Science of Running

Genetics of sport- Does Doping change genes?

2013-02-17T15:47:00.002-06:00

Genetics of sport- Are we searching in the wrong places?

The topic of genetics of endurance sport is a fascinating one. For as long as I’ve been a competitive runner, the question of whether nature or nurture gave rise to the pocket of dominating distance runners in East Africa has been around.

Researcher Yannis Ptisliadis exemplifies this search. In an article last year, he was quoted as saying that, 10 years ago he would have said that East Africans were better because of genetics, but now he’s not convinced. His change of heart was the result of his group, and others, trying hard to find some genetic difference that some of the best Kenyans and Ethiopians had but finding only minor associations that didn’t fully explain the phenomenon.

So, is it right to conclude that there are no or very little genetic reasons for success in elite East African runners?

I’m not a geneticist, or anything close to it, but a few years ago the field of epigenetics really caught my eye. Epigenetics can be best summed up by the analogy by Dolinoy et al. (2007) that “if the genome is compared to the hardware in a computer, the epigenome is the software that directs the computer’s operation.” It’s best to think of epigenetics as a mechanism to up-regulate or down-regulate gene expression.

The fact that a variety of stressors could actually affect gene expression was fascinating. I’ve delved into the topic a bit elsewhere, and even threw out some rough hypothesis on whether maybe that East Africans due to living at altitude, high activity levels, a different nutrition, etc. could affect things on an epigenetic level to create a perfect storm that results in being predisposed to distance running success.

A fascinating review article by Ehlert et al. (2013) entitled “Epigenetics in Sports” helps clear up the picture on genetics and elite sport, and how epigentics may play a role. I highly recommend you read it for those interested (and at least some knowledge of genetics, as it can get kind of confusing), but I thought I’d highlight some of the more interesting parts and talk about it’s implications.

The problem with association studies:

The review starts by laying the foundation that researchers are working on a broken premise. The idea that we can search for single or multiple genes that influence performance is too simplistic. The way most studies work, is they look at a wide variety of gene candidates in both an elite grouping and a control grouping and see if they can find any standouts. So it’s essentially a comparison, where we take elites and a control group and see what is different.

The general consensus on single gene and multiple polymorphisms is inconclusive at best. When I was in school, the big thing initially was the ACE gene for endurance. The problem is after the initial study, duplicate studies failed to collaborate the finding (rankinen et al. 2000). The same goes with multiple gene association studies. Ehlert et al. make a pretty thorough case for the multiple limitations association studies have, which I suggest you read, but the easiest and simplest is to look at the search for the genetic component of Diabetes mellitus. They point out that research has been extensive and there have been many large scale genome-wide association studies. They’re not saying it’s not valuable research, but rather that using a similar design in smaller scale to a complex problem might not be the best route.

So are genetics not the answer?

Ehlert et al. outline the premise that genes play a role but it’s not that simple. Instead epigenetic processes cloud the picture.

I’ve outline epigenetics before here if you want a refresher:

http://www.scienceofrunning.com/2010/09/epigenetics-in-athletics-part-1-what.html

The epigenome essentially modulates gene activity, acting as a semi-permanent up or down regulator for genetic activity. I look at epigenetic modifications as a way for your body to make subtle changes for the environment. A large number of these changes happen during fetal development.

So, the classic studies I remember from grad school were when a mother went through a traumatic/high stress experience during pregnancy (such as 9/11 if you were in NY) then the baby has a hyperstress response and chronically high cortisol levels throughout their life. Another quick classic example would be if a mother goes through famine during pregnancy, then there was an increase risk for obesity and food related diseases. The theory is that when these stressors are applied to the mother/child the developing baby gets epigenetic changes to prepare for its environment essentially. So, if there’s famine, certain genes are up/down regulated, which might make the baby more susceptible to obesity or diabetes when food is plentiful.

What’s really interesting though is that, epigenetic changes are present throughout life. Fraza et al. (2005) compared sets of twins and found that twins epigeneomes were different based on their lifestyles.

Researchers have started using rat studies to see how nutrition during development or early childhood and/or behavior affects the epigenome. So far there have been studies showing protein restriction, high fiber diets, high folic acid diets, and a slew of others all cause epigenetic changes that can affect life expectancy, disease risk, etc.

Taking it a step further, there is some preliminary evidence that performance is a partial result of an altered epigenome. According to Ehlert et al. Terruzzi et al. found that in a group of elite athletes several epigenetic changes were significant. Similarly, short term studies have shown that training effects DNA methylation. In fact, a recent journal article on the famous ACE gene claimed that “Epigenetic regulation of the ACE gene might be more relevant to endurance physiology than the I/D polymorphism”

(http://jap.physiology.org/content/early/2011/11/21/japplphysiol.00828.2011.full.pdf+html)

Based on these findings, Ehlert et al. make the case that training, diet, and lifestyle should have large impacts on the epigenome.

Implications for performance and athletics:

Lifestyle, diet, and training may play a bigger role in causing changes on the epigenetic level than previously thought. While, researchers are still at the beginning stages of figuring this puzzle out, and it is entirely possible that there is another layer of complexity beyond this, it’s still exciting to think about.

Nutrition:

The fact that animal studies have shown that manipulating certain vitamins effects methylation of DNA is intriguing. It adds a whole new level of complexity to diet and nutrition. So far, research has shown that diet plays a large role during development stages. For example, research by Pemrey (2006) shows that overeating during developmental years (8-12yrs old roughly) might impact type 2 diabetes likelihood epigenetically. How much a role it plays epigenetically beyond that is anyones guess at this point. The question arises whether your mom eating a certain diet or taking certain vitamins impacts how well you process carbohydrates or fats could be huge for performance.

Thinking in terms of east Africans, does a diet very high in sugar generally give some sort of advantage for running?

Doping:

A very interesting topic was raised in Ehlert’s paper on the use of performance enhancing drugs and epigenetics. In the review, they mentioned several studies that showed that giving animals various hormones effected the epigenome. The most studied so far have been Growth Hormone, IGF-1, and anabolic steroid administration in rats. What is crazy, is that the studies found that administration of these hormones caused epigenetic changes that could potentially last for a long duration.

The implication in humans is that if you are doping, the acute effects might be gone after your 2yr ban, but the changes at the genetic level still persist. Meaning even off the juice, an athlete might be benefiting from his prior use. (After all, other rat studies have found an epigenetic impact on fiber type development).

It’s pretty scary to think about that hormones not only used for their acute benefits of recovery, repair, or muscle growth, might cause permanent genetic changes.

Training:

While it’s more of scientific than practical interest, it seems like training should cause epigenetic changes. So instead of simply breaking down the training adaptation process into signaling pathways and the like, it might be possible to look at DNA methylation for instance to see what effect different training regimes have on the epigenome.

Altitude:

We know that there are several different blood response patterns to altitude (various groups show different adaptations in terms of hemoglobin and hematocrit to altitude), so is it possible that some of this is partly epigenetic? What role does being born at altitude have over a life time. Or better yet, does exercise at altitude during the developmental years cause some epigenetic change. No one has the answer yet in terms of athletic performance.

Researchers are beginning to look at epigenetic changes to low altitude (http://www.xtreme-everest.co.uk/article.php?article=847) so it’s a matter of time before more research comes out in terms of endurance performance.

So What?

It’s an interesting new realm. The take away is that genetic studies aren’t the be all end all and once again it’s a very complex process. It’s not an either/or question.

So if you are asking if the East Africans are genetically superior, the answer is perhaps partly. It’s not the simple answer that researchers set out to find a decade or so ago. Instead, like everything, it seems to be a combination of genetics, epigenetics, lifestyle, and training.

It also means that genetic testing for athletic performance, which a lot of companies are starting to jump on, is probably useless.

Ehlert study:
http://www.ncbi.nlm.nih.gov/pubmed/23329609

My interactions with Lance Armstrong

2013-01-16T15:59:00.000-06:00

With Lance Armstrong's confession being the major news item of the moment, I figured I'd throw my two cents in and give my perspective. I had a short interaction with Lance when I worked with Nike. Essentially we had to help Lance with his running form and training a little as he transitioned into triathlons.

It was an interesting experience, given how much I despised drug users, and looking back enlightening. Why? Because it gave me a brief glimpse into why people might have chosen to bury their head in the sand instead of facing the facts presented before them. This continual burying of heads is what kills fair sport. It's not just the athletes, but also the media, journalist, fans, coaches, and perhaps most importantly agents and sponsors. I'm not sure if there is an answer to the problem of doping.

But I would start with a radical departure that might include taking aim at those who control things and have power.
-Doctors- any doctor supplying an athlete be banned from working with athletes in that sport (if an athlete is caught working with him, he gets banned). Work with US govt. to maybe make it a hit on their medical license.
-Sponsors- Right now it doesn't matter if athletes dope to sponsors. If they run well and don't get caught, great. If they get caught, then they just distance themselves and don't take a hit. Create penalties that if the sponsor knows, they get fined X dollars. If a coach the sponsor pays has athletes busted, make it where there has to be an immediate termination of that coaches contract.
-Coaches- Have a rule against coaching drug users. If someone you coach tests positive, have a consequence. If you get to 2 or 3 athletes who have tested positive, ban from coaching.
-Agents- Similar to coaches. Have them take a hit if there athletes test positive.

Basically, create consequences for those beyond the athletes. Just some quick thoughts.

You can read the full article on competitor.com below:

http://running.competitor.com/2013/01/news/magness-my-interactions-with-lance-armstrong_64596

Long term development: Coaching HS, college, and professional runners

2013-01-04T17:00:00.002-06:00

I was fortunate enough to give a presentation for the Gulf Coast Scholastic Track Coaches Association Clinic this weekend. In the talk, I focused on the keys to long term development. I don't like giving generic talks on training, so my hope was to explore some of the differences between coaching at different developmental ages. I use HS, college, and Pro to classify, but it's really tailoring training to their actual "training age". I've posted the power point presentation below, and hope you enjoy it.

Clinic.

Long term Developement in Distance runners from sjm1368

What do Orthotics and shoes actually do? Looking at data from a professional runner

2013-01-02T12:49:00.003-06:00

Often times in research we focus on norms. We look at the average effect of different interventions and then apply them to everybody. In this way, as a whole we get what the effects are for most people. By doing this, sometimes we miss the individual effects. So in today’s first blog of 2013, I want to share with you some data on the effects of running shoes on data with one individual athlete, Jackie Areson, who runs professionally for Nike.

In this data, what we did was stick her on a treadmill running at the same speed for every trial and set up my poor man’s high speed video analysis system (Casio Exilim + free motion analysis software), and took side and back views of her running. What I was looking at was a comparison of shoes impacts on her mechanics. Using barefoot as the “normal” and comparing from there. We looked at all sorts of different Nike shoes (because that’s her sponsor), her old shoes she trained in in college (Brooks Ravena) and then just for the heck of it, each shoe with custom orthotics and without custom orthotics (she does NOT wear them) to see the effects orthotics had on her mechanics.

So what you'll find below is a chart comparing I’ve included pictures below for you guys to take a look at that give a good indicator of things and includes a few other shoes not included in the chart (because remember, this data is analyzed the old fashioned way so it takes a while to analyze it all!).

		Pronation	Pronation	Footstrike
	Orthotics?	change	Change (deg)	Degree	Ground Contact	Flight Time	Footstrike	Heel-toe drop
Lunar Fly	NO	7	10	93.6	0.214	0.114	whole	10mm
Lunar Fly	YES	7	9					10mm
Katanas	No	9	10	92	0.195	0.128	midfoot	4mm
Lunar Racers	No	9	13	93.4	0.2	0.123	whole	7mm
Lunar Racers	YES	9	11	98	0.209	0.119	Heel	7mm
Pegasus	No	8	10	100.7	0.214	0.104	Heel	12mm
Pegasus	yes	9	11	101.6	0.214	0.109	Heel	12mm
Vomeros	Yes	10	12	96.5	0.204	0.114	heel	11mm
Barefoot	No			93.8	0.195	0.119	forefoot	0mm

Footstrike degree- 90deg= knee and ankle of foot are at 90deg angle. So greater the degree, means further out ankle is in front of knee at footstrike.
(Heel toe drop is using data from outside sources, not measured)

Pictures of shoes at footstrike- NO Orthotic on left. Orthotic on right (except for Nike free, Katana, and streak XC- NO Orthotics on those)

What did we find with Jackie.

1. Orthotics almost always switch to a more pronounced heel strike (probably for a few reasons- They add weight, bulk, and increase the heel to toe drop.

2. Orthotics don't decrease pronation really, and don't have a uniform effect across shoes. They tend to change things in different degress.

3. Footstrike is greatly influenced by shoe type. It's hard to pick out definite trends, but the less heel-toe drop the more likely she lands forefoot or mid/whole foot. Additionally, the lighter the shoe the more so. Interestingly (and the data isn't up there) but for some reason she lands more whole foot with the Brooks Ravena then with comparable shoes in terms of heel/toe drop and weight. My guess is because of the high toe spring changes her loading/landing pattern (because at this period of time, she protected her past foot injuries by not "pushing off" her big toe.) Also, the contrast between flats and shoes is remarkable.

4. Using the simple measure of ground contact time tells you how minimal a shoe is. It's a kind of "duh, that's obvious" conclusion, but a simple measure of comparing barefoot ground contact time versus shoe GC might be a useful measure. The difference (at the same speed) could give an indicator of how much the shoe "interferes". So maybe a simple yet effective measure might be change in GC with each shoe? (Just hypothesizing but how cool would it be to go to a shoe store and run barefoot, get a GC, then compare shoes effects on it, instead of doing pronation junk?)

5. Pronation- It varies. And having junk in your shoe to stop it really didn't do much at all for Jackie. (and yes, pronation is natural, I just included in this analyse because it's easy to measure, everyone measures it, and I wanted to show the effects shoes had on it...)

Hopefully this data makes you think a little bit and gets you to see the individual differences that shoes create.

Anybody notice any other trends?

Revisiting Singles vs. Doubles- This time with Mice

2012-12-03T12:31:00.001-06:00

Back in the day, the importance of a distance run was thought to be that of putting constant pressure on the heart so that it will adapt. In other words the theory went that you wanted to keep your heart rate up for a prolonged period. So the logic went, the further we can go the better.

What we now know is that adapting to training is a super complicated process that involves numerous different adaptations on multiple different systems. So is it as easy as more is always better? I’ve delved into this question many times in regards to doubles versus singles. By the old school logic, singles should always be better. It makes logical sense that 10 miles once is better than 5 miles twice. But as I pointed out before, that logic isn’t always sound. It’s one of my favorite topics to delve into (more here) and it’s always worth looking into.

An interesting new study came out where they took a look at the effect of one 30min run versus 3x10min runs throughout the day in mice. It’s not quite your doubles versus singles argument, but it’s an interesting concept.

What makes the research a bit more fascinating (and also harder to translate to real world application) is that it was on mice, which means they could dissect and analyze all sorts of things that we normally can’t see. We get to see what is going on at the cellular level instead of relying on crappy surrogate markers like VO2max.

What they did was take mice and stick them on an 8 week treadmill training regime. Half the group they had do 30min a day all at once 5x a week, while the others did 3x10min split with 2 hours rest in between. Then they measured all sorts of lovely signaling pathways activation to see what was going on.

What did they find?

1. Performance- Pre and post training Each group improved their distance covered from 224 to 464 (30min) and 217 to 471 (3x10min), speed, and work to similar levels.

2. Capillary- Both groups had similar increases in capillarization. No significant differences between the two groups.

3. Pathways- Citrate Synthase activity increased in both groups to similar levels and VEGFR2 increased similarly in both groups. Slow Twitch fiber % increased in both. TSP-1 decreased by 50% in the 30min group and 68% in the 3x10min group. P38 MAPK increased similarly in both. Figures 2-3

What do these random letter combination things mean?

VEGFR2 refers to one of the receptor for vascular endothelial growth factor (VEGF-A) which is basically one of the regulators for capillarization. TSP-1 is the protein that essentially works in contrast to VEGF-A. So if you get a decrease in TSP-1, you generally get an increase in capillarization. So taken together, increase in VEGF and decrease in TSP-1 in this study meant increase in capillaries. P38 MAPK is involved in the PGC-1 pathway which regulates mitochondria proliferation among other endurance related changes.

So what?

Yes, it’s only mice. But what is interesting about this study is that you saw similar increases in performance, capilarization, and mitochondrial biogenesis. This would run in the face of the old school running/training thought process. It doesn’t mean everyone should get out and start training three times a day and never run far. What I think it does do is give just a little more evidence for why doubling (or maybe tripling?) may work. And before I get crucified by the old school singles are king people. All I'm saying is that maybe each has their place and this study simply adds intrigue to the idea.

In my own coaching, I’m a big fan of the occasional even split short double for recoveries sake and if studies like these are to believed you’re not really missing out on the stimulus for adaptation. Just judging by past experience that was always my feeling with the high school kids I used to coach ( Running Times article here) We’d do singles for the most part in the summer and then doubles during the school year because there were only so many times you could run around the boring loop at school without wanting to kill yourself.

What I found was that endurance was maintained as long as they had a single long run on the weekend.

So what’s that mean? I have no idea. But maybe to build endurance we go with singles and shift to more doubles which are easier on the body for maintenance. Then the question gets asked about other forms of exercise or what is the effect of doing cross training as a shakeout or a shakeout after a workout, or on and on. So many questions, so much to figure out.

Periodize your easy runs? Maybe. Most of the time we just ignore easy/distance runs and don’t put much thought into them. Maybe it’s time to.

References:

Malek et al.(2012) Similar Skeletal muscle angiogenic and mitochondrial signaling following 8-weeks of endurance exercise in mice. Discontinuous versus continuous training. Experimental Physiology

Waters RE, Rotevatn S, Li P, Annex BH & Yan Z (2004). Voluntary running induces fiber typespecific angiogenesis in mouse skeletal muscle. Am J Physiol Cell Physiol 287, C1342-

1348.

A Scientific look at Viagra enhancing endurance performance? No, not that kind, actual running performance…

2012-11-29T15:09:00.001-06:00

Chicago Bears wide receiver Brandon Marshall made a little bit of noise in the news when he said:

"I know guys, it's such competitive league and guys try anything just to get that edge…I've heard of guys using Viagra, seriously, because the blood, it's supposed to thin . I don't know. Some crazy stuff. It's kind of scary with some of these chemicals that are in some of these things, so you have to be careful."

(http://www.newsday.com/sports/football/bears-wr-brandon-marshall-heard-of-players-using-viagra-to-gain-edge-1.4275134)

Which led offensive coordinator Mice Tice to comment: “"Viagra? I've never heard of such a thing. He's making that up. He's got to be making that up. You've got to be kidding me."

So, where did this all come from?

Well, if you've been reading this blog for a while, you might remember I called the Viagra improving performance thing way back in 2009 when I was some kid in grad school making crazy guesses on stuff (not much has changed…) (http://www.scienceofrunning.com/2009/09/complex-to-simple-beware-of-gurus-and.html)

The first study came out in 2006 by Hsu et al. and found significant improvement in a number of factors. That was in the research world. In the real world, people seemingly caught wind of it’s effects as can be seen by this nice little clip of the British TV show Top Gear from 2010:

But does it work and what’s the deal?

Viagra actually got it’s start as a performance enhancer at altitude. The simple idea behind it was that it causes pulmonary vasodilation, so the thought was that maybe this effect would help increase endurance at altitude under hypoxic conditions. The theory is that you’d prevent a drop in Oxygen Saturation levels and get a nice bump in Cardiac Output. So in essence, Viagra would mitigate the effects of high altitude/low oxygen levels.

So what does the research say?

The first thought of using Viagra for exercise adaptation started with a study that looked at taking it during a Mt. Everest ascent. They found that about half their group saw significant improvements in performance and cardiovascular performance markers while making the ascent. The aforementioned 2006 study took the idea to the next level and found that at simulated altitude (12.8% O2 or about 3,900m altitude) taking Viagra beforehand improved performance on a 6km time trial by 15%, improved stroke volume, cardiac output, and O2 saturation levels. Sounds good right?

Well more recent studies have found slightly different results. A 2011 study by Kressler et al. looked at the effects with more moderate altitudes. They compared 3,900m, 2,100m, and sea level. What did they find? At high altitude, it helped with oxygen saturation numbers, keeping them higher during a 15km time trial and a steady state exercise, but other than that Viagra had no effect on any of the performance measures.

Similarly, another study by Jacobs et al. (2011) looked at Viagra and performance at 3,900m altitude and found similar results. This time they took endurance trained men and women and put them through a 6km time trial. No significant change in performance and only a difference in Oxygen Saturation levels (in women only). However, they did find that some people had significantly greater performance (one male improved by 36sec for example)

So what the heck is the deal? Does Viagra work or not?

Responders and non-responders:

Of course the answer isn’t that simple and once again we’re brought back to a common theme: individual variation.

If we go back to the original 2006 study, although the group as a whole improved significantly, what they actually found was that they had two groups. One improved performance by an average of 39% and one improved by an average of 1%!

That’s kind of a big difference. Similarly, if we look at the 2011 study, they noted that there were outliers who had very significant improvement.

The reason is simple. At high altitude, each person’s limiter is different. Viagra seems to aid in one specific area. If that area is your limiter, performance will be improved. If not, well too bad. For example, if you compare me and Jackie Areson’s oxygen saturation levels at different altitudes even with just sitting there and not exercising, you can see our bodies response/compensation to altitude is completely differently (and yes, it’s a fun thing to do…Just sit in an altitude tent for a few hours with an O2 saturation thing on your finger J).

Altitude (Feet)	Steve O2	Jackie O2

3200	97	98
4400	96	98
5100	95	96
5900	94	96
6500	93	96
7100	92	95
8000	90	94
8200	88	94
8800	85	93
9000	84	93
9900	81

So what causes the difference? No one is entirely sure but a couple notable things are of interest. First, in the 2006 study, they found that responders tended to have lower O2 saturation levels. That makes sense because if we look at the studies and see that Viagra generally increases O2 sat levels, then it makes perfect sense that those who naturally respond to altitude with lower O2 sats might get a boost in performance if those levels don’t drop as much. Along similar lines, there’s been lots of research showing people susceptible to high altitude sickness “experience greater pulmonary vasoconstriction and exaggerated increases in Ppa when exposed to hypoxia (Hsu, 2006).”

So…Does Viagra improve performance?
At very high altitudes? Possibly, depending if you are a responder or not. If you want to take a wild guess if you are a responder or not, measure O2 saturation at high altitude and see if you are comparatively low or not.

At moderate altitudes like those which runners might actually train at or someone like Brandon Marshall might play at in Denver? Doubtful unless you have severe Exercise Induced Arterial Hypoxemia.

At sea level? Doubtful son.

So…all those NFL guys taking it. Does it work for them? I’m going to be very doubtful. They don’t play at high altitude. They might get some ummm interesting side effects which NFL players probably don’t need, but a performance boost? Doubtful.

What's interesting about this to me is two things. First, how athletes will take almost anything if there is a hint of it improving performance. I wonder how it spread to the NFL actually where very few games are played at even moderate altitude. Secondly, it's another perfect example of individuality of response. We all have different physiological limiters, thus why we can't all train the same way and expect to improve...

And lastly, did I really just write an entire article on investigating the performance benefits of Viagra?

References:

http://jap.physiology.org/content/100/6/2031.long

http://www.ncbi.nlm.nih.gov/pubmed/21451938

Stimulus and Adaptation- A complex and simple look at the training process

2012-11-21T13:21:00.001-06:00

I’m going to be a bit ambitious here and try and break down the process that is training. If you read my last post on stress, hopefully you realized the myriad of factors that might affect training and adaptation. What I want to try and potentially accomplish is to break that process down and look at each segment. I’ve been giving up on these post for a few weeks. It’s frustrated me because it’s something that’s hard to wrap your head around, but here’s my best go of it.

When I was in grad school, my advising professor, Jason Winchester, had us write a paper where we took a certain type of training applied to a person and then take it down to what that would do down to the genetic level, and then back up to what kind of functional change would occur. You can get incredibly complex doing this method, but the point of the exercise was to know that we don’t just go from lift weights to increase in muscle size. There’s a process that the body goes through. The basic gist of the process is summarized by the nifty chart below:

The point is that it isn’t as simple as simply going to do a workout and then getting better. Your body follows a process of adaptation. So the stimulus is applied, homeostasis is disturbed. When homeostasis is disturbed messengers get sent that trigger a signaling pathway. If the pathway is activated enough or repeatedly, it will eventually translate into a genetic response that if that gets triggered enough results in a functional adaptation.

In this model what we need to know boils down to:

1. The training adaptation we are looking for.
2. What stimulus leads to that adaptation.
3. What does the training stimulus trigger?
4. What pathway is activated?
5. What translate that pathway activation to actual response?
6. How much “activation” is needed until we translate that to a functional adaptation?
That’s a heck of a lot to know. What’s the point right? It’s overly complex…Well, let’s address that shortly.

So if we look at altitude training as an example:

Stimulus- Training in a hypoxic environment

Messenger- Reduced O2 levels in blood and muscle

Signaling pathway: Hypoxia inducible factor (HIF-1) is activated.

(From my lit review) HIF-1 is a main oxygen homeostasis regulator in the body. Two subunits, HIF-1α and HIF-1β, make up the HIF-1 complex. Under normal conditions, HIF-1β is present, but HIF-1α is constantly being degraded by the proteasome (Dery 2005). When oxygen levels are lowered, the degradation of HIF-1α is inhibited, this stabilizes HIF-1α. The stabilization allows for HIF-1α to bind to transcriptional co activators and enter the nucleus of the cell. Here, HIF-1α binds to HIF-1β, forming an HIF-1 transcriptional complex (Marzo et al. 2008). This HIF-1 complex then binds to the Hypoxia Response Element (HRE) on the EPO gene. This in turn leads to EPO expression (Stockmann et al. 2006).

Genetic Response- EPO expression occurs. Eventually results in EPO production

EPO then needs to be transported to and bind with EPO receptors. EPO receptors can be found on erythroid stem cells in bone marrow (Marzo et al. 2008). The binding to the receptor on the cell membrane results in a signaling cascade that results in the activation of the transcription factor STAT-5 and two enzymes, PI3K and MAPK. These enter the nucleus and induce transcription of specific genes that result in the inhibition of apoptosis, programmed cell destruction (Marzo et al. 2008, Jelkmann 2004). The end result is that this prevention of destruction of developing RBC results in an increase in RBC.

Functional Adaptation- Increase in Red Blood Cell mass which results in increased endurance

Now before you jump on the “too complicated” bandwagon, let’s step back for a second. I’m going to make the notion that the above chart, and understanding its implications is paramount for success. BUT, I also think you need to be able to simplify it to be useable. So let’s step back and go through the process of dissecting the above chart.

Starting simple:

When I was talking to my college team at Houston the other day I basically summarized training as a process of stimulus and adaptation. That’s it. Training can essentially be broken down into those two parts. You apply a stimulus and your body adapts. How your body adapts depends on the stimulus applied. So we can take that chart above, take out the middle three and you get:

Stimulus-> Adaptation

What you’ve essentially done is take out the mess, and make some assumptions.

1. We assume that the person follows a normal route of adaptation.
2. We assume that the recovery is correct and long term adaptation takes place

What we need to know:

1. The training adaptation we are looking for.
2. What stimulus leads to that adaptation.
a. How much is enough?

Essentially our goal is to figure out what we are trying to accomplish and then what it takes to accomplish that goal at this specific time with that person. So it’s rather simple.

As an example, let’s say my goal is to increase aerobic support for a 5k runner. So I might want to increase his lactate threshold. That’s the goal. So let’s take Tommy Schmitz as an example and say his last tempo run was 4miles averaging just below 5:00. Now, I might give him 5miles going 5:10,5:05,5:00,4:55,4:50.

Why? I’ve increased the distance a bit, made it progressive so he starts just slower than threshold and ends maybe just faster. It’s a new stimulus. If everything goes well, he’ll increase his endurance in that specific fashion.

Simple enough. Know what you are trying to do and what it takes to accomplish that goal. This is the basis of coaching. Apply a progressive stimulus to get a desired adaptation. A heck of a lot easier than knowing what signaling pathway results in some gene activation that might do something nice.

Assumptions and external factors:

So far we've stuck with dealing with the idea that all that matters is the training stimulus. You apply that correctly and this cascade of events occurs. You make the assumption that X translates to Y. We’ll call this the set it and forget it model. But…what really happens is that along that way from stimulus to adaptation a crap load of stuff needs to take place. So now what we look at now is “interference and synergist” for the stimulus and adaptation.

Basically, what things help or hurt the process. They can help or hurt at any level along the way. And this is why the complex model is needed. The complex model gives the basis for understanding why external factors impact adaptation. When we use the simple model we are saying do X workout, get Y result. When we look at the complex model, we say oh crap, lots of stuff can go wrong. If you know the basic underlying process for the complex model it allows for better creation of training and less risk of error.

Let’s first look at some of the factors that can influence the process and (a few) examples.

1. Arousal and emotional state- Since my last post was about stress we will start here. First stress affects adaptation. I’ve covered it. Secondly, arousal state before and during a workout can affect the adaptation. How? Get our adrenaline going and it changes the degree of stimulus a workout is giving. Get lots of adrenaline and the lactate response changes, the CNS activation of muscle changes, and so on.

2. Nutrition- Nutrition impacts everything.

a. If we take in carbs before a run, it changes the fuel utilization of that run.

b. Take carbs in the middle of a long run we’ve just switched the stimulus from the goal of running the body low on fuel so it adapts, to now running long at a quicker pace while maintaining fuel levels.

c. Take protein and/or carbs after a workout and we’ve just changed the recovery process and protein synthesis within the workout. Don’t take it and recovery differs.

d. Building blocks for adaptation- If you don’t have the iron or protein or whatever necessary ingredient is needed, full adaptation won’t take place.

3. Environmental factors

a. Working out in a hot environment? Muscle recruitment from the very start is changed. The limiter changes now too.

b. Doing hills? Muscle recruitment changes. A strength component is added and a decrease in reliance on elasticity happens.

c. Working out on soft grass? Bye bye elastic component of your stride and hello reliance on more “work” instead of “free energy”. Muscle tension is changed as well. Thus now biomechanics change and your neural adaptation to running on grass changes.

4. Recovery

a. Nutrition recovery changes adaptations.

b. If you take some NSAIDS

c. How much you sleep effects the cementing of the learning process (i.e. reinforce any biomechanical/skill changes), the hormonal state (testosterone, HGH, etc.), and protein synthesis.

This is just a smattering of examples and there are countless others. It’s not meant to overwhelm but rather to give you a scope of the issue.

Now, where can these things impact the process?

1. Stimulus application- Stress, anxiety, arousal state, CNS activation, nutrition- All these things can impact the stimulus of the workout. They can either increase or dampen it down.
2. Conflicting pathways- There’s an interplay between many signaling pathways. So the classic one is between AMPK and mTOR. If one is activated, it impacts the other. Thus why if you are trying to get muscle hypertrophy and you go for an aerobic run right after lifting heavy weights, you just dampened down the training effect of the heavy weights. Why? Pathways interact.
3. Not enough adaptation reserve- stress, recovery, sleep- We only have so much room for adaptation. If outside stress decreases your adaptation reserve, guess what, less adaptation to your workout.
4. Translating to functional adaptation- nutrition, protein, building blocks- You have to have the building blocks to translate to permanent adaptation. If protein synthesis isn’t there, you aren’t going to rebuild muscle. If iron is too low, you aren’t going to make new Red Blood Cells.

So how much does the little stuff matter? Some examples:

Caffeine- Central Nervous System stimulant- changes motor recruitment a little. Manipulates central governor/pain perception. So now you are “amped” for every workout. Now you are going above and beyond in every workout. What happens? There’s a mismatch between the feedback your body is giving and the actual stress. You’re able to go to another level and your body doesn't think it’s that hard because of the artificial enhancement. Do this repeatedly enough and it might hurt you a bit or you become habituated to the artificial levels. That’s why I say save the caffeine for when you need it.
Antioxidants/NSAIDS/etc.- Impacts training stimulus/messenger and adaptation. If the messenger is increase in free radicals, then would taking something that eliminates that stimulus for adaptation be good? You’ve dampened down the stimulus.
Mouthwash- This is one of my favorite examples of why little stuff matters. Beet Root juice is the new in vogue performance supplement of choice. It increases performance/endurance and since all you have to do is drink a lot juice and the only side effect is your pee might be get a little. Well, take some mouthwash before/after that beetroot juice and what happens? The beet root juice doesn’t work because the mouthwash gets rid of key bacteria needed for the process to work

How do you know what helps or hurts the adaptation process?

1. Research- read journals or my blog
2. Reason it out- Use the chart above and if you know the process you can take an educated guess if something might dampen down a stimulus or retard adaptation.

So what?

Now that I’ve overcomplicated everything, what’s the point? The goal of the coach, athlete, scientist, whomever, is to know when to go complex and when to go simple. The human body is incredibly complex. I spend waaaayy too much time looking into all this science junk because it intrigues me and I still get lost.

So my point in trying to dissect the training/adaptation process in two contrasting models was to reinforce the idea that you have to know when to go complex and when to go simple. You have to have the ability to do both and more importantly know when.

In the world of coaching, I try and figure out the complex. I use that signaling pathway junk whenever I’m asking what I think a new type of workout will do. Once I figure that out, and I think I have a good handle on the workout, then it shifts to the simple model. I’m always trying to simplify, but you have to understand the big complex junk before you can get to that step.

Use the models, come up with your own, be creative. The point is to understand what happens along the route of workout to improved fitness.

In simple terms this should guide your program. You need to know what you’re trying to accomplish and how to get there. That is the key to coaching.

The Stress of Life: How stress can impact your workout

2012-11-06T14:05:00.001-06:00

The Stress of Life:

Adaptation is a fairly simple process. You apply a stimulus, or a “stressor” to the body and it adapts. Go lift weights, break down some muscle, and your body responds by making the muscle stronger. The actual process along that path is very complex and we’ll go into that shortly, but really training and adaptation is as simple as that. Stimulus-> adaptation.

As coaches, we obsess over the workout part. We carefully plan what needs to be done and when it needs to be done in order to get the adaptations we want. We know when to apply that threshold run to get a generalized aerobic stimulus or when to start those 400 repeats to cover the other side of the spectrum.

In fact, the entire coaching profession is based on the assumption if we give a workout and give enough recovery, then they’ll adapt.

That’s generally a safe assumption to make, and often times it comes true. If something goes wrong, we generally think, oh we pressed it too hard and they couldn’t adapt, or we didn’t give them enough recovery, and so on. After a while, as coaches, we get a handle on how much someone needs to be pushed and how much they need to recover to continue along the path of gradual adaptation.

But…are we missing part of the picture?

We control everything that is running related, but that creates a situation where we tend to think in isolation. If we give X hard workout on Monday then follow it up with maybe a shorter easy run on Tuesday and Wednesday, then we’ve covered the hard part and the recovery part. Everything should be good. But what about life outside of running?

General Adaptation Syndrome:

The concept of stress wasn’t always as prevalent as it is today. A Scientist named Hans Selye essentially formulated how we respond to stressors and thus paved the way for us exercise nerds knowing how to program training based on adaptation.

He stumbled upon doing a lot of experiments on some mice and applied various stressors to them (think heat, cold, poking and prodding, etc.) and found that no matter what the stress, there was a generalized response to them. So the body had a sequence of events that it went through no matter the stressor. This and a bunch of other studies gave rise to the concept that we respond to stress in a certain patterned way. So, regardless of what the stressor is, there’s a generalized response that accompanies the specific response.

Most people think of this in terms of physical stressors only. But the reality is that your body is programmed to respond in similar ways to mental stressors too. So, you get mentally stressed out, your cortisol levels jump, you’re on edge and your sympathetic nervous system is firing more, just to be prepared.

Adaptation to workouts:

As coaches, you know there’s only so much each athlete can handle in terms of volume and intensity. These are your stressors in training. If we go over some amount for each person, they’ll “burn out” and performance will suffer because they simply haven’t adapted and absorbed the training. The key concept to remember is adaptation. We have to be able to adapt to the stressors.

What Selye found is that if he removed the stressor soon enough, the mice would adapt and become better able to resist that stressor. If he left that stressor there too long, in many cases the mice would die or become less resistant to that stressor. So the key was giving them enough of a stressor to adapt but not too much.

Tieing it all back together now, if we have our running related stressor (workouts), and we apply that at the same time as when some other stressor is going on in our athletes life, will he have enough room for adaptation?

The answer is sometimes no. You only have so much “stress” you can adapt to. And as we learned earlier, there is a general response to stress so that there is overlap between doing 4x1mile repeats and being stressed because your boyfriend just dumped you or you are about to take a mid term. Prepping for that mid term gives you many of the same stress responses that you had in prepping for that workout. So if we got both going on at around the same time, we’ve got your body trying to adapt and handle two different stressors.

If it’s too much for you, your body won’t adapt to the workout. Even if the workout in itself wasn’t too hard, when it’s combined with something else that is a stressor it might push you over the top.

In essence, your body only has so much it can adapt to. It’s best thought of as an adaptation reservoir. You have so much “energy” you can use to adapt and handle different stressors. If you use up the reservoir, it’s depleted and you won’t adapt until it’s filled up again. So if we go and do that hard interval session in the middle of finals and our athlete maybe just broke up with his girlfriend and is generally freaking out, will he adapt?

Where’s the science?

A recent research article by Ruuska et al. (2012) examined what happened when they took a group of untrained adults and put them through a very specific and controlled aerobic exercise program for 2 weeks. They tried to control the workouts so they were all at 75% of their max HR and for the same duration. They also gave them a stress questionnaire to see what their levels of stress were during this 2 week period. After the training, they measured a slew of physiological variables including the traditional VO2 kinetics, but also performance variables such as power output.

What happened?

The change in performance variables was a little as no change all the way up to a 40% increase. The level of improvement in both Vo2 and power output was associated with stress level, meaning that the lower “stress” levels they had, the more they improved. So for all the individuals who had a lot of stressors in their life, had no or very minimal changes in fitness. They didn’t adapt.

But, that’s not the only study that shows this association. There have been several studies that have found HR variability, which is used as a surrogate marker for the state of the CNS(Central Nervous System), associated with training response (Tulppo et al. 2003).

More Science

If you comb through the research you’ll start to notice that several stress or stress buffering hormones or markers all relate to adaptation. For instance, another few studies mentioned in the Ruuska et al. piece showed DHEA-S has been associated with whether there was a training adaptation in elderly adults, with people low in DHEA-S (which acts to counteract stress in many ways) not showing improvement in fitness (Huang et al. 2006).

A study by Lee et al. (2006) found that DHEA-s was related to adaptation to altitude.

Why is this interesting?

Because if we looked at adaptation to altitude for a few of the elites I've worked with, they did not show positive adaptations in blood markers or in training if they had high cortisol levels going into and during altitude. So the higher the cortisol levels, the lower increases in Hemoglobin or RBC mass on several athletes. This was a somewhat common theme, and with some I had to really get creative in making sure to knock down the stress or to up their nutritional support to make sure they could adapt.

Altitude in itself is another stressor (so you get the same generalized stress response) so when you combine it with someone who already has a high stress level (high cortisol) and/or low stress buffering (low DHEA-s) you’ve got to change something or else they won’t adapt.

Just a hunch, but I’ve thought that part of this high/low responder to altitude thing is simply a stress response thing. So, word to the wise if you go to altitude, check cortisol and DHEA-S or Testosterone before you go!

What does this practically mean?

1. Pay attention to what goes on outside the training world. I know this is crazy hard to do in the high school or collegiate world because there is always stress on students, but be aware of it and feel free to adjust if needed as a coach.

2. Individualize I harp and harp on this concept on this blog, but how much “adaptation reservoir” someone has determines how much work load they can handle. For elites, what I’d do is look at the various markers in the blood. Look at Testosterone to cortisol ratios, basal cortisol levels, DHEA-S, etc. You can also look at someone’s Heart rate variability or even something as simple as resting HR or the change in HR from lieing down to standing up. There are no perfect measures, but the point is, if you see something out of whack, then know you have to adjust.

There are certain athletes who have high stress responses. It just means that you have to be extra careful in not pushing them over the edge. Knowing that a high stress response athlete might only be able to handle X, while someone else at the same ability level can handle X+1. Don’t just give the high stress athlete the increase volume/intensity because that’s what they “should” be doing for someone who races at their speeds. Realize, that getting continual adaptation is the key, and perhaps pressing too far will lead to no adaptation.

For athletes:

All of the above is important, but also use the information to prioritize your life. When you’ve got a big training block coming, try to minimize outside stress. That doesn’t mean live like a hermit, because people have different activities that are stress reducers, but it means try and minimize triggers for stress.

Secondly, look at how you approach practice. I love the sayings by Renato Canova where he talks about how Africans generally approach training with lower stress and anxiety than their American counterparts. Realize that getting super anxious and stressed out before a workout could do more harm than good.

The take away message is that stress, whether it’s internal or external, effects the body in similar ways. There’s only so much we can adapt to. If you’re outside life gets too complicated, maybe that’s why you aren’t adapting to the workouts? And for coaches, maybe they can’t do as much as you thought, not because you aren’t giving them enough recovery after, but because you haven’t taken into account the external stressors of life?

Rethinking the cool down AND XC coach at University of Houston

2012-09-09T11:43:00.000-05:00

First, let's get the personal life/move out of the way. I took the job as XC/distance coach at my alma mater, University of Houston. I'm thrilled to be back in TX and at UH. We've got a great bunch of athletes here and looking forward to doing big things! Also excited to be working with another pro in Sara Hall, who is an absolute pleasure to work with.

Announcement:
http://trackfocus.com/college-track/former-oregon-project-coach-steve-magness-named-university-of-houston-assistant-cross-country-coach

Second...Cool downs!

The Cool down- what does it do?

I’ve contemplated for a while writing about the role and function of cooling down after a workout or race, but never I have never fully been able to put all the pieces together to do so. The cool down seems like such a normal/given thing. It’s a rite of passage to be able to be done for the day. It’s so ingrained that no one asks the question why anymore.

Why?

Let’s first look at the traditional viewpoint of the cool down. If we were to ask what a cool down is used for most answers would relate to bringing your body back to normal. You’d get answers like to get rid of lactic acid or waste products, to slowly bring muscle temperature down, to gradually reduce Heart Rate (HR), and all sorts of other related answers.

But do these things matter? Lactate is cleared within 30-60min anyways, so maybe a cool down speeds it up to 15-20min, but that’s not a big deal because lactate is not evil. Muscle temperature and core body temperature would drop quicker by just standing around, as would heart rate. On the contrary a cool down would keep blood flow elevated for longer, so perhaps transport of “stuff” would be enhanced. But the truth is. We have no idea why the cool down actually physiologically does anything.

Is this another case of being overrated like stretching?

Everyone in the world uses a cool down post workout whether it is HS, college, or Pro’s so there has to be a reason or benefit. Unlike stretching (which people who were keenly aware just kind of stopped doing) there’s never been a movement to stop cooling down. That to me, and the fact that empirical evidence from coaches all over supports the use of one, lends credence to the idea that cooling down is in fact a good thing. My contention though, is we’ve been asking the wrong question when trying to figure out what a cool down does in the running world.

Adaptation, not always recovery:

While the emphasis on what a cool down does has been on returning to normal and recovery, which it probably aids to a degree, I can’t help but think that we’re missing part of the picture. The cool down job or activity post workout is actually part of the workout. It’s a crucial component that actually furthers adaptation.

What state is the body in at the completion of the workout? We are probably left with muscles running low on glycogen, high on lactate, have a low pH, a large number of muscle fibers having cycled in to do work and exhausted, all sorts of neurotransmitters in the brain at high levels, and the brain’s central governor screaming at us to stop. That’s quite a lovely state to be in right?

Once we stop, things calm down a little bit and start the return back to homeostasis. But then we start jogging again and what happens?

We’re now doing more running, albeit at a slow pace, in this depleted state. It’s not increasing our depleted state too much in most cases but we’re still recruiting muscle fibers to work when they’re in this state. Is it possible that with a ton of them already fatigued, we’ve altered the recruitment slightly so that fibers that normally don’t work at such an easy aerobic intensity are now working? If so, then we’re training fibers that normally don’t work at such low intensities to be a little better aerobically. Secondly, if we look at lactate. If we have a decent amount of it built up and we start running, are we perhaps training our muscles to take up and reuse lactate better while running then if we were just lying around?

If we look at the brain’s role, could continued exercise, even at a low intensity post hard workout actually signal the brain that we’re okay and we can push these boundaries a little bit more and survive?

I don’t know the answers exactly, but…

What I’m getting at should be obvious but it is this: The cool down might be a training effect more than a recovery enhancer. Both probably play a role, but it’s typically thought of as the later only.

Where’s the evidence? I have little because there is little to no research on cooling down.

What I do have though is intriguing.

We know that a cool down of aerobic exercise (i.e. a jog) following a strength workout will impact the adaptations that occur from the total workout. Depending on the combination and what kind of athlete you are dealing with, a cool down can either enhance strength gains or be used to limit hypertrophy. Essentially throwing aerobic exercise in after a strength session can impact the adaptations you get. You can see this on a signal pathway level in comparing what pathways get activated versus which don’t. Just by including light aerobic work after (which many would consider a cool down) can alter the effects of the previous strength workout. Similarly, there have been some intriguing studies on stretching after strength work that shows it can change the amount of hypertrophy. The point is this, a cool down activity can modulate what the main workout produces in terms of adaptation.

The cool down therefore should be looked at as an enhancer to the main workout.

How to modulate?

I have no clue. I’m guessing. Completely. Educated, but still guessing.

So let’s look at our options beyond a typical short jaunt. Remember that we are in our kind of fatigued state at the start of the cool down…

Long cool down- Simply go for a longer cool down. Instead of the easy 2mi or so, go for 4,5,6mi. This is what we used to do in HS after races. Why? Partly to get in mileage, partly for no reason, and partly because we went really slow so we could get the girls on the team to run with us and cause mischief…but it was mostly for the putting in the extra miles…

So what could a longer cool down for you? You’re getting a light aerobic stimulus on fatigued muscles, meaning your probably training some fibers aerobically which normally aren’t. Secondly, you are dampening down the effect of something highly anaerobic if you do it after a anaerobic event (think 4x400 or a very fast speed session). This is briefly touched upon in Jan Olbrecht’s wonderful book Science of Winning. Why would you want to dampen down the effect? If you have a kid who is a high responder to anaerobic work and you don’t quite want it overwhelming the aerobic side of things.

Strides in cool down- One of the more intriguing cool down manipulations I experienced was a set of 10x100m strides with a turn around recovery as part of the cool down from a hard track session by Igloi disciple Joe Douglas. Why might this be good? Well two thoughts. First, it’s not long but its faster so once again your pushing activation of muscle a little more in a fatigued state. Secondly, you’re going through a bigger range of motion running wise, so it prevents that tightening up or change in tension too much.

Stretching cool down- As I mentioned before, in combination with strength training, while there have been only a few studies, stretching sometimes enhances strength performance. The theory is mostly based on the idea that the combined effect increases hypertrophy. Another possible mechanism is that stretching seems to increase select hormones, at least in animal models, such as IGF-1 (Yang et al. 1996). What does this mean? That stretching AFTER a workout might do something. Right now there’s slight evidence for increase in hyprtrophy. Remember that when stretching you are actually essentially tearing collagen bonds, so its possible that the adaptation occurs via a response to damaged tissue. So lots of questions to answer. Do we stretch for hypertrophy post workout if that’s the goal? Do we stretch to get a hormonal response to increase recovery? Or should we avoid stretching because it may increase damage to a muscle tissue that’s probably already damaged from the workout?

Strength in cool down.

Last but not least what about adding strength to the cool down. Whenever I trained out in Virginia with Scott Razcko we always did GS (general strength) right after runs/workouts. I think this is intriguing for two reasons. First, it has to be a great way to work on strength endurance. Think about it. You’re adding a strength component in a pre-fatigued state. Secondly, what happens hormonaly? Depending on the strength exercises selected, is it possible to get a hormonal change that enhances either adaptation or recovery?

And what about recovery?

Yes. Cool downs likely help recovery for feeling good the next day. Why? Well no one knows for sure. The increased blood flow thing for a while is one theory that makes sense. There could be a hormonal component. Then you have canova’s data where he stated that after an easy run you can get lower morning lactate levels. But one of my thoughts is this: a cool down simply manipulates tension in the muscle. You go from doing something hard and fast which will eventually jack up tension, and a cool down simply works to modulate that down a little bit. It’s why you probably feel better the next day if you cool down instead of going straight to the car…

Is there ever a time where you don’t want to cool down?

At first this seems blasphemous, but stop and think about it. Could there be a time when you don’t want to? It’s probably few and far between but would not cooling down give predominance to some anaerobic adaptation post “anaerobic” workout? I’m not sure I have the answer but it’s an intriguing question to think about.

So what?

The take away here is that we don’t have a lot of answers, but we do have a lot of intriguing possibilities. It’s time to change the way we think of a cool down. It should be another planned part of the training in certain situations. Once you shift it from being solely a part of recovery and instead see it as a way to manipulate adaptation, then questions arise and possibilities open.

Moving on

2012-07-09T17:06:00.003-05:00

Brief intermission from normal blog stuff for an interruption from my real life.

Most have probably seen but I'm moving on from the Nike Oregon Project. It's been a great learning experience for the last almost 2 years, but it's time move on and do my own thing. Thankful to Nike for giving me the opportunity and very happy with the work I've done with the athletes over that past period. This article sums it up nicely so I don't have to rehash:
http://www.runblogrun.com/2012/07/magness-moves-on-by-jon-gugala-note-by-larry-eder.html

Really looking forward to the next opportunity. Since the story "broke" have had some nice correspondance with a variety of people from the running community. Excited to see what we can develop and where things go from here. It's been a crazy hectic past bit, but am trying to sort through things and look at the feasibility of various projects and ideas.

Thanks for all the help and support from those of you out there. Much appreciated. Got some cool stuff for the blog, and I promise to finish up part 2 of the last post soon.
Steve
stevemagness@gmail.com

Physiological Model of Training- Why it and "zone training" are outdated

2012-06-15T13:39:00.000-05:00

Physiological vs connection model.

(This is going to be a long one…heads up…..)

I hate zone training. It’s a pet peeve of mine. I hate the idea and the concept behind it. But so many coaches out there use it, and in actuality we all tend to classify workouts into different zones. I’ve wrestled with trying to explain my hatred for zone training and what I’d call the alternative method for a while, but it’s a difficult thing to wrap your head around. I knew I hated it, but I couldn’t effectively explain why to outsiders. I’d dance around the why’s but never had a satisfactory answer. Part of the reason was I didn’t have a simple way to explain the alternative. I could throw a bunch of information and examples to describe it, but there was no easy descriptor. Before getting into what the alternative is, lets look at what exactly the physiological model is and how we got there.

Defining a model:

The physiological model of training is one that relies on the premise that there are a few big physiological parameters that govern performance. The big ones mentioned in research and the literature are VO2max, Running Economy (RE), Lactate Threshold (LT), and sometimes lactate tolerance or anaerobic capacity/tolerance depending on publication. The idea is that these four things combine to create performance.

The central premise of the physiological model is that IF we improve one of these parameters, then performance improves.

But how does this relate to training? The model takes another step and says that there are certain intensities or zones that will improve X parameter.

So the full model really states that IF we do X training, Y parameter will improve and thus performance improves.

If this was a logic class it would look something like this: X->Y=↑ P

Sounds reasonable right? Well, hold your horses…

Strict adherence:

Before fully diving into what’s wrong with this model, it’s important to fully understand it so that it doesn’t look like I’m creating a straw man argument. As with anything there isn’t one strict concept of the physiological model, but instead many slight variations covering the spectrum. I’d like to give an example of that and show the limits of a normal physiological model.

Not meaning to pick on Dr. Jack Daniels, but his updates between his 1^st and 2^nd edition of the book Daniels’ Running Formula perfectly illustrate this. In his first edition, he outlined what have now become the classic zones used in many programs. What’s interesting, and what is typical of a strict physiological model system, is that in between these zones were what’s referred to as “no man’s land” training.

(Thanks to the blog http://sisyphusrunning.blogspot.com/2011/08/no-mans-land.html for this)

In his book he defines this no man’s land zones as:

“No man’s land of training. Training intensities that fall into ‘No man’s land,’ are either too easy or too hard to reap the benefits you want. You are not, as may sometimes be assumed, achieving the purpose of training the two systems on either side of the chosen intensity. What you are doing might be termed, “Quality-junk” training. At the least, it is training aimed at accomplishing an unidentifiable purpose. Always have a purpose for every training session; ask yourself the following questions: ‘What system do I hope to improve by doing this workout ‘and ‘What am I really trying to accomplish?”

This is what I’d call a strict adherence. If you train too fast or too slow of the zone it’s “junk” because it isn’t targeting the special zone which should target some parameter. This sounds good, but the issue is that training doesn’t occur in isolation and as we will soon find out those training zones don’t even attack those parameters terribly well. It’s missing the central point of training, that it is a stimulus. Yes different stimuli will result in different results, but everything is a stimulus to a degree. If you are too fast or too slow, it doesn’t negate the adaptations, it just changes them slightly. Secondly, you have to remember that this thinking is with the model behind it. There is no purpose for the “no man’s land” zone training IN THIS MODEL. How accurate that is depends on how well the model reflects what is actually going on. Because every model has holes and doesn’t perfectly reflect what is going on. In this case, the model fails to accurately reflect what’s going on as we shall soon see.

What is interesting (and very astute of Daniels) is that in his 2^nd edition of the book he takes what I’d call a more loose interpretation of the model. Why? Because he expands his LT/tempo section of the book to say that unlike in the first edition, tempos can be slower and longer than the LT zone and still get great benefits.

Now that we get what the model is, what’s wrong with it?

(The above section might come across as harsh to Daniels but that isn’t my intention. Instead I think it’s cool that Daniels realized the potential of other zones of training and amended his thoughts. A smart coach!)

What’s wrong with the model?

As a quick reminder the physiological model relies on the following logic:

1. There are certain parameters that define performance.

2. Training each one of these parameters improve performance.

3. To train these parameters you work at X intensity.

Hopefully you’ve noticed a few holes in this logic. Let’s go through them.

First, those big parameters don’t really do a wonderful job correlating with individual performance. Yes, some studies show strong correlation to a mixture of them, but you can’t really separate out good runners from great runners. Research shows that combining the big 3 of RE, VO2max, and LT explains around 70% of the variation in performance (Di Prampero, 1986). So, good, but not great? Vo2max in particular does a relatively poor job. You can check my fallacy of VO2max article if you want more details. For now I’ll briefly quote one relevant section:

“Showing the separation of VO2max and performance, the Vollaard et al. study found that the change in VO2max was not related to the change in time trial performance (2009). Studies demonstrate improved performances without changes in VO2max (Daniels et al. 1978). Also, studies show that VO2max can improve without changes in performance, which is seen in a study by Smith et al. that showed improvements in VO2max by 5.0% without an improvement in performance over either 3,000m or 5,000m (2003). In addition, in looking at long term changes in performance in elite athletes, changes in performance occur without subsequent changes in VO2max.”

As far as the other parameters, yes they all correlate to performance to a degree when looking at groups. So that is valid. The question is do changes in these parameters correlate with improvements in performance? The answer is it depends. In several studies you’ll see an increase in LT, RE, or VO2max as well as an increase in performance. In others, like those mentioned above with VO2max you’ll find no change despite an improved parameter. Another quick example is a study by Vollaard et al (2009) that found that RE and VO2 changes didn’t explain performance improvements, or in their words: “This study demonstrates that improvements in high-intensity aerobic performance in humans are not related to altered maximal oxygen transport capacity”

Similarly, with lactate threshold. An increase in threshold is sometimes tied to a decrease in performance as demonstrated in the world by Jan Olbrecht. This is usually a result of the lactate threshold increasing while anaerobic ability is decreasing. For more on this concept see Jan’s work.

Which brings us to the point of training not occuring in isolation. We can’t independently try and improve these parameters in all runners and expect performance to increase. There’s an interaction between the training types. For instance, there’s a strong back and forth tug of war battle between LT work and the so called lactate tolerance work. This interaction effect is somewhat addressed by periodization, but when training is thought of in isolation such as do X and improve Y parameter, it’s often lost.

So, not surprisingly, we start with a somewhat decent premise and get a bit shakier as we move away from it. But where things really fall apart is in the next step, which is the most important because it translates lab work to the real world, which is what we are all concerned with anyways.

Training zones don’t really work?

Perhaps most importantly then, the training zones don’t really correspond with improving the parameters. And even if they do to a degree, there are multiple ways to improve the parameter. Let’s look at these zones individually to get an idea.

VO2max

In this new quest to improve VO2max, it was first ASSUMED that training at VO2max was the best way to improve it. The logic was simple. Spend as much time at maximal oxygen consumption as possible and it has to increase right? Sounds logical enough…So the next step was figuring out what paces would elicit VO2max.

Why do we train at roughly 3k pace to improve VO2max? Well, we got to that point because a bunch of researchers took on the challenge to see what was the slowest speed which would maintain VO2max for a relatively prolonged time. Depending on what research article you look at, it generally came out to be something that lasts roughly 7-10 minutes. Or about the time it takes to run a 3k. Therefore, 3k pace became VO2max pace. Yes, running faster than that elicits VO2max too, but it’s not the slowest speed. We had the intensity. Onto the next step.

A bunch of researchers did more studies seeing different intervals that would allow you to spend the most time at VO2max during the workout. That’s where we get Billat’s famous 30-30 workout and a slew of others. After this we had our optimal interval speeds, lengths, and recovery.

So it was all set. Do these workouts at X speed with this recovery and you are set. The problem?

Well the research didn’t exactly back up the idea that to improve VO2max (even if it mattered much…) we should do that. I could go on and on but a nice little review of training to improve VO2max by Midgley (2006) sums it up nicely:

“Training intensities of 40–50% V˙ O2max can increase V˙ O2max substantially in untrained individuals. The minimum training intensity that elicits the enhancement of V˙ O2max is highly dependent on the initial V˙ O2max, however, and well trained distance runners probably need to train at relative high percentages of V˙ O2max to elicit further increments. Some authors have suggested that training at 70–80% V˙ O2max is optimal. Many studies have investigated the maximum amount of time runners can maintain 95–100% V˙ O2max with the assertion that this intensity is optimal in enhancing V˙ O2max. Presently, there have been no well controlled training studies to support this premise.”

So there we go. We don’t know if that is the best intensity or not to increase VO2max. Tons of research, but no clue.

I also like one of their other statements:

“Synergistic and interference effects between optimised training protocols designed to target specific physiological performance determinants and the influence of individuality then need to be established before sports scientists can make recommendations to runners and running coaches,with a high level of confidence, on components of an effective training programme.”

Individuality. Interaction. IMPORTANT.

So what we’re left with is a magical zone that we’re not sure if it even attacks what it’s supposed to attack (and if that even matters?)

What does this kind of thinking get us? Well, a quick example is certain studies came out a long time ago that said after 50-60mpw amount of mileage, VO2max doesn’t improve, so why would we run more mileage if that’s true since VO2max is the be all end all (Berg, 2003). This isolationist approach neglected the complexity of performance so we ended up with a bunch of coaches thinking you don’t need to run much mileage…whoops.

LT:

The lactate threshold is one of my favorite topics as I like to do lactate testing, but in the Jan Olbrecht inspired way, not the traditional way. I’ve covered that in my blog elsewhere, but there are some important lessons from that distinction. For instance, the actual threshold itself is influenced by factors besides “aerobic” ability. So the anaerobic side or lactate production side influences it too. So it’s entirely possible to get an improved LT curve while actually decreasing in aerobic capabilities (if the anaerobic capacity is decreased…). So once again interaction is key, but what about training at LT to improve LT, and thus performance.

Well if we look at the research, training at LT CAN improve LT. That’s good to know. But so does training at various other paces. Once again there is no magic training zone. In fact if we look at the one study on well trained runners, if they increased their training volume at near LT by 103%, it didn’t do anything to the actual threshold (Lehmann et al. 1991).

In other studies, with recreational runners, you saw big increases in LT after 2-3 months of training at threshold and then no further improvement in LT afterwards with continued training. What this tells me is if they wanted to keep improving the threshold, the stimulus had to change. They had to do some work above LT, some mixed intervals, aerobic intervals, or alternations. Whatever they chose, the stimulus had to change

In a review on training to improve threshold, Midgley et al. (2007) stated:

“In summary, we found only one study that investigated the effects of an increase in the volume of

vLT or vLT training on the lactate threshold of distance runners.[25] This study reported no significant

increase in the lactate threshold. Several training studies have reported a significant increase in

the lactate threshold of distance runners in response to the inclusion of supra-vLT training velocities,[15,29,39] although these findings have not been consistent.[34,36]”

Once again, we’re looking at, ya training at LT improves it, but so does a lot of other stuff. And it depends on the type of athlete on how best it’s done.

Running Economy
But what about Running economy? Run fast and you get more economical? That’s the magic zone to improve RE, right? Well, sorta. If you look at research, again depending on the group studied, running fast, at VO2max, and at LT have all improved economy in various studies. Wait, so has weight lifting, plyometrics, whole body vibration, altitude, training in the heat and on and on (Berg 2003,Foster 2007). Obviously some improve it more than others, but the point is that like with all the other parameters, there are numerous ways to improve them. It’s not some magical zone that best targets it.

Ignoring whether or not RE is actually a good measure (that’s a topic for another time), it seems silly to assign one zone to improve this, when truthfully people are still arguing over what the heck improves it.

The point of this little tirade is to not say that training at these intensities is bad. It’s good. The point is that by sticking to this strict zoning concept we ignore both the individuality of the athlete and of the training response. In this system it assumes that an LT run does the same thing regardless of whether the athlete is a fast twitch runner or Slow twitch. While, we know that the effect can be vastly different because there physiology is different. Same goes with VO2max training or any of the other zones.

Nail in the coffin:

For my final nail in the coffin for why the model sucks, let’s look at a training study on sedentary people that had them all train at 70%VO2max. So they all trained at the same exact “zone”. What happened? Let’s check out the data (from Vollaard et al. 2009):

What happened was simple. A ton of different individual reactions to the same exact training load and training zone. All the way from big picture changes like performance , VO2max, and VE all the way down to enzymatic changes. There was a whole lot going on and a wide variety of responses. What this tells me is that stimulus matters. For some people the same training “zone” will give a different stimulus.

The same was found in a more recent study of untrained individuals. They followed them for a prolonged period and had them do all exercise at 60% HR reserve. What happened? Well a big variation in improvements in the big variables even though they were all training at the same intensity and volume (see full study here: http://onlinelibrary.wiley.com/doi/10.1111/j.1600-0838.2010.01139.x/full)

While you might say this was with untrained individuals so what's the point, I'd counter that with untrained individuals you'd expect almost anything to work! I mean you're going from nothing to something, so the fact that there's a huge variation is interesting.

And finally, if we want to go all the way down to the genetic level, here's what happens to people again all training at the same intensity. Look at the variation in high responders versus low responders for a whole slew of different genes: http://jap.physiology.org/content/110/1/46/T2.expansion.html

Why do we do this?

The answer is simple. In Daniel Kahnemann’s book Thinking Fast and Slow he describes essentially how human’s think. In there he talks about the concept of how when we get a difficult question, we often times replace it with an easier question and answer that. It’s subconscious so we don’t know we are doing that. But that’s essentially what we’ve done here.

We have a difficult question: How to improve the complex notion of performance?

And we’ve replaced it with “How do we improve these parameters?”

The second question is much easier to grasp our heads around then the first. It’s fine to simplify and reduce, but in this case we have to ask if the second question really answers the first. My contention is that it doesn’t.

How’d we get here? The story version:

Back in the day, coaching was almost purely trial and error. You learned from those who had come before you and tried your own manipulations. If something worked, it stuck for a while. The great coaches quickly were emulated until the next new idea or phase took over. The classic example is Arthur Lydiard experimenting on himself in terms of mileage before assigning training to his illustrious crew. Trial and error works. It just takes some time and occasionally a lot of error.

That got us most of the way towards modern training concepts, but something happened starting in the late 70’s, early 1980s and continued through the 1990’s. Exercise Science actually became a more defined field with actual research on performance. We began to be able to readily measure parameters like VO2max, lactate, etc. on well trained runners. Furthermore, we began to conceptualize what may effect performance. This was the rise of the VO2max paradigm. All those cool results that showed our best had really high VO2max started coming out and for those athletes who didn’t have crazy high VO2max values, the concept of RE was developed and explained the rest. Soon portable lactate analyzers came about and we could measure that evil fatigue component called lactate. More testing, more variables.

Fast forward a little bit and we have the big 3 of VO2max, LT, and RE and then a few other variables that were occasionally thrown in to determine performance. This got translated to the intrepid coaches looking for an edge. It was the beginning of the age of Science. It was cool to make things sciency, and it offered a world of possibilities. Everyone was looking for the next edge, so science became that.

That’s when it got translated into the coaching world. With Coe and Martin’s book in the 1980’s, Daniels’ Oxygen power following, and many others it became the thing to do. The promise of explaining performance in a neat formula AND being able to make training almost a mathematical model was too tempting to pass up.

The model is thus part of our human notion to want to compartmentalize, our need for structure, and our seeing Science as the next ultimate step to sole all of our problems. The models basic foundation and premise are broken though.

Done rambling, so what?

It’s not that the workouts are bad. It’s not that we shouldn’t run at threshold or 3k pace or faster. It’s that the model is bad. The model is broken. And if you strictly follow the model, you miss out on a bunch of sweet stimuli that need to be touched on. You also loose the ones thing that is essential to coaching, creativity. Instead, it becomes a plug and play system that discourages creativity and innovation.

Hopefully through this rambling mess you get a few things. If all fails, I hope it gets you to step back, think, and question.

But what the heck do we do about it, if I make this claim that the model is broken? After all I can't just sit here and tear something down without suggesting an alternative.

That’s part 2…

A bunch of Scientific research from ACSM conference

2012-06-08T17:02:00.001-05:00

Last week was the big American College of Sports Medicine annual meeting. I wasn’t in attendance as I was at the Prefontaine classic. So instead I had the pleasure of browsing through the 3,500+ abstracts that were presented at the conference. There were a lot of interesting studies to pop up, so I figured I’d share my highlights of the abstracts. In the coming weeks, I’ll go through some of the more intriguing studies to come out and give their real life impacts.

(Some are more in depth than others because I was taking hand written notes as my computer broke…So, if you want to search the abstracts, I’ve included the authors when I remembered. Also, remember that experimental procedure and subjects matter. So just because I say X did Y, it doesn’t apply to everyone..)

My comments on the studies will be in blue.

(Full abstracts can be seen here: http://acsmannualmeeting.org/wp-content/uploads/2012/04/12AMFinalProgramCombined.pdf )

Exercise Induced Arterial Hypoxemia:

· -The higher the VO2max, the more likely for oxygen saturation to be less than 91% at sea level. 71% of well trained reached low oxygen saturation levels (Chapman)

· -Mechanical ventilator constraints are a contributor

· -Faster runners- pulmonary diffusing capacity of nitric oxide is limited

· -Aveolar-capillary membrane conductance is a limiter (Lavin et al.)

Impact: Limiters and physiology change as you deal with people futher outside the norm. For highly trained athletes, O2 saturation drops might play a role. This might be the reason various interventions in terms of respiratory training are successful. It depends on the population you are addressing. It’s simple to test if an athlete has EIAH. Simply buy a pulse oximiter for $60 and then test during a really hard workout.

Inspiratory Muscle Training/Diaphragm:

Speaking of EIAH, there were a few interesting studies on inspiratory and expiratory training.

-"After IMT, highly-trained competitive cyclists demonstrate decreased whole-body VO2, and LM and RM deoxygenation during exercise with heavy inspiratory loading. These data suggest that IMT reduces respiratory muscle

demand and decreases oxygen extraction by the active muscles, which may reflect IMT-induced changes in respiratory and limb locomotor muscle oxygen delivery."

Electrical Activity of the Diaphragm in Trained Subjects During Progressive Cycling to Exhaustion Trials

Dan S. Karbing, Nicolai L. Mifsud, René M. Jørgensen,

CON CLUSIONS : Results showed poor within subject agreement over time for EAdi. Possible causes include probe placement and subject variation over time. In contrast, trends in EAdi changes with workload were similar within subjects. In general, EAdi increased from WL of 40% to 55% and 70%. On average, a plateau at 85% WL was indicated in agreement with previous studies of EAdi, but individual subjects showed no clear pattern of changes in EAdi from 70 to 85% WL.

What I loved about this study is that it showed diaphragm activity was highly variable. The diaphragm and breathing are starting to get attention once again in terms of limiting performance after going through a phase where it didn't really matter.

Lactate:

-Negative effect on differentiation of human myoblasts

-regulates proliferation, apoptosis, and differentiation (Jung)

Myoglobin:

-Contrary to prior beliefs, myoglobin is not only in cytosol. Plays role in regulating mitochondria respiration

Fiber Type:

-muscle activation patterns can alter fiber type through six 1 gene.

Essentially the fiber type can be “trained” based on its use.

Satellite cell: (SC are essential for the muscle repair and growth)

-Increases 4 days post but not 10 days after a bout of strength training

-Concurrent endurance blunted satellite cell proliferation. (Thus why endurance training and strength training performed together can reduce hypertrophy)

Ultrasound:

-Ultrasound increases muscle cell proliferation in isolated muscle cell giving a potential investigative reason for ultrasound to work

Ibuprofen:
-Increase skeletal mass in older adults by decreasing IL-6.

Interestingly, in older adults, ibuprofen INCREASED hypertrophy. According to the authors, it most likely does so by decreasing IL-6. The interesting thing is this runs contrary to other research done in younger people. There’s much to investigate on this but it could point to a different limiter in terms of hypertrophy depending on age (and likely related to hormonal differences

-"Consumption of 1,200 mg·d-1 of ibuprofen for 3d following an initial novel bout of eccentric contractions significantly diminished the well-established neuromuscular adaptation (repeated bout effect) that commonly occurs following injurious exercise. Athletes should use caution when utilizing NSAIDs to treat lower extremity muscle pain.

Once again, some more research showing that NSAIDs might block some nice adaptations or recovery. Save it for when you really need it!

Whole body vibration

-Improved running economy in college distance runners in terms of both caloric unit cost and distance unit cost. (Ching-Feng Cheng)

-Improves vertical stiffness (Coglianese)

While it’s only a few studies, it’s interesting that WBV improved economy, and in some other studies power, in the short term. It would be interesting to see what the long term studies would show. For why it happens, as mentioned, another study showed an increase in vertical stiffness which may play a role in increasing RE.

Weight Loss:

· Weight loss results in decrease in T to C ratio

Fatigue

· Low frequency fatigue is caused by reduced SR Ca2+ release

· CNS tolerates greater magnitude of peripheral fatigue when source of skeletal muscle afferent feedback is confined to small muscle mass (Rossman, Venturelli)

o (One large feedback versus many diffuse signals- many fatigue signals-CNS shuts down stuff sooner)

· Cognitive demand (math) increase muscle fatigability

· Metabolite detecting markers decrease post exercise=down regulation of afferent signaling in order to reduce fatigue sensations (Van Haitsma)

Some very interesting studies coming out on fatigue and in particular on how fatigue is relayed.

Signal pathways:

· NCoR1- opposite effect of PGC-1a

· mTOR

o intervals before strength blunts mTOR

§ (Once again shows why timing matters when you do stuff)

o Whey- 20g post resistance training= increased mTOR activation

· A7integrin=upregulated in response to mechanical strain- regulates p70S6k signaling which increases fiber hypertrophy.

· PGC1-a

o Upregulated for up to 6hrs post exercise in novice

· Sumo-1-

o Triggered by oxidative stress/hypoxia- peaks 15-30min post exercise

· Attenuated response of PGC1-a and MURF-1 after just 10 days of training (about 1/3 of the increase after 2^nd time trial) (Hinkley)

o This one is interesting because it shows that training has to adapt to elicit further response of a signaling pathway. The stress has to be manipulated. Thus why you can’t just do the same thing over and over and get results.

Epigenetics:

-exercise alters DNA methylation- aerobic+ resistance altered more sites than RE only (6976 vs 970) and only 197 genes common in both (Radom-Aizik, Haddad)

I love epigenetics. It’s one of my favorite side interests, so to see a study looking at epigenetic changes due to exercise is very interesting. In past studies, there’s been data to show that some epigenetic changes get passed down. What would be interesting to know is how much exercise related epigenetic changes can get transferred to the next generation. Additionally, what’s intriguing on this one is the number of sites modified in endurance+resistance versus resistance only. AND that there wasn’t a huge overlap.

Altitude:

-Time-trial performance is impaired to a greater degree in hypobaric compared to normobaric hypoxia at the same ambient PO2 equivalent to 4300 m despite similar cardiorespiratory responses.

This one is very interesting because it shows that Oxygen isn’t the only thing that matters. Pressure seems to play a role too. So altitude tents alone won’t do the entire job?

· -Nitric Oxide/Nitrates decreases the effects of altitude.

o Use when racing at altitude, or when needing better workout at altitude.

· -Lower HRV- leads to parasympathetic withdrawal and increase in sympathetic activity (Rodriguez)

o Shows that stress response at altitude changes and you have to consider it when training.

· -Living high, training low= increase in cortisol. AND increases muscular protein degradation/catabolism.

o –Shows that when at simulated altitude, need to probably increase protein intake, and be aware of the increased stress response and likely decreased recovery from training.

I think the take away from the above studies is to think of altitude as a stressor, just like any other workout or new training stimulus. I'd venture to guess that why a large majority of people who go to altitude and don't see positive adaptations, is because they "overtrained" at altitude because they didn't realize it was an additional stressor.

Training effect of altitude on breathing:

"CON CLUSIONS : Decreases in the oxygen cost of breathing accounts for

approximately one-quarter of the improvement in running economy in elite distance

runners after altitude training. The data suggests that the added ventilation with chronic

training at altitude acts as an additional training effect for the respiratory musculature,

which may contribute to altitude training-mediated performance improvements."

Heat:

-Heat preconditioning (30min hot bath) eliminates increase in IL-6 and CK following eccentric work (Wang)

Blood donation:

-Donating blood causes temporary spike in NOS and EPO (500ml donated)

Muscle

-marathon training modifies muscle architecture (higher pennation angles and shorter fascicle lengths) (lateral gastroc more likely to change than vastus lateralis/

Power:

-in rats, peak power training decreased FTb fiber SDH (mitochondrial) activity.

Intriguing because it shows the interplay and balance that is essential in finding that speed vs. endurance balance. If you sway too much on one side you can mess up the balance.

Protein

-whey increases mRNA expression post resistance training

-L-arginine with resistance exercise blunts GH response

-Leucine=activator of protein synthesis proteins, HMB inhibits protein related to protein degradation (Wang)

-choc. Milk better at decreasing muscle damage then whey protein fix (Fornal)
Protein is becoming a bigger deal, even for endurance athletes. And it not only matters that you take it in, but also when and how much.

Biomechanics and Shoes:

-VFF improve RE after 2 week adaptation period in national level runners (Warne)
-De Paoli- Inexperienced barefoot more economical barefoot than when shod.
-Zero drop shoes change foot angle at touch down so its closer to barefoot (Bohne)
More interesting stuff on shoes and the barefoot trend. What I like about the VFF and RE study is that they at least gave them an adaptation period instead of doing the stupid RE in shoes then right after in VFFs.

Additionally, the zero drop shoe study shows what we've all been saying for a while. Heel height plays a specific role in the angle of the foot at landing.

"Does Gait Retraining To Decrease Vertical Loads Reduce Bony Loads In Runners?"

Rebecca E. Fellin1,

:External and bony loads appeared to decrease post gait retraining.:"

-Increased hip strength resulted in decreased ROM for both pelvic drop and trunk rotation during the stance phase of running in collegiate athletes.

Biomechanics and Fatigue:

-Fuhr et al- found that "These results indicate that changes in mechanics occur throughout the simulated 10 km run and these changes are magnified as runner’s fatigue. Mechanical changes such as these may be compensatory in nature. Increased elbow flexion may have assisted propulsion by increasing the amount of lift acting on the body and ultimately increasing the individual’s total flight time. This, combined with increased knee flexion, seem to be key coping strategies to maintain pace with fatigue induced step frequency decreases.

Cool study that shows what all of us track coaches see. As Fatigue occurs (in this case over a 10k race) mechanics change. The take away on this study is the changes in arm stroke to compensate for fatigue. The question is can we delay this need to alter mechanics until we really need to. And secondly, is there a preferred way to compensate for fatigue. For example, many runners try to do the lift the knee thing when fatigued, which I'd say is incorrect. Are there certain things to teach to go to when fatigued? My advice has always been to focus on the arm swing. Depending on the athlete, either increasing frequency or stroke range of motion could be helpful. I think what way they go depends on what there "normal" mechanics are. If they are an athlete who generally maximizes stride frequency then you probably aren't going to be able to compensate to keep frequency up and instead would have more luck in increasing stride length. Or vise versa.

Muscle Damage:

Discussion: These results suggest that muscle damage induced by ECC increased

corticospinal excitability, which was seen at high stimulator output levels. This could

be attributed to increased EMG activities and force fluctuation during voluntary
contractions of damaged muscle.
Eccentric muscle damage changes EMG activity.

Baseball:

-Using a heavy or light bat while warming up, shows a trend in decreasing bat swing velocity when swinging your regular bat.

I love this study because it shows that once again something that baseball has been doing for a century is idiotic...(i.e. donuts on the bat in the on deck circle). There are other studies that found the same thing.

Carbs:

Immediate Energy Signaling During Physical Activity

-Study by Grant, Turner, et al. showed that swishing around Carbs enhanced neural activation network. It increased activity in the motor cortex and "regions involved in reward processing."

This explains why swishing around carbs and spitting them out seems to work. Your body and brain is a wonderful thing. It's pretty cool how feedback works.

Study on nutrition and efficiency:

"CON CLUSIONS : Significant differences in gross efficiency were obtained following alteration of nutritional intake in the 3-days preceding and during exercise. This suggests that nutritional intake should be carefully controlled and monitored to ensure the validity of gross efficiency measurements.

Core and RE:

RESU LTS : Right and left side bridge, flexor, and back extensor endurance times were significantly (p < .05) increased following training. Interestingly, despite increases in core endurance, a significant (p < .05) decrease in RE was observed.

This study was interesting because it found an increase in core endurance, yet a decrease in economy...which is what all the core fanatics say is supposed to be improved. This doesn't mean that core is bad, it just makes you ask the question of why economy was decreased...or it tells you the measurement of RE is kind of crap...

Caffeine:

-"Caffeine was ergogenic during leg, but not arm cycling and this effect may be attributable to preserved muscle activation in the KE."

Training in pollution:

-"The results show that regular exercise in urban environment with high traffic - related air pollution increases markers of respiratory and systemic inflammation. In line with our previous findings where the exercise-induced increase in BDNF does not occur with exercise in polluted air, this study shows no improvements in cognitive performances with training in polluted air."

In this study they looked at training in Brussels versus the country side. Very interesting that training in city manipulates systemic inflammation.

Pregnancy:

Aerobic training improves mitochondrial function in human placenta by increasing mitochondrial respiratory complexes activity and decreasing H2O2 production. This intervention favors fetal oxygenation and substrate delivery and could

help protection on gestational disorders associated to impaired mitochondrial function.

This is not relevant at all to me...but it still is really interesting....yaaaa I dunno..

Eccentric Training:

-"Following eccentric exercise, we observed an increase in blood flow and blood volume within the microvasculature of the gastrocnemius over 48 hours."

An increase in blood flow and volume might help explain why eccentric work seems to work so well.

Strains/muscle injury:

-"The data show that muscle strain injury causes morphological changes to the NMJs. Due to the short time course used here, changes in NMJ morphology among injured myofibers is likely not due to regeneration or a change in myofiber size. This focus toward the NMJ represents a paradigm shift from more prevalent myocentric perspectives on injury."

Neuroscience:

-"We observed that cardiorespiratory fitness levels play a role in the effects of exercise on activity in frontal and visual brain regions involved in food processing. These data appear to suggest that LF individuals have a greater suppressive

affect in brain regions that regulate appetite."

How cool is this? Fit people can suppress that urge to eat much better than non fit.

Pacing:

-Foster- accumulated RPE. Instead of just doing a session RPE, Foster et al. did accumulated RPE over a race and found that 50% effort completed at 60% of the distance. So the last 40% of the race takes 50% of the effort.

Accumulated RPE is a cool, simple way to look into effort over race distance. It makes intuitive sense that more of the effort is divied out during the last part of the race.

VO2 over 800m race:

-"For Japanese collegiate 800-m athletes, VO2 remained elevated throughout the latter half of 800-m running, implying that the decline in running speed towards the end of the event could not be attributed to a fall in VO2. The ability to prevent a profound decrease of pH until 400-m may be the key to maintaining faster running speed near the end of the race." (VO2 peaked at 425m into the race)

Running economy:

-Pole vaulters exhibited better oxygen cost than XC runners.

Simple question...IF PV have better O2 cost than XC runners…do you really think PV are more efficient or do you think the measurement sucks?

-Stiff Achilles beneficial because of increase stiffness of tendon.

Pool Plyos:

-In one study they looked at doing sprint drills and plyos on the land versus in the water and looked at the change in sprint speed over 40-100m. These weren't crazy fast people (mid 13s for 100), but the pool group improved speed to the same degree.

I love this study because it supports something I happened upon way back in HS, doing pool plyos. Yes, you lose some of the stretch reflex and increase Ground contact time when you do it, but doing pool plyos and more importantly pool power work is a GREAT tool for distance runners who generally suck at it and are prone to injuries from that kind of stuff. I love explosive pool work in particular, but this study shows that it at least works.

Individualization of Immune response:

-"The immune response reflected a change in the number of blood cells of the athletes after performing exhausting physical activity, these cells acquire their normal levels after a week recovery period. It is important to emphasize that in

an individual way each athlete showed a different response to training. The results presented in this study were an average, in some cases the athletes showed higher or lower values concluding that integral physical personalized training is strictly necessary for triathlon as a sport and also to avoid over training."

I LOVE this study. Why? Because it shows the individual immune system response to exercise. This has profound impact on recovery for athletes and is just another example of why individualization matters. I'll have a blog on this soon.

Sleep:

-"One night of sleep disruption lowers the heart rate response and amplifies the mobilisation of NK-cells in response to acute exercise. These data indicate that altered sleep patterns could interfere with the trafficking of cytotoxic lymphocytes in response to acute exercise and might play a role in athlete infection susceptibility.

Self selecting intensity increases positive affective response:

-"These results suggest that perceived autonomy is related to affective responses to exercise"
This was a cool little study that showed that when people were assigned an intensity that had higher negative affect and when they had a self chosen intensity for exercise they felt more positive affect. What this means, is don't be anal about assigning exact paces for everything. Save that for when you need it.

Toe exercises:

-"The towel gathering and the great toe flexor exercise significantly decreased MLA (arch length). In regard to the great toe flexor exercise, the tendency was stronger. On the other hand, the exercises of 2nd-to-5th toe flexors and 3rd-to-5th toe flexors increased MLA.

Training Volume of Olympic rower:

-"In the observed period, 5827km (127km/week) were covered by the W1x, including 4202km on water, 910km on ergometer, and 715km in running and cycling. When divided by intensity zones, 75.2% of the distance was distributed in zone 1. The percentage of zone 2 and zone 3 was 22.4% and 2.4%, respectively. After dividing the training year into preparatory period (October to middle of March) and competition period (middle of March to OG), it was found that the training at or around lactate threshold (zone 2) decreased significantly from 34.4% in the preparatory period to 8.7% in the competition period, which was sacrificed by increasing the training volumein zone 1 and 3 from 63.5% to 88.6%, and from 2.1% to 2.7%, respectively.

Very cool to look at the training volume and intensity and compare it to runners.

Supplements:

-Bakers yeast B glucon- Decrease cold symptoms post marathon and improves mucosal immunity post hard workout and decreases IL.

-Betaine increases GH and IGF-1 and decreases cortisol

10-20-30 workout- Research flaws and Why there are no secret workouts.

2012-05-08T13:13:00.000-05:00

10-20-30 workout- Research flaws and Why there are no secret workouts.

Every once in a while a scientific studies simple concept crosses over the main stream and explodes in the exercise world. A decade ago it was Billat’s famous 30/30 which consisted of 30sec at supramaximal speeds with 30sec jogging. It was supposed to be the secret workout that improved VO2max and lactate threshold at the same time. A fewyears ago it was the famed Tabata exercise protocol which consisted of a series of short sprints with short recovery that was the new magic workout that was supposed to improve aerobic and anaerobic abilities at the same time.

There is about to be a new secret workout. It’s called the 10-20-30. It’s short, has a catchy name, and showed up in a recent research article in the Journal of Applied Physiology.

The magic workout showed an increase in VO2max, 5k performance, and 1500m performance while reducing training by half! What more could you ask for in America? Quicker results with half as much training time and volume.

So what’s the problem?

The Actual workout:

Let’s read what the participants actually did first:

“For a 7-week intervention period the 10-20-30 replaced all training sessions with 10-20-30 training consisting of low, moderate and high speed running [<30%, <60% and >90% of maximal intensity] for 30, 20 and 10 s, respectively, in 3-4 5-min intervals interspersed by 2 min of recovery, reducing training volume by 54% (14±0.9 vs. 30.4±2.3 km(.)week(-1)) while CON continued the normal training.”

So, participants who had been training at an average of 24km per week , cut the mileage in half and just did this simple interval/fartlek workout a couple times per week instead for 7 weeks. They improved from 23:06 to 22:16 for 5k and 6:09 to 5:49 in 7 weeks. There were also no significant enzymatic changes between the intervention and the control. So a few things to keep in mind are the low training volumes, the low performance, and the protocol itself…

What researchers probably missed:

I hate harping on researchers because it’s a hard thing to do, but a consistent theme in scientific research on training programs (and why it makes it so difficult to do them) is that there’s almost an ignorance of anything that happened previously before the study. It's one of my major pet peeves in pure training research on runners and why I prefer to look at research that looks at the effects of the workout regimes, or looks at the totality of the training.

Let me pose a question to you coaches out there. What does this look like?

Normal training- 24km of jogging…then switch to

7 weeks- 3 intervals workouts a week with cut back mileage

If you answered a pure base phase followed by an intense speed phase, you’d be right. Or if you answered a low volume version of the original Lydiard schedules, or the way that the Finns trained in the 20s-30s with a winter of jogging and walking followed by almost only intervals, you’d also be correct.

So the results in this study should not be surprising. It took a bunch of people used to running easy mileage, and added some intensity. You would expect massive improvements. Yes, they dropped the volume, but with runners running so little that’s not going to matter a whole lot over 7 weeks. Yes, they replaced normal distance runs with intervals but that won’t matter much in pretty untrained people either with the intensity increase.

They essentially performed a base to speed/peaking protocol. One that was the norm 80+ years ago essentially in the distance running world. The workout itself is just the black swan, or the elephant in the room that grabs attention and distracts us from what is really important. Don’t base your conclusions off of the obvious thing. It’s the surrounding noise and details that aren’t fun to look at that probably explain the outcome.

The bottom line:

For recreational jogger who trots around, adding intensity is good! This isn’t an either or situation, do some easy runs, do some intense runs. It’s not rocket science.

For well trained athletes, this is just another variation of a faster speed workout. It’s not magical. It’s another tool in the shed. You’d probably get the same results with a number of other workouts. There is no magic workout that you need to do every week. Variety of stimuli is the key and figuring out what stimuli to hit and when is the key to training and coaching.

Don’t fall into the trap of searching for some magic workout. It doesn’t exist. Even if research might initially point in that direction, if you take a deeper look it’s not there. In the upcoming months, you’ll be sure to see this workout explode and take off as the next cure all. It’s not. Be forewarned and don’t fall into the trap.

This study and the subsequent increase in popularity should be seen as a demonstration of how to critically look at research. Don’t just look at the conclusions, but look at how they got there

Why timing matters

2012-04-15T17:02:00.000-05:00

Why timing matters

Knowing what to do or what supplement to take doesn’t cut it anymore. Knowing what and why is great but there’s another dimension that is often neglected and that is to ask the question of when. While it is easy to get lost in the minutia that is increased knowledge of genetic signaling pathways and training adaptations, this increased body of knowledge also provides us clues to that question of when to do things.

Timing is critical for one simple reason; it can completely alter, boost or negate, the training effect that you are working so hard for. Why spend so much work suffering through a workout or trying to do certain activities to maximize recovery, if by simply popping a pill or having the wrong order of exercise you can significantly negate the previous work. We’ll delve into some of the examples of where timing matters, but more importantly I hope that you start to ask the question of when to do things and if it matters. It’s a question that we don’t have all the answers to, but one that is overlooked and deserves investigation.

Caffeine

In a recent article on competitior.com I raised the question of whether caffeine is always a good thing in terms of performance. One of the messages I was hinting at was that when you take caffeine matters. Taking it before a workout or race decreases some immune system response, while taking it after can keep the CNS “up” for a bit after being taxed, which might make you feel better in the short term but repeating too often could potentially lead to some not too desirous effects. So when you take it in terms of the workout, and before what workouts matters heavily. As suggested in the article, deciding the timing of when to take caffeine and when not to is critical. Find a balance

Antioxidants:

I’ve written about this topic numerous times and by now the message might be a bit bland, but free radicals and oxidation occurs during endurance training, and it just so happens that it’s a signal for adaptation. The main pathway it affects is the PGC-1a pathway which leads to mitochondria increases. What happens when you take antioxidants is that it minimizes the activation of this signaling pathway therefore negating some of the exercises benefits. A couple years ago this was a somewhat theoretical argument, but the evidence keeps mounting. Recently, in Keith Baar’s lab they found that antioxidants did in fact suppress PGC-1a.

The question is if you still insist on popping some Vitamin C, E or any other antioxidant for reasons such as increasing iron absorption with Vit. C, then when can you do it? Unfortunately, there’s no clear answer, but its clear that when you take them matters. Take it right after the workout and you just suppressed adaptation, take it far away from it and nothing happens to the workout. Of course there aren’t enough hours in the day, so what’s the gap needed? There is no answer, but I subscribe to a 2 hour guideline. Why 2 hours? Because if we look at a few studies that have looked at PGC-1a activity, it peaks at 2hrs versus other times tested closer or further away from the workout. Therefore, space it out by 2 hours if you need to take it.

Another issue of timing mattering is that it depends on what the workout is as to whether or not you need to follow the rule. In general anything that stresses oxidation and adaptations such as mitochondria increases (so anything hard or long..) counts. On the contrary, if you are looking for hypertrophy from a strength workout then, you might actually want to take antioxidants afterwards. Why? Because in this case metabolic stress decreases the signal for adaptation for hypertrophy. So if you are a weight lifter, pop that Vit C if you want post strength session.

For those wondering what about fruits and all those wonderful foods that contain antioxidants, it’s pretty interesting but it seems like doses in vitamins are the problem and not the natural occurring ones.

Anti-inflammatories:

Another one I’ve covered numerous times so I won’t delve too far into it, but in this case inflammation is another signal for adaptation. The key is normal or just above normal inflammation is a signaler, not crazy excessive inflammation (as if you sprain your ankle horribly). Once again, when you take it matters. A study looking at taking anti-inflammatories during ultra marathons showed that inflammatories actually increased inflammation. So that might not be a good idea. On the other hand, taking certain NSAIDs before a race has occasionally shown to modify pain perception and therefore increase performance. Lastly, other research has demonstrated that taking anti-inflammatories post workout decreases training adaptations. So, once again, three scenarios of timing, three different outcomes. My recommendation is to follow the 2 hour rule again post workout for the most part, for similar reasons.

Iron:

Over at Sweat Science, Alex went over a study that showed that when you take iron post workout impacts how well it is absorbed. The general consensus was that taking iron within 6 hours of a hard or long workout decreases absorption. This is of particular interest for female runners trying to increase iron stores. If you continually take iron post workouts, maybe that’s one contributing factor that is creating the situation of you fighting an uphill battle in getting ferritin levels up.

Melatonin:

In 2009, when I was still training and went over to Europe with my friends and training partners Mo Joseph and Nikeya Green, one of the things I noticed was other athletes in our little group in Leuven were popping some meltonin. Why? Because adapting to the time change sucks…horribly… so much so that in our little dorm style rooming for the first few days we had an empty dorm room which was designated the can’t sleep room where if you were up at 2am and couldn’t sleep you’d just go there and see who else couldn’t sleep and hang out. Anyways, the popping of melatonin is an interesting one because it works! But only if taken at the correct time! If you take it at the right time, it actually really hurts you adjust to the time difference. Of course, none of us knew that then, but it’s a great example of timing mattering.

Without getting so complex that I don’t understand anymore, according to a review by Waterhouse (2007, Lancet) melatonin “delays the body clock after waking and advances it in the afternoon and evening.” So essentially if you take melatonin when your body is naturally low on it, it shifts the body one way, while if you take meltonin when it normally is high in the body it shifts the body the other way. So it depends if you are looking for a phase delay or phase acceleration in terms of taking melatonin. As for general advice when to take it, on YOUR body time, taking melatonin between 4pm and midnight causes a phase acceleration, while taking between 1am and 10am YOUR current body time causes a phase delay. So what time you are used to matters when you take melatonin. So, if I’m travelling from Portland to Europe and it’s 6pm and I pop some melatonin to help me get to sleep, it’s actually 10am my body clock time…so I’m setting myself back that first night potentially! Every night shift that by an hour or two until fully adjusted and you have a decent rule of thumb. Similarly, timing of light exposure matters and is another good example of this whole timing thing, but that’s another example.

Training

This should be an obvious one but sometimes the obvious ones are the easiest to overlook, but when you do certain workouts, it matters. We can use endless examples here, but we’ll stick to a few of my favorites and hope that you all can figure out the rest.

One that I always cite as a classic example is that the training adaptation changes based on if you do strength training before or after endurance work. The two pathways competing for adaptation interact and can help turn each other “on” or “off”. So if you do strength training and then follow it up with a good little run, you’ve shut off the pathway for muscle growth (which could be good or bad depending on what you’re training for). Additionally, we can look at some recent research that showed that how you adapt neurally depends on the timing of what was done first. This applies to not only endurance versus strength timing, but also the sequence of your strength training workouts.

Another quick example, is the timing of long runs or runs following long runs. When we are looking at training adaptation signals, one is a decrease in muscle glycogen. Once we are low on glycogen, some sweet adaptations take place to signal our body to deal with this better next time. It depends on the case, but sometimes it’s a good thing to train low. So there are two ways to look at this beyond relying on the long run to get the glycogen decrease effect. If we look at doing a long run and then 10hr later (i.e. long run in evening followed by next morning run), the glycogen stores certainly aren’t restored. So using a long run followed by an easier but still relatively long run is a good way to get double the low glycogen (i.e. 17mi followed by a next morning 10miler). Another option which I employ occasionally with my runners is the Friday workout followed by the Saturday long run. The Friday workout (especially if its something like a threshold run) can decrease glycogen just enough so the next day you’re starting with low stores and can dig a little deeper into glycogen depletion on the following days long run. It’s a great way to increase strength endurance.

Recovery

Finally, timing matters in recovery enormously. Take carbs in at the right time post workout and you maximize insulin sensitivity and replenish glycogen slightly faster. Take protein at the correct time and in the correct amount and you increase protein synthesis. Or take an ice bath at the right time and your legs feel good and poppy the nest run while take it at the wrong time and your recovery is hampered and you feel a bit flat.

I’ve discussed the above situations before, so I won’t go into detail, but one I’d like to expand on is protein ingestion. Of course taking it in during/after strength training in certain cases can increase protein synthesis promoting repair and growth. But one thing that most distance runners don’t think about is protein ingestion throughout the day. When I was in grad school, me and my fellow classmate, Matt Andre, who is getting his PhD at Kansas, would spend time after class throwing out theories together. One we came up with is whether taking a hit of protein before bed or even in the middle of the night would increase protein synthesis and therefore recovery. Similarly, with an athlete I coach we were experimenting with ways to increase recovery and came up with the idea of taking “hits” of 20g or so of protein every few hours to kind of give protein synthesis and the hormonal profile a boost. Well, it turns out we weren’t that crazy after all. At a recent nutrition conference put on by some heavy hitters in the science at GSSI, these topics were both brought up. It’s pretty exciting to see actual research backing it up, but the lesson isn’t that we were on the right track, but that timing of when you take stuff matters! It’s more than just total calorie or protein counts that matter.Secondly, we were just theorizing without much data to go on that we were aware of at the time. So think for yourself and if it makes sense give it a go.

These are just a few examples of the importance of timing which you can learn from, but the real key is getting you to think about when you do things and if it matters. Don’t overthink it as sometimes it doesn’t make a difference, but ask the question anyways. Being inquisitive and curious is the key to being a good coach.

Stress, Caffeine, recovery, and the immune system

2012-03-27T16:38:00.001-05:00

I just started writing articles for Competitor.com and the first one went up today. In it I take a look at the negative side of taking Caffeine pre-race or workout. Caffeine is generally thought of as only a performance enhancer, which it does well, but there are drawbacks if you chronically use it. In the article I take a look at what happens to the CNS and the immune system when Caffeine is ingested all the time.

Do The Performance Benefits Of Caffeine Come At A Cost?

http://bit.ly/Hcoiim

Secondly, Alex Hutchinson, who now has his blog Sweat Science on runnersworld.com wrote an article for Outside magazine in which I give my take on why stress is a good thing. Alex does a good job taking us through why sometimes we want damage to accumulate. In the article you'll also get a take from one of my athletes, Jackie Areson, who changed some of her nutrition supplement strategies based on the theory.

Stress Tested

http://www.outsideonline.com/fitness/recovery/Stress-Tested.

Enjoy!

Measuring Galvanic Skin Response….say what?

2012-03-02T23:28:00.001-06:00

Galvanic Skin Response….say what?

If you read letsrun.com and look up anything about me I’ll be branded as some science only nut who relies on too much science and forgets the “old school” way. If you were at my coaching presentation the Distance Summit put on at Queens University, after my “science” presentation you would probably label me as some anti-science guy, or at least anti-traditional science guy. (Plug: If you want to watch me (and other excellent presenters) ramble on for 2+ hours you can buy the DVDs here. I get no kickback; it was just one of the best conferences I’ve been to in terms of knowledge dropped: http://store.coachrunning.com/

The point I made at the conference is that you have to know HOW to use science. Science isn’t evil and it isn’t a cure all. But what it can do is provide some useful insight and data if you use it correctly. One of the other things, you may have noticed if you read this blog, is that I’m a fan of what I call resourceful science. Which means figuring out different ways to measure practical phenomenon.

One of the recent things I’ve been experimenting around with is something called Galvanic skin response (GSR). To make a long story short, GSR essentially is a way to look at sympathetic nervous system response. It’s been used primarily in research related to arousal states and in combination with other metrics in traditional lie detector tests. In this case, I’ve been using the affective Q sensor, which is essentially a watch like device that allows us to measure GSR on the go, or in real time.

So how does that relate to running? Well, no ones for sure yet, because there hasn’t been a lot of research on GSR and running or exercise for that matter. But if we hypothesize and speculate for a minute, several different potential uses can be thought of. Below is some things I’m looking into and further down is some data from three workouts from Jackie Areson, who recently got 2^nd at the US indoor champs is competing in the World Indoor Championships in Istanbul, Turkey.

1. 1. Arousal states to different workouts

We all know that various kinds of workouts tend to “stress” us out before hand more so than others. Renato Canova always makes the comment that Kenyans do a much better job of not using “nervous energy” to get through each and every hard workout. What we’ve been doing is wearing the Q sensor for the hour or so preceding the workout to get an idea of how the arousal state increases leading up to the start of the workout.

For example in the three workouts below, you’ll see that GSR during the latter portion of the warm-up before the 7mile straight tempo is much higher than before the other two workouts.

2. GSR during various workouts

Another interesting thing that can be looked at is what happens during the workout. There are various patterns that can be found. For example, during the long steady tempo, there is a rather linear very steady increase throughout. While on the alternating tempo which was basically 600m at 5k pace alternated with 1000m steady for 4.5mi, you see a higher peak with only some short leveling off. This probably occurs because of the still quick “rest” period that doesn’t really allow full recovery followed by the faster “hard” periods. Similarly, compare it to the interval workout which was much higher intensity but with recovery jogs in between that allowed you to come back down a bit.

3 3. Recovery or time course to return GSR to baseline

Lastly, another obvious thing to look at is the time course to baseline. We can quantify how long it took for GSR to return to pre-workout baseline levels post workout and/or post cool down. This allows us to get a rough idea of Nervous system state, and can be used to see what recovery metrics might enhance or delay this. For example, we can look at what happens when you stretch, do general strength, hop in an ice bath, or eat food post workout and see if there is any effect on the time course of recovery.

4 4. A lot of other things!

Some other metrics we’re looking at are what effects GSR during recovery in between intervals (walk/jog/run/exercises). What keeps GSR up during the in/between time of finishing the warm-up jog to the actual workout (drills vs. strides vs. stretching). What calms or excites each athlete pre-race or workout to get them to their optimal arousal state.

Alternating tempo

Straight long tempo:

900/500/800/400/700/300

Who cares?

The point is that it’s a relatively unexplored area and its exciting to be essentially messing around with stuff to try and figure it out. It’s at the stage of just because we can measure it, doesn’t mean it’s important. However, the hope is that we can collect enough data with elite runners and notice patterns or trends that correlate with other variables then it might give us another objective measurement. And if not, then hey, it’s some cool data to mess around with!

(and if all else fails, it’s still fun to see the GSR spike in real time if you intentionally stress someone or say something to make them uncomfortable...or if you don’t want to be intrusive to someone else I can only imagine the arousal response on something like a date…so many possibilities to try!...and yes I will be the ultimate science geek wearing this thing around during different situations…)

Crossfit endurance, Tabata sprints, and why people just don’t get it

2012-01-12T18:51:00.001-06:00

Crossfit endurance, Tabata sprints, and why people just don’t get it

Not terribly long ago, I stopped dating a girl because she did crossfit.

Okay, it wasn’t the only reason, but it was a major factor. I mention this not to show how messed up my dating life/requirements may be, but to show how strongly I feel about the marketing scheme that is Crossfit. I’ve always wanted to write a blog post about it, but the article in this months Runner’s World has finally pushed me over the edge. I’m writing this blog to give a 2^nd opinion and to combat the marketing hype that surrounds crossfit. I wouldn’t take much offense to crossfit and would let it do its own thing, except when you start telling people that this is the way of the future and that Ryan Hall would run faster if he did this stuff , then I have a problem (Yes, CFE founder has made this claim)

For this post, we’ll focus on Crossfit Endurance because it got some major publication in this month’s Runner’s World and has been getting some hype lately. If you were at my presentation at the American Distance Summit in North Carolina, you got to hear me take a few jabs at crossfit (and Renato Canova even threw in a jab or two!). Since it’s a question I get asked a lot, lets take a look at crossfit endurance.

The claim and exploitation:

Crossfit Endurance and CF in general is a randomized non-system of training. It’s basically a set of random workouts that are high intensity circuit based workouts. In CF this refers to a variety of high strength circuits and in CFE it combines this with high intensity intervals like the famous Tabata “sprints” (sets of 20sec hard/10sec easy). There are no easy runs. It’s simply mix short intensity work with slightly longer high intensity work and that’s all you get.

Crossfit exploits a couple different natural reactions people have to get people on their bandwagon. First, they create a straw man “us vs. them” mentality. We’ll go over this straw man tactic a bit later, but they try and cultivate this idea that just because it’s different and new means its got to be better. They throw in some pseudoscience or misinterpretation of science and they’ve bolstered their selling point. Further exploiting peoples natural habits, they promise better results with less time commitment, which in today’s “busy” world is probably the number one selling point for many products or ideas. If you’ve ever watched late night infomercials, you might start to see some similarities…

Lastly, once you’re in they do something pretty creative. They first created their own new performance metric on which you’re judged. Because being good at all the other methods of establishing performance isn’t good enough, so now you’re judged based on some criteria that crossfit develops. Being a specialist at something is apparently bad? Additionally, they really go after this hard work/pain = improvement and results idea. This is also known as the Rocky effect. But if you’ve been in the coaching business long enough you know that hard stupid work doesn’t get you anywhere. You can’t just do work that is painful just because it hurts and expect to get better.

Getting beyond some of the basic philosophical tenants of CF that are ridiculous, let’s look at some of their claims in regards to endurance performance and training.

What crossfit doesn’t get:

The central claim is that you can get the same endurance benefits (or better) from doing high intensity work and limit any slower to moderate paced running. They go on to claim that endurance training ages you faster and is detrimental to performance. Their claim rests on their misunderstanding of VO2max as being equal to or critical to performance.

Let’s use their main research backed claim to look into their claims.
Tabata sprints and the high intensity misunderstanding:

A researcher named Tabata did a series of studies on untrained and then moderately trained individuals in which he gave them a workout that consisted of 20sec hard/10sec rest for 4minutes. When this program was researched, they noted that VO2max increased by a large amount and that certain aerobic enzymes also increased. Using this and similar studies as their basis, CF has championed the idea that you can get the same, or better, performance off of doing intense work like that done in the study. Lets use this as a way to look at why these claims are false.

#1 VO2max does not equal aerobic performance:

While I’ve written before about the measurement of VO2max and how it relates to performance and you can read more in depth on it in those blog posts, it bears repeating the conclusions reached by Vollaard et al (2009):

“Moreover, we demonstrate that VO2max and aerobic performance associate with distinct and separate physiological and biochemical endpoints, suggesting that proposed models for the determinants of endurance performance may need to be revisited (pg. 1483)”.

The basic idea is that VO2max and performance are separate things. Just because VO2max is increased or decreased, does not mean that performance will change to the same degree or even at all. This is a key concept to understand because often times studies will track training’s effects on VO2max and not performance. For instance, in much of the research cited by CF or even cited in journal articles that talks about the benefit of high intensity training or strength training, they talk about changes in VO2max.

#2 Intervals increase aerobic ability of FT fibers

At the coaching clinic I presented at Renato Canova made a nice point that somewhat fast interval training can increase the aerobic ability of Fast Twitch fibers. It’s best to think of it as an interplay between FT and ST fibers. In that different intensities and volumes will increase aerobic or anaerobic enzymes in each type of fibers along the spectrum. What that means is that although high and low intensity might both hit similar aerobic enzymes, they do so in different ways and in different fiber types.

#3 Why does VO2max improve?

Understanding why VO2max improves is another key to understanding this whole debate. VO2max does not simply reflect aerobic ability. Instead VO2max is influenced by several mechanisms. First off, if you’ve read Noakes central governor or if you’ve read recent research on VO2max testing protocols, you’d know that VO2max isn’t an actual max. You’re body self limits it. One way to improve VO2max in a test is to be familiar in pushing closer to that “edge”. If your body knows you can go there, it loosens the limits a little bit. Very hard interval training lets the body know it can handle high stress loads.

Secondly, we know that VO2max is influenced by muscle fiber recruitment. So if we increase the amount of recruitable muscle fibers during a test, the VO2max will rise. What’s a way to increase muscle fiber recruitment? Sprinting, strength training, etc. It’s one of the reasons why you see VO2max increases in untrained athletes but not so much in trained following strength training. The trained ones are pretty good at recruiting more and more fibers as they get closer to fatigue. The untrained, not so much.

#4 What Happens when we build a base and follow it up with intensity?

A major problem with research studies is that they are all short term. It’s the nature of the beast. But let me pose a few questions to all of you.

What does the typical recreational endurance athlete do?

If you answered jog around or do easy and moderate runs with little hard workouts you’d be correct. Most recreational runners for instance simply go run. Why does this matter?

What happens when you take people just doing mileage and add intensity?

If you answered they improve over a short time, you’d be correct! Think back to your HS days when you spent a summer building a base of almost just mileage and then you hit the season and your coach starts throwing interval training into the mix. You get a nice boost in performance right? This is essentially what happens in these research studies. They take recreational runners who just do easy/base stuff and then throw 6 weeks of training hard on them and they improve. Ask any coach and they’ll say this is just a simple old school peaking/training program. In fact, it might resemble your typical HS application of Lydiard training.

#5 What CrossFit endurance does is reminiscent of training done in the early 1900s:

I harp on people to know their history so that they don’t repeat training mistakes. In the history of endurance training it’s been a constant back and forth between intensity and volume of work. Early on there were very very big swings. So we went back and forth between training that was almost all easy slow running and that which was all hard interval training. As training has evolved we’ve gotten closer and closer to that sweet spot and mix.

What CFE has done is ignore all that and try and go back to a time when all that was done was very hard very fast interval work. It worked to a degree, but performance got much better when we modulated things so that there was a nice mix.

Essentially, Crossfit is living in like the 1940s. We’ve learned from those times and evolved.

#6 A straw man of LSD vs. high intensity:

Crossfit, and many others, typically create a straw man where they compare their training to a type of training that isn’t used but by very beginners. They paint running training as almost all LSD (long slow distance), when the reality is if you look at any elite, college, or high school training program there is a nice blend of volume and intensity. No one is just jogging around each day. Yet that is what they have you believe. This even happens in research when they compare interval training with just jogging around, as if jogging around was the norm for training.

What happens in the real world of course is that there is a nice mixture and blend between volume and intensity. Essentially, they are arguing for something that doesn’t occur.

#7 Two ways to improve aerobic endurance

In fact, if you look at how some endurance adaptations happen, you can see that to increase things like mitochondrial density, several different intensities trigger similar adaptations. This goes along with the point on enzyme activity and FT/ST fibers. But if we look at this nice graphic from Laursen (2009), we can see that two different pathways to achieve some of these functional adaptations are activated by endurance and interval training. So why the heck would we want to use only one pathway when two different means of getting these nice adaptations are there. If you just attacked the problem from one side, you’d maximize that side quickly and have nowhere to go!

Additionally, we know that repetitive stress and activation of signaling pathways is what triggers adaptation. It’s one of the reasons why we train pretty much every day for maximum performance even if some of it is low intensity. That low intensity easy to moderate work helps to enhance recovery and applies a consistent signal for adaptation. Pure rest in this case isn’t better (which is often the counterargument).

#8 Periodization matters:

It seems simple enough that people would know that how you plan and periodize training matters. Training isn’t a random collection of hard exercises or workouts. There has to be some sort of logical sequence and progression. If there’s not, then you can expect to get exactly what you trained for, random results.

The bottom line is that so called high intensity interval training (HIIT) which is the new fad word with strength coaches is good. But for endurance performance it’s even better when it is supported! You have to support it with something. Endurance work of various kinds and even pure speed work (with lots of recovery) serves as support for the intense stuff.

#9 Interaction matters:

Endurance and strength gains fight each other a bit for adaptation. While I don’t want to get bogged down in the details, if we look at the signaling pathway for some endurance adaptations and then muscle hypertrophy which are two goals of CF and CFE, we can see that they interact and in fact impair each other in some cases. For example, doing endurance work right after strength can impair hypertrophy because the mTOR pathway(which signals hypertrophy among other things) is basically switched off with endurance work. This isn’t meant to show that they are mutually exclusive, but instead to show that when you do things matters. Sometimes a whole heck of a lot! Thus why you have to think about and plan things, not just do random hard workouts.

This goes for not only sequencing of endurance and strength work, but also in regards to sequencing different strength workouts. You have to know what pre-fatiguing muscles does to the subsequent training effect. And you have to know what the effect is on the Central Nervous System. Crossfit doesn't think about this at all. They don't care.

#11 Individualization
My number one pet peeve. There is no individualization. Workout of the day. That's the norm. Beyond that, everyone does the same crap for the most part. I could go on for days on the importance of individualization, and CF and CFE fail miserably.

What does this all mean?

What happens in the long term?

Again, I’m going to ask a rhetorical question, for you HS coaches out there what happens if you mess up the balance and do too much intense interval training after that base phase? The answer is the kids fried. You see it all the time in High School. A kid hits the interval training hard, runs some amazing early season times and then fizzles out and is fried by the end of the year. That’s what happens training wise. If you want lactate proof, this is what happens aerobically if you mess things up. You shift the balance to working anaerobically too much (Test #3) and you produce more lactate at each pace, and you are done!

The reason is that there is an interplay between easy to moderate running and intense running or even strength training. If you work too much on the intensity or strength side you shift things towards that way. In practical terms your lactate produced at each speed might go up or you might decrease aerobic ability a little bit. Same goes if you do too much volume with not enough speed support. You’re speed side would be neglected so that would go down. It depends on what you are training for but achieving some sort of balance is key.

Additionally, if we look at very long term implications for performance we know that the foundational aerobic mileage does a few things. First in long term studies on Cross Country skiers, the high volume of training created a fundamental shift in fiber type towards those which improved their performance. So we got a ST fiber type shift for guys who needed lots of ST. Secondly, the high volume of training leads to long term increases in efficiency. Yes, high intensity work or even lifting can do this too but again it’s through different mechanisms. Lifting for example can increase efficiency via modulating stiffness of the system. Or essentially creating a stiffer spring. High Volume training on the other hand works via increase the efficiency of both motor program patterns (because of the repeated nature) and at the muscular level in terms of oxygen utilization and waste product removal. Again, two different ways to hit the same functional adaptation (improved efficiency), so why would we just want to work on one of them.

So we have research showing that in very elite runners, long term high volume training is needed to make functional changes. We have practical experience in that throughout history we’ve shifted towards the volumes we do now and that practically every single good runner does a solid amount of mileage (with good intensity mixed in) and we have the theory of why mileage should work.

If we simply put crossfit endurance through the same kind of review we have:
Research- short term studies on high intensity training shows improved VO2max and in some cases performance, but we have looked at why those don’t apply neatly already. No research on crossfit endurance in particular

Theory- It goes against all known scientific theory for how endurance performance should be improved and how it actually happens.

Practice- No good runners do it. We know from history what happens and what kind of performance you get even if you do a lot of high intensity work with very little volume.

And lastly, it doesn’t help that they subscribe to every fad from diet to pose method of running that there is.

Finally, if you want a very interesting research approach to the high volume/intensity paradigm read Stephen Seiller’s nice summary here:

http://sportsci.org/2009/ss.htm

And finally, I’d like to point out that finishing and racing are different. I’ve heard far too many times that so and so did crossfit and finished a marathon so it must work. No offense and sorry to sound elitist, but if I took off 6 months and did nothing I could still finish a marathon. It doesn’t mean my program of doing nothing worked.

What does this all mean?

While this was a lengthy rant, it only touches the surface of the Crossfit or Crossfit Endurance phenomenon. My point wasn’t to critique everything they did (that might be later) but to teach you why some of their claims they make, even research based claims, might be wrong.

In the future we’ll look at some of the specifics behind crossfit.

Altitude babies, Rats, and Epigenetics

2011-12-26T12:43:00.001-06:00

New born rats, altitude, and epigenetics:

Over the past few years, the term epigenetics has kind of exploded in the popular science world. I’ve discussed it at length in this blog and how it might have implications with a wide range of topics from obesity to African running dominance to how we adapt to altitude.

One of the basic ideas is that what happens in the time period before and just after birth is when a newborn is kind of adapting to its adjustment. So if we look at diet, if a mother is going through famine during this time frame, then the baby changes to be prepared for this environment. So it’s response to certain foods or its insulin response is adjusted. Similarly, there’s been some studies looking at mothers who have high stress loads during and right after pregnancy result in babies have altered stress hormone responses for the rest of their life.

I always joke with my friends that whenever I have kids, I’m going to stick them at altitude during pregnancy and right after just to develop super altitude adapted kids (and my friends always respond with you better find a wife who is crazy enough to let you do all this wonderful experimentation…and that you’re kids are gonna be messed up…but that’s besides the point…). Which brings me to the point of this…

A study in the Journal of Applied Physiology was recently published that took a bunch of rats that were at high altitude in Bolivia and made a group of them live in a simulated sea level environment. So you basically had an altitude group and a sea level group, but it was only from 1 day before birth to 15 days after birth when they were in these two different environments. Then they were brought together and lived their normal rat lives together. Well, they checked them periodically through their life and ultimately at 600 days post birth.

What is interesting is that those 16 days during development affected parameters for the rest of their lives. For example, the “normoxia/oxygen” group had lower hemoglobin and hematocrit for the rest of their lives. They also had “reduced right ventricular hypertrophy (both sexes); lower air space-to-tissue ratio in the lungs (males only); reduced CO₂ production rate, but higher oxygen uptake (males only);”

It’s pretty interesting that 16 days in the rat lifecycle affected various parameters for the rest of their lives. It just goes to show how important that development period actually is and it brings up some questions about altitude training and whether just copying altitude born athletes is the key or if we should attack it from a different way with sea level born athletes.

I’m not really sure what the practical importance of this is, except maybe my crazy joking of having high altitude babies might be on to something…

(study abstract here: http://jap.physiology.org/content/112/1/33.abstract?etoc )

2011-12-21T16:52:00.000-06:00

A few weeks ago I was fortunate enough to be at the Canadian athletics coaching symposium to speak with Alberto Salazar on a couple of different topics. It was a great experience and I picked up a lot of interesting ideas from other presenters and those in the audience who I chatted afterwards with. While there, Jay Johnson asked me to sit down and do a podcast covering a wide range of topics from HS training to sprinting to what I do now with elites. So head on over to Jay's site and take a listen.

http://www.coachjayjohnson.com/2011/12/podcast-003-steve-magness-interview/
Also, a couple articles I wrote or contributed to for Running Times are online now so if you haven't checked those out, there might be something useful in them:

When to pull the plug on your season:
http://runningtimes.com/Article.aspx?ArticleID=24550

How to do a hard workout after a race:
http://runningtimes.com/Article.aspx?ArticleID=24260

Lessons from outside the running world

2011-11-28T10:41:00.001-06:00

This is going to be an interesting attempt at a blog. One that takes seemingly unrelated subjects and ties them into my main focus, running.

If you were to flip through any of the myriad of books I’ve read on some pretty random subjects, you’d see the margins littered up and down with notes. If a stranger was to read them, they probably would make no sense, because they’re almost all about connecting whatever random subject I’m reading about back to running. It doesn’t matter what the subject is. Recognizing similar patterns in other subjects, or taking overarching themes and tying them to your specialty is key to broadening your horizons and not falling into the same dogma that gets presented over and over again within a specialty. Making connections is a skill that should be learned. Given that, I’m going to delve through several of my books and highlight some of the abstract lessons I’ve learned and what that means to my specialty, running.

This is somewhat related to a previous post where I gave my kind of overarching principles and rules for everything:

http://www.scienceofrunning.com/2010/04/my-rules-of-everything.html

Complexity-

One of my favorite sayings is we constantly underestimate the human body and its complexity. You can see this in almost every field, but in exercise science some recent controversies that demonstrate this are the hydration issue and the running shoe cushioning issue. Reading other science type books does nothing but cement the idea of the complexity of the body. My quick example will be from the book Evolution in four dimensions, where in one part there is a discussion one pigenetic changes to DNA leading to evolutionary changes. The authors state that recent findings result in an ability to change their way of thinking. “We are now free to think in realistic molecular ways about rapid genome restructuring guided by biological feedback networks.” This quote was made in reference to how for years, it had been assumed that the gene was all that mattered. Nothing changed, environment mattered little and the gene dominated. However, more recently we know that that isn’t how it works. Another quick example is that of hydration where we assume that weighing ourselves and forcing down fluids is better than listening to our body and thirst mechanisms. The lesson here is obviously to be aware of the complexity of the body and its almost genius.

We’re in the age where technology allows for improvement. That translates over to the somewhat false idea that we can engineer things to be even more optimal. As mentioned earlier, the overbuilding of shoes is a great example. Another more relevant to performance change would be the reliance on “fake” foods or vitamins. For more information on this, see sweatscience.com and the recent findings on whole vs. partial foods and what our brain senses, or see my many diatribes on why antioxidants after/during exercise isn’t a good idea.

Knowledge reflects what we experiment on and study:

This is a seemingly obvious statement, but the impact is profound. We only know about what we study in science. In reading the book Evolution in four dimensions, they make the nice point that since early genetic studies were on flies and then bacteria, our ideas on how genes and evolution work was based almost entirely on what happened in these organisms. The problem became when we transferred that into overarching principles for all of genetics. This happens all of the time in every science. Theories are developed and become dogmatic because they fit with what was initially studied by happenstance almost. You can see this in running science literature or coaching.

We only know what we study. So if some early pioneer focused on VO2 measurements because that’s all they had to measure with, then that becomes important simply because we could measure it. The same goes for lactate during the 90’s, and so forth. This is one problem with a strictly evidenced based program. We know far too little to be able to measure what matters, performance, and in many cases we don’t even know what we should be measuring.

Short vs long term- pg. 57From the book the 10,000 year explosion- “sometimes the apparently inferior choice has a better upgrade path: Evolution can’t know this, and we aren’t particularly good at recognizing it ourselves….”Natural selection may solve the same problems differently in different populations, and what appears to be the most elegant solution at the time may not in fact turn out to be the one that works best in the long run”

The principle of immediate versus long term results is a paramount. The above idea fits well in running in several ways. First off, in terms of workouts, there are certainly workout types or methods that would produce very good short term gains, but then would sputter out. It’s important to keep the big picture in mind and realize that sometimes we do things because we know they will increase your ceiling in the future. A good example is running form changes. Sometimes when you make form changes you get an immediate decrease in running economy, because the movement is new and awkward (and that’s what researchers will point too…). However, what proper form changes do is increase the potential ceiling of efficiency. So that once you get adapted to the change, how efficient you can actually be increases.

The second part of this quote is very pertinent to coaching. Sometimes the easy solution doesn’t work in the long term. For example, we might see big improvements by throwing a bunch of fast interval work with no mileage background for a few weeks. But what happens most of the time is the athlete gets sudden improvement and then plateaus or bottoms out. So fast work might be the easy answer to the question “How do I improve for the race in 3 weeks?” but long term it might not be the best option.

Adaptation length-

Again from the book the 10,000 year explosion, they give a nice example of how adaptation time matters. In terms of food, the popular example is how the Polynesians or aborigines have more western diseases then even western cultures, probably because of very recent changes in diets. The western cultures have had a much longer period of time to adapt therefore the stress response isn’t as great.

I like to translate this to the length of time that an athlete has had of a particular training stimulus. A runner who has years of mileage and tempos will be much more adept at doing those workouts or that load, then one who has done low mileage and lots of fast work. What that means, is that even if two athletes run the same times, it doesn’t mean they should be doing the same total workout load of one particular aspect. Instead, you have to look at where they are in terms of adaptation.

Connectivity- “science requires communication and cooperation between people who are unusually good at puzzle solving.”

This is self explanatory, but connections are key and you need someone to bounce ideas off of and tear apart those wonderful theories you have. It allows you to get a viewpoint that doesn’t include your biases. Sometimes the most productive conversations I have on training/running are with those who know running well enough, but who are very smart in fields outside the exercise science/training world. They aren’t trapped by traditional thinking and will ask the question “why?” on things we just accept and take for granted. It’s amazing how many things you just skip over and your brain doesn’t even think about, that probably should be questioned.

Averages-

“If you are advising or treating individuals according to the average effects of a gene, you may be doing the wrong thing.” Average mask individual variation- that’s the whole point of an average.” Both from Evolution in four dimensions.

The fact that everything relies on the average is a common theme. If you look, almost every single research study is based on the average. That is a necessary evil, but far too little attention is paid to variability. This is the single reason why we can’t have an entirely research founded practice in training or coaching. If we just did what the studies said exactly, then we’d be training the way X average person in X population should train. What about the outliers (of which we mainly deal with in elite sport…). Individualization is key. Don’t forget that when coaching, and don’t forget that when evaluating research. Just because X works on average, doesn’t necessarily mean it will work for your individual.

Again, not to nitpick, but it’s why we can’t just say “X worked in research, so it should work for you.” This applies to every field and it’s why the best in whatever field are the ones who can take principles learned and think outside the box using those principles. They simply don’t prescribe some workout or some diagnosis because it worked for the average person.

Part vs. whole- “Whether or not a length of DNA produces anything, what it produces and where and when it produces it may depend on other DNA sequences and the environment. The stretch of DNA that is a gene has meaning only within the system as a whole” e4D-

We tend to isolate variables and concepts and take a reductionist approach to everything. Do x “Vo2max” workout to improve one variable, do x Threshold to improve another. We forget that the interplay and interaction is what is truly important. What a workout does is defined by what surrounds it. Renato Canova once put it nicely when he said that an athletes fitness can change even if X indicator workout is the same if what has surrounded that workout has changed. It’s why one single workout in time doesn’t matter.

This also relates to nutrition where we see a reductionist approach to we need X vitamin or nutrient or macronutrient and it doesn’t matter how we get it. Recent research, however, shows that the brain is much smarter than we are. It changes how it reacts based on the combined effect of whatever we are taking.

Forget- Darwin thought use and disuse and heritable variation occurred, but over time this part of his belief was lost and forgotten. So everyone thought he didn’t think the above was how it worked.

“at this point in time, as at most previous stages of the history of evolutionary ideas, certain findings in biology are being ignored or underplayed”

We go through a cycle of forgetting and remembering what’s been done before us. You see this in the reintroduction or rememphasis in certain training methods in the coaching world. That’s why it is incredibly important to know your history. And if you can, know your history from a primary source where you attempt to look at it through their eyes during that time period. For example, going back and reading Lydiard’s original work gives a greater appreciation of what he was trying to do, then reading someones summary now, 50 years later. We lose a little bit of the original message.

Know your history. The more history you know, the more you realize why certain methods stuck around and certain ones were discarded. You’ll also learn methods that were successful that may have been overused but still have a place in your arsenal (think Igloi training…).

Commitment- In the book Sway, they talked about the reluctance of football teams and coaches to adapt to new styles, “they had used the grind it out and hold on to the ball strategy for so long that it was simply hard for them to let go. They were committed to continuing down the road they had always walked. They were so committed, in fact, that it was virtually impossible for them to take a different path.”

This relates to another one of my favorite sayings, it’s okay to fall in love with an idea or philosophy, but don’t marry it. If you start identifying solely with an idea or “marry it” then you put yourself in a hole and will resist change even if that is what needs to be done. This is particular important in training because there is so much individual variation that at times you are going to have to go against your norms and do something different. It’s one of the reasons I hate when people say “I’m a high mileage guy” or “I’m a speed guy” in terms of their coaching philosophy. Well, that’s great, but your pigeonholing yourself and there will be a day when an athlete comes along that needs the opposite of your philosophy and you will have to change if they are going to be successful. Can you?

Value attribution- Another one from the book Sway. Value attribution is our tendency to imbue someone or something with certain qualities based on perceived value, rather than on objective data. “we may turn down a pitch or idea that is presented by the wrong person or blindly follow the advice of someone who is highly regarded.

In the book, they describe how the value that people attributed to drinking the same Sobe drink affected their score on a subsequent test. Meaning that if they paid more for the SoBe, the scored better because if they paid for it (and attributed value to it) then the claims must be true.

“we often ignore all evidence that contradicts what we want to believe.” From Sway

Lastly, we’ll end with this quote. Don’t take offense if evidence points to a different conclusion than you thought. Read it, analyze it, and see if it fits in. It doesn’t have to change your opinion, but if there is enough of it, you might want to consider. You see this all the time in Science. Whether it’s global warming or shoe pronation/cushioning. Take evidence as data. Don’t ignore it for convenience.

There ya go. There’s my mishmash of random recent lessons I’ve learned from reading books outside my field and how they relate to my field. I highly suggest stepping out of your comfort zone at times and trying to see if you can tie overarching concepts back into your own specialty.

The Sole of the Shoe: Looking at inside the midsole

2011-11-07T19:02:00.003-06:00

The sole of the shoe:

With this whole barefoot/minimalist/running mechanics thing exploding right now, one fo the more productive outcomes in science is the realization that the body is smarter than we give it credit for. All those old biomechanical models that presented the body as rigid mechanical body don’t quite accurately reflect what’s going on. Instead, the body works in a nicely complex way where stiffness, tension, and muscle activity are adjusted on the fly based on feedback the body receives. So it’s constantly calculating and preparing for what’s going on. So that means adjusting for the ground surface type, the position of the legs and feet throughout, and so on. Essentially, your body has an in built cushioning system.

You might remember those Adidas shoes that had a computer chip in them that attempted to adjust the cushioning every stride? Well, in this case, the body already does that and better than any technology we have currently can do. (Which makes me wonder, if the shoes adjusting cushioning constantly for the ground, and the body is adjusting the cushioning based on the shoe, among other things, that just seems like a bad situation of constant adjustment going on that is fighting against each other.)

http://www.pocket-lint.com/news/2015/adidas-updates-its-computer-controlled

A couple recent studies published in Footwear Science help illustrate this point even more so. First, a study entitled “Relationships between impact variables from running in 20 different footwear conditions” showed that the traditional mechanical tests used to measure cushioning do not translate over to what actually happens cushioning wise when a person is running in those said shoes. While it might be obvious, this is significant because that’s how they classify the “cushioning” that a shoe has….And it doesn’t actually translate to real world application. So we have a situation where the classification doesn’t match what actually happens.

A second article, “Impact characteristics in shod and barefoot running” took several different custom shoes with wide varying midsoles (from 4mm thickness of cushion to 20mm). The basic conclusion was that in terms of impact forces and loading rates the amount of midsole thickness didn’t matter (for statistical significance). And Barefoot running changed the impact charactistics largely through an adjustment in foot strike and placement.

The point of the above is to reinforce the idea that the body is a complex dynamic system.

Which brings me to the point of this:

Cobbling shoes:

Recently, I decided to cut up a couple different pairs of shoes just to take a look at the insides. It’s rather interesting what certain shoes have in the midsole and the perceived reasoning behind them. You always hear the fancy names thrown around for the technology, but it’s pretty interesting to see it hands on. So that get’s me to the point. If we assume that the following is true:

-We know that the body adjusts stiffness and muscle “tunes” itself to the surrounding environment. So it adjusts based on the surface the foot will hit.

-We know that shoe structure impacts proprioception which changes our in built “cushioning”.

THEN, it would make sense that sense our body adjusts for what it is going to hit that the midsole of the shoe influences our bodies adjustment. Therefore if we look at the midsole of the foot, the fact that it Is not uniform begs the question of how does the body adjust to it?

For instance, if we look at running on a soft/unstable surface versus a pretty stable surface like concrete, then we see differences in muscle tuning and preactivation. So, if we have a midsole that has a variety of “stuff” in it, what is the body adjusting for? I don’t have the answer to this question but it seems interesting and plausible.

For example, if we take a look at the two shoes here. One has a firmer outer lining of the shoe with a very soft midsole in the middle. So, does the body prep for the initial striking of the firmer outsole when you either land on your heel or on the lateral edge of the fore/midfoot. Or do you prep for the super soft middle of the midsole?

Similarly, if we look at one of the other examples here, if you are a heel striker, does the firm crashpad get adjusted to, or the soft white midsole or the air pads underneath the forefoot and heel? It seems like the constant change in cushioning would change how our body accurately adjusts or "tunes" to the surface. It's akin to the story Biomechanist Benno Nigg tells about the Circus performers who install a flexible shock absorbing floor and the injuries skyrocket. Why? Because the way the floor was made you had sections near the "support" stiffer than the furthest points in between the support, which were very pliable and responsive. So you created a situation where you had a way too soft area and then firmer areas, so the body never knew what to prepare for. The injury rate decreased as soon as the floor was changed by the way.

And finally, we get to another shoe design that puts gel basically along the center of pressure of where a heel striker would travel. That seems like a great idea, but again, perhaps you create a level of unstableness and mixed firmness that might create a bit of confussion.

The point of all of this is does the mixing of hardness in the shoe itself create a slightly unstable situation, like if one we’re to step partially on sand and partially on hard dirt?

I really don’t have the answers to these questions at all. It just strikes me as interesting and I wanted to ask the question.

My gut feeling is that creating a highly non-uniform midsole would create a situation where the body doesn’t know exactly what to adjust for and it creates a situation where the foot functions artificially. Because of the variance in hardness you influence the natural motion of the foot in the shoe itself. So it might sink more in certain places or alter the loading in certain areas based on the variance in stability.

I could be off here, but if research from Irene Davis’ group shows that even socks influence the proprioception of the foot, then a crash pad or gel and air insert at various places in the midsole could certainly have an effect in what our body does to prepare for the ground.

Just something to think about..

Training to Kick

2011-10-06T16:53:00.003-05:00

How to train a kick:

In the last post, we took a look at the physiology behind the kick. That’s all well and good but it’s pretty much useless unless we can translate that knowledge into something practical. So let’s give that a go based on theory and practical experience. Here’s my guide to creating a kick:

Finding the weak point and attacking it from multiple ways:

If you are at all familiar with my training style, one of my central premises is to attack a problem from multiple different directions. The same thing applies to the kick. What we ideally do is look at what each runners strengths and weaknesses are in terms of why they can or can not kick, place the emphasis on developing that attribute, but make sure we cover the opposite side too.

That means the first question that needs to be asked is, what’s the balance between their aerobic strength and anaerobic capacity? Obviously increasing both is needed, but this answers the question of whether they run out of gas during the race (lack the strength to stay more aerobic deep into the race) or whether they have the speed ability to actually kick. This will develop the proportion of emphasis. You want to attack both sides, but sometimes one side needs a little bit more emphasis because it’s a bit weaker. Given that, let’s go into the different ways of developing a kick:

The steps:

If you remember in the last post I gave a general outline of what you need physiologically. Let’s use that as a template and I’ll show you how to develop those abilities:

Get to the end more aerobic than anyone else

Essentially we need to get to the “kicking point” as aerobic as we can without delving deeper and deeper into our anaerobic and muscle fiber reserves. To do this, we’ve got to build the aerobic system. The first step is easy and any coach could tell you how to do that. We need a general aerobic base, which means mileage, tempo runs, aerobic intervals, etc. to build the foundation. That changes slightly with mid-distance 8/15 runners where we have to develop the aerobic system more through igloi style intervals

Once a general aerobic foundation is built, then the key is getting more aerobic at race pace. My favorite way to do this is through Canova style alternations. Why? Because it’s a nice progressive way to work aerobically while increasing race specificity. My typical example for the 5k would be start at 200m at race pace alternated with 1400m at a steady pace (just slower than marathon pace to start with) for a couple miles. Then progress that until you’re running 800/800 or 1000 at pace/600 steady, with the fast pace staying at around 5k pace and the steady getting a little faster.

So a general template would be to start with increasing threshold work (unless a speed orientated 8/15 guy, then less threshold stuff…) duration and then speed. Mix that with some slightly slower tempo work of longer duration (6-10mi tempos). That gives you the general foundation. Then to work on specific aerobic ability, add “stuff” to the tempo, add alternations, and add some aerobic “igloi” intervals.

Have a larger degree of anaerobic capacity to use and a larger motor unit pool to call upon.

These two physiological goals tie together nicely, so we’ll cover them jointly. The other main component of a kick is having the ability to recruit additional muscle fibers when fatigued and call upon our anaerobic energy reserves. Before working on the ability to use these under fatigue, we have to increase the total capacity of each of these which are done through similar mechanisms.

We have to lay the foundation and develop the ability to recruit a larger percentage of our muscle fibers in a fresh state first. No one can fully recruit all of their fibers because we have some protective mechanisms involved to prevent this from happening as catastrophe would likely result. However, you can train to edge the percentage of fibers you can recruit towards that 100% max. Research shows that elite athletes in various sprint or explosive events are much closer to max recruitment than regular athletes or untrained people.

To increase total fiber recruitment, we need to do activities that have a high force requirement and ideally do so in a specific running manner so that we recruit the same muscles in the same sequence that we do when running. For distance runners, this simply means we need to sprint!

(For mid distance or shorter athletes, we can often build a foundation of muscle recruitment via doing explosive/ballistic type non-specific activities first as they “violate” the size principle to a degree and make it where Fast Twitch fibers are preferentially recruited. Then you follow that up with a specific period where you try and translate those gains to the specific action of running through sprint work.)

I prefer to use a method where you start off with hill sprints because of the reduced injury risk and the fact that the hill will increase fiber recruitment and then transition to sprints on the track. The reason for this is that we get a little bit more specific as the training progresses as we get a bit more reactivity from doing flat sprints and a bit more strength when doing hill sprints.

To work on the energy system side of things (the anaerobic capacity) we have to go fast for a little bit longer so we’re stressing the anaerobic systems ability to produce energy maximally. That means extending sprint work both on the hill and on the flat. The key is that these are anaerobic capacity workouts. They’re not designed to get us to deal with large amounts of fatigue or running fast when tired or anything like that. Given that they require long rest, and the best way to do them is initially as an add on at the end of sprint work. Later on they can be their own “workout” but most distance runners can get away with just doing a bit of an add on. A typical example progression of all of this work would be:

6xHS

8xHS

10xHS

6x60m

8xHS

6x80m

6x100m

8xHS+ 1x15sec

6xHS +1x20-25sec

2x60, 2x100, 2x130m

2x150, 2x200

250, 200, 150, 100

Be able to use them in fatigue!

Now that we have built up the capacity, then the goal is to learn how to use all of this “stuff” under fatigue. There are numerous methods to do this, and I could go into tons of detail on each. So that this doesn’t get too long I’ll outline the general principles and then give some examples.

The basic idea is that now that we have the ability to recruit additional fibers and the like, we now need to extend that ability to being able to recruit them under fatigue and to extend their endurance. To accomplish this we combine a mixture of higher strength activities to recruit the fibers with either faster stuff (i.e. under fatigue) or longer stuff (i.e. extend the endurance). I generally go about it by training to extend the endurance and develop some strength endurance and then go about doing it under heavy fatigue.

Strength endurance:

You should move from general to specific. Meaning, start with just hilly runs or like one of my past coaches Scott Raczko liked to do, hilly long runs. That establishes a base of strength endurance. From there, move to hill fartleks or what I like to call up/downs which just means short aerobic hills with a run up/jog down at about 5k effort (200m in length is good). From here you can move to more specific work.

You can search my previous blog posts for strength endurance development for more information. But the use of circuits and in particular Canova style circuits are of great use.

The most specific phase is when we combine strength activities with heavy fatigue. One of my favorite is to include either hills or bounding in the middle of fast work. So at first it might be doing a set of intervals followed by a few hills, then back to a set of intervals on the track. Later on, it will be a more specific activity where we actually try and force recruitment of additional fibers in the middle of the workout. Any of the High School kids I’ve worked with will tell you about my affinity for running 500’s where they go 200m at 800m pace, 100m bound, and 200m kick in one continuous motion. Another good way is to mix sprint work in between interval sets or at the end of a set of hard intervals.

There are numerous examples, but here’s a couple quick ones:
-3 sets of 500m w/ 5min rest going 200m at 800m pace, 100m bound, 200m kick in

-3 sets of 3x800 at 5k pace with 4x200m hill in between sets run hard.

-3x (3x800) w/ 4x60m sprints in between sets

-Intervals run on a flat/hill/flat section where it’s 200m hard on the flat, 100m uphill, then a final hard 100m on the flat once you crest the hill

-Strength endurance circuits alternating strength exercises w/ running uphill (see videos).

Have the ability to change gears:

Doing this stuff on it’s own is easy. You might have the best sprint mechanics, be highly aerobic at race pace, and all that jazz, but the ability to transition from your race pace to the final 200m or so is often what seperates the kickers from the non-kickers. Therefore you have to tie everything together nicely instead of having a bunch of different singular components. What this means is practicing the switch/transition.

To do this you simply do some race simulation work and some cuing of the changes. The first step is to work on transition mechanics. That means running 200s with the first 100 at race pace and the last 100 a gradual acceleration for example. The goal of the coach should be to help the athlete learn how to transition and control that increase of speed. Most athletes will simply try and do the same thing only quicker if they want to run faster. With those types of athletes, we have to equip them with the ability to increase stride length or range of motion, so that they have two options available when it comes time to kick. That may mean working on opening up the arms for example. With other athletes, the tendency might be to try and reach out to cover more ground. We’d have to take the opposite approach as above with these types of athletes. The bottom line is that we need to put the pieces together and figure out a way to transition from that steady rhythm they have to the sprinting ability which we have developed in isolation.

That’s my rough guide for developing a kick. What exactly you do depends on the athlete and their strengths and weaknesses. But the overall requirements of a kick remain the same. It’s just up to you as a coach to figure out the right way to mix the ingredients.

The Science of the finishing kick

2011-09-19T07:17:00.000-05:00

Kicking it into gear.

I’ve explored the phenomenon of the kick a little before but with recent research and with the fact worlds has just happened, let’s explore the kick phenomenon a bit more. First, let’s look at what actually happens physiologically, and then what we can do about it.

The physiology of the kick:

Energy systems dynamics:

An interesting new study sheds some more light on why we might be able to run faster, particularly at the end of a race. You can read about it here (LINK) but they took cyclist and had them do either solo time trials or against a computer which was really their previous selves. What they found was that when racing someone, they were able to increase their speed and the sole reason was the anaerobic energy component. In other words, the cyclists used the same amount of energy aerobically, but in the faster trial they were able to tap into more of their anaerobic capacity. This has implications in regards to motivation which we’ll discuss shortly, but for now lets look at what this and other research means for the kick in terms of energetic.

If we define the kick as the last 100-400m or so of the race where the pace is increased you have to look at two factors in terms of what effects the kick.

How we got there- If we look at things in terms of energetic, the person who gets to X point in the race when it’s time to kick the most economically will be in best position to tap in his energy reserves. If we think in terms of energy systems, this could be the person who is most aerobic at X point. Looking at lactate, previous data has shown us that some elite Africans tend to get to this X point with lower lactate levels then their counterparts. What that means is that they haven’t used as much anaerobic energy to get to the point, thus they have much more in reserve to throw it down. This reason alone is why “faster” pure speed athletes sometimes can’t kick. They may have better speed, but they’ve used all their “speed” (and anaerobic capacity) just to get to that point, so when they try and go, there is nothing left.

How much we got left- Given the above, there’s another factor that plays a role energetic wise. How big that anaerobic energy tank is. Someone could get to the X point the most economically, but if he has a very small tank of anaerobic gas to use, he’s still not going to have a good kick. If we think in terms of lactate, then having an ability to increase their peak levels to a high amount at the end of the race is critical.

So for the ultimate kick, the idea energetically is to get to the point X as efficiently as possible and having a big tank of anaerobic energy to throw down that wasn’t tapped into during the race. If we think in terms of lactate, it’d be having a low lactate at X point then being able to jack it up to a really high amount at the end of the race.

Motor unit recruitment

Another similar factor that has been studied is motor unit recruitment. This ties into and is similar to the above energetic model. If we look at studies on kicking, they show that the increase in speed is directly related to an ability to increase muscle motor unit activation. It makes sense. The more motor units we can activate, the more power/force we can produce.

Once again, this is like energetics. As we fatigue during a race, we have to call in more and more muscle fibers to do the work and we have to cycle them through faster. If we’ve cycled through everything when we reach our X point, then there’s nothing left to access and we have no way to increase force production. Therefore the goal is to be able to be very efficient in terms of muscle fiber use getting to point X, and then having an ability to access a large number of motor units at the very end. So once again, the goal is efficiency to point X, then having the neural ability to recruit more fibers.

If we look at some past studies measuring EMG, there’s a clear correlation between the increase in speed during the kick and the increase in EMG signal, or motor unit recruitment. Being able to send a stronger neural signal to recruit more fibers is key during the kick. How’s that done? By having the neural pathway ingrained so that you can access it, and by having sufficient “motivation”, which we’ll discuss shortly.

Biomechanics- ability to change gears (strides rate/length)

These ideas all tie together to a larger degree and one of the results of the two above mentioned factors can be reflected in the stride mechanics. There are two ways to increase speed. Either increase stride rate or stride length. Each runner tends to have their preferred way to do it to a degree. Some are more length dependent, some more rate, and some a nice mix of both. Everyone uses both ways, but the exact combo depends. What’s interesting is that when we pick up speed to kick, something has to change, and that for the most part, people tend to increase via whatever way they haven’t maxed out during the race. So if they’ve kept their stride length slightly lower and relied more on a high stride rate throughout, then they’ll jack up the stride length, or vice versa.

The bottom line is we have two ways to increase speed and it’s best to have both at each of our disposal. If you have two ways to go, then you’ve got an out if you are so fatigued that you can’t increase stride length for example. A good example of this is shown in this data from the 2007 world championships:

http://www.scienceofrunning.com/2010/11/speed-stride-length-x-stride-frequency.html

Motivation

Lastly but certainly not least is the issue of motivation. The aforementioned study on the cyclist also points out a seemingly obvious but subtly important issue. When we have competition or are motivated, we can improve our performance. That’s a no brainer right?

But what’s interesting is how. We always have stuff in reserve. Our body is too well controlled to let us push so deep that we risk injury or death (my boss Alberto Salazar might be the only exception here…). So it has all sorts of safety mechanisms to shut us down (or fatigue us) before we reach that point. One of the most obvious is once we get near deep fatigue, the brain might start shutting down muscle fiber recruitment.

What’s interesting is that motivation, or importance, changes this equation slightly. It lets us push just a bit further. In essence, our end “governor” point is extended just a bit. The extreme example of this are those stories where you hear some lady lifting a car to save their child or someone lifting a big boulder to save someone. These are feats of superhuman strength where our bodies have essentially weighed the risks and decided risking muscle/bone rupture/breaking is preferential to death in most cases. So, the limiters are gone and boom, we have super strength.

The same thing happens to small degrees in races. If we are highly motivated, if the competition means something, and if we are in the thick of things and believe we can hit some goal, then we’re more likely to be able to extend that governor and call upon a stronger kick.

What’s it all mean?

Get to the end more aerobic than anyone else

Have a larger degree of anaerobic capacity to use.

Have a large reserve of motor units you can call upon

Be able to use them in fatigue!

Be close enough and feel good enough where your body extends it’s limits a little- be motivated and challenged with goals just far enough to challenge yet close enough to be achievable.

How to train a kick?

This will be the next follow up post. And here's my heavily biased favorite kick for a guy who sucked at kicking for a few years...:

Watch more video of Ryan Dohner on flotrack.org

Factors affecting distance running performance: A literature review

2011-08-20T15:33:00.001-05:00

Free Lit Review on the Science of Running and performance!
I've decided to make my literature review for grad school available to all because I'm too busy to do anything with it at the moment and it's better to allow others to get some useful info out of it then sit on my computer.

This document is a full literature review of all there is to know about the science behind distance running. Going beyond a literature review, it also contains a critique from my coaching perspective and some insights on how to translate the science to the coaching field. It took more time than I care to remember, so I'd like it be of some use to someone besides me and hope those who decide to read through it find it interesting and thought provoking. I welcome any comments or questions about anything contained in the document.

It's 130 pages including well over a hundred citations. The best part is it is free. I like sharing information and figure that some coaches and athletes might get something out of it and that's good enough for me. If you find it extremely useful and want to contribute any money, feel free to do so with the donate button. It is greatly appreciated.

Download and donate at the following link:
http://www.scienceofrunning.com/p/get-science-of-running-literature.html

Table of Contents

Chapter 1: How Running Happens

Motor Programming

Sending and Receiving the signal

Muscle Contraction

Energy Needed

Muscle Fiber Types

A Recruitment Issue

Passive Mechanics

Chapter 2: Fatigue: Friend or Foe?

How Fatigue manifests itself

How Fatigue occurs

Oxygen’s role

Chapter 3: An Oxygen Problem

The measurement: VO2max

Oxygen intake

Oxygen Transportation

Oxygen utilization

The VO2max limiter.

Chapter 4: The Fallacy of VO2max

How the VO2max concept developed

Efficacy of basing training paces off of VO2max

Should we train to improve VO2max?

Chapter 5: Lactate, Acid, and other By-products

Buffering/Dealing with high acidosis

The Lactate Threshold

Maximum Lactate Steady State

Lactate Testing

Chapter 6: Efficiency

The Measurement: Running Economy

Biomechanical Efficiency

Neuromuscular Efficiency

Metabolic Efficiency

Problems with Running Economy

Chapter 7: The Brain-Muscle Connection

Neuromuscular and Anaerobic factors in performance

Fatigue and the CNS

Temperature Regulation

The Psychology of it all

Chapter 8: The Genetics of Training

Steps of Adaptation

Long Term Adaptation

Training Applications

Chapter 9: Theories of Training Adaptation

General Adaptation Syndrome and Dose-Response

Individuality of adaptation

Chapter 10: Volume and Intensity of Training

Volume of Training

Intensity of Training

Interaction of Volume and Intensity of Training

Training in the Real World

Supplemental training

Training Frequency

Chapter 11: Periodization

Periodization in Endurance Sport

Individualization

Chapter 12: Training Models- Example of Integration of Theory and Practice

Chapter 13: Where do we go from here?

European Travels- High Speed race video

2011-08-04T18:09:00.005-05:00

While I've been doing this little new job I have which includes bouncing around Europe for a while, I've kind of neglected this blog a little bit. Before I write anything substantial, I figured I'd fill the gap with some high speed video I took of a couple of professional 800m races that took place in Lignano, Italy.

When i get time, I'll go through a little bit of the process of post-season evaluation that I go through using Tommy Schmitz as an example. He had a kind of crazy season filled with some rookie mistakes by me and some ups and downs but came away with a nice 3:39 PR and another 2 races under his old PR, so no complaints, but I'll go through what went right, wrong, and how to fix things.

Also, here's a brief interview I did with Runner's World on how my job's going so far:
http://racingnews.runnersworld.com/2011/07/a-brief-chat-with-steve-magness.html?utm_source=feedburner&utm_medium=feed&utm_campaign=Feed%3A+RwDailyNews+%28Runner%27s+World+Racing+News%29&utm_content=Google+Reader

Until then, enjoy the videos: