Now Doug has given me great advice over the years and what better excuse to drink a beer after a 17 hours fast and workout than a tribute workout! Here was yesterday’s workout, took all of 7 minutes:

Some might decry the workout for  a bit of sloppy form on the deads (agreed) and maybe that my negatives weren’t as slow as they could have been (agreed) but the point of the workout was maximum intensiveness so as to earn the beer. That means gnarly deadlifts and hardcore negatives. Next week, like Doug, I return back to my controlled, slow, deadpan, broken-jawed breathing HIT. This, however, was a gut wrenching intensity…and a ton of fun!

Onward!

—

So I was reviewing some old PDFs I had lying around (inasmuch as a digital file can “lie” around) and I came across an article from Scientific American regarding fast twitch motor units and training as it pertains to athletes. In this article, there is the discussion of how, in the authors’ particular study, they found that after a group trained for a period of time and then was detrained, their relative percentage of fast twitch muscle fibers increased dramatically. The designations used in this article are Type IIa to Type IIx however, while even my exercise physiology textbook designates a IIx sub-catagorization, more recent studies have used this designation:

Back to the study at hand. Take a look at the relative amount of fast twitch motor units that are created (or rather, that the body adapts toward) after detraining:

So the relative amount of IIx fibers doubled after 3 months of detraining. Damn you Art De Vany for being right about everything.

The Hunch

So here’s the “just a hunch” part, where the labcoating begins: maybe people who get great results with HIT do this better than those that do not. I’ve been thinking about this a lot as I’ve ventured into my new experiment and thinking about gains in the past. I’ve been freaky-strong training only once a week and bigger than I am now, albeit not by a huge amount (~10lbs lean mass). It could be that my physiology is spendthift but it also could be that by training so infrequently you’re creating a miniature version of the curve shown above, changing the relative amount of fibers toward a fast myosin expression thus getting way stronger and perhaps a bit larger. Lots of anaerobic stimulus from the incredibly intensive, very brief workouts may have the potential to express a fast twitch machine without adding much mass.

What if you want more mass? I’m looking forward to testing this on myself as well but maybe the periodic, drastic upregulation of volume ala a blitz-type burst becomes the way to a bigger engine. Hypertrophy seems to be muscle more “here and now” when it comes to the stimulus. Perhaps all of this fast-twitch turnover primes the pump for a short period of much higher volume. You have a much larger percentage of fast motor units at your disposal thus any effort you exert for a given volume has the potential to create a much larger homeostatic disruption. You’ve got these giant engines, occasionally you should run them through the rev range. Not only is the alarm state reaction (ala a flu shot) much greater than if you had been training all of the time and reduced the relative amount of fast motor units, but your ability to endure such workouts for very long is physiologically truncated by your fiber ratios (more fast than slow).

Can I prove this? No. Is there some evidence that I can daisy-chain together that at least suggests plausibility? Perhaps, if you believe the study above. This is the extent of my testing for the next few months. The bodpod will tell the tale.

I write this mostly for myself, as a return to what got me to damn near my genetic potential in the first place. High intensity weight training to total muscular fatigue, focusing on emptying the tank as fast as possible and judging progress by internal cues rather than forcing external metrics (e.g. raising weight just because or fidgeting to reach a better TUL).

If I end up training with weights more than 1 hour per week, I’m doing it wrong. I bet I can get it back down under 20 minutes like the old days. Hell, less than 10 minutes (per week) has let Vee achieve 18+ inch arms.

That post was just over 1 year ago and since then I’ve started grad school and have maintained a very busy training schedule. However, the perk of grad school is that I get Bodpod body composition measurements for a very reasonable cost. So on September 9th, 2011 I had a bodpod scan that gave me the following:

-Weight    173.898 lb
-Lean Body Mass    150.614 lb
-Fat Mass    23.283 lb
-Body Fat Percentage    13.4%

At that point I took on a constant loading program espoused by the late John Christy. I did this due to the fact that I didn’t have a trainer at my disposal to really drive me through high intensity workouts akin to Dr. Doug McGuff would espouse. I love carpet time but in order to achieve this you need to be able to give yourself over to a trainer you trust and Keith, and he’ll tell you this, is not a HIT trainer per se. That’s not to say that he’s not capable of kicking ass. So my workout was high-intensity oriented given that I didn’t have a trainer: big compounds with microloading. It also helps to know that I was coming off a hand injury that kept me from pulling hard or doing good chins. Here was my workout in early October:

• Trap bar Deadlift: 220 x 12, 200 x 12
• Weighted Chin: +12.5 x 12, BW  x 12
• Weighted Dip: +30 x 12, +15 x 12
• Shrugs: 200 x 12
• Gripper: 92.41 x :45 x 2/each hand (static hold)

And here is where I was last week:

• Dip: +100 x 3, + 75 x 4, +45 x 5, +23 x 6
• Chin: +70 x 3, +47 x 4, +23 x 5, BW x 6
• Trap Bar Deadlift: 360 x 3, 326 x 4
• Dynavec Multi-Directional Hip Extension: 145 x 15
• Nitro Pullover: 210 x 10

And for what it’s worth I can now do much more weight for higher reps. For example I can do weighted dips with 65lbs around my waist for 10 reps. This should mean more muscle, right? Let’s look at a Bodpod from last week:

-Weight: 174.508 lb
-Lean Mass: 150.438 lb
-Fat Mass: 24.07 lb
-Body Fat: 13.8%

Say what?! Big strength gains and no muscle gain at all? This is what is called “Adaptive Coordination” and is how athletes locked in a weight class sport continue to get stronger in spite a lack of gain in muscle tissue. After trying to reason my way out of it, I went and got a Dexa Scan done which gave me this result:

Bodyfat: 13.1%

Fat-Free Mass: 153.4lbs

Fat Mass: 23.2 lbs

Bone Mineral: 8.5lbs (HELL YEAH! MORE THAN KEITH! EAT IT!)

The Dexa had me at 176.6lbs, 1 hour later without any food or water intake, which makes up for the difference in lean mass between the bodpod and the Dexa. The cool thing about this, if I’m to look for a silver lining, is that I eat unweighed, unmeasured paleo and it keeps me rather lean. Not bad. However, I got stronger but not bigger, why?

My ability to lift weight improved due to a variety of things. This is just a short list of things I improved in the past 8 months:

1. Inter and intra muscular coordination
2. Motor learning
3. Motor unit/fiber recruitment efficiency
4. Golgi tendon inhibition
5. Heterochronicity
6. Fatigue resistance
7. Postural changes
8. Co-contraction
9. Connective tissue changes
10. Improvements in cadence and turnarounds
11. Motivation
12. Pain tolerance
13. Perception of difficulty
14. Confidence
15. Experience

No less than 15 different things that can go up and allow weight to go up without muscle going up. There is a longer discussion about lifting ability versus lifting capability that is beyond the scope of this article.

The next stage: Bass + Blitz = Bomb Diggity?

So the next step is to see how I do with a full-on return to pure-HIT strength training. Specifically giving myself over to a trainer, my boss, and getting thrashed once a week in the weight room. On Saturdays I’ll run some Sprint-8 type intervals followed by a long weight vest walk. I won’t keep track of calories but I will eat more on those days just because I can.

If this looks familiar, it’s because this is exactly how Clarence Bass trains. At least that’s how he trained 14 years ago and no article I’ve read recently indicates otherwise. And like Mr. Bass, I’ll vary my routines while maintaining marker exercises: everything from Dr. McGuff-style workouts to Doug Holland-style deadlift+beer sessions. The latter will likely be once per month.

However, there is benefit of periodic volume and intensity increases. I’ve discussed the concept of the “critical point of change” as applied to power law dynamics, specifically the use of workout chaos to increase effort due to lack of coordination and the blitz to drastically ramp up demands and intensity at the same time. The thing is I’ve never actually done a blitz, not well, likely because I was too exhausted to get excited for one and/or the recovery demands are quite an undertaking. Think 4500+kcal/day, contrast bathing, weekly massage, loads of sleep, as little life stressors as possible. Ask Dallas about his clean mass gain and he’ll tell you just how hard it was to do for 5 weeks but 2 weeks is about the limit of a drastic, silly, obscene increase in effort, demands, and recovery work. Summer is where this could take place. I’ll plan on doing something like that in July and doing a bodpod right afterward. If it works, it validates both the ABCDE diet AND the No-Bull Mass Gain diet, at least somewhat.

“There is no failure, only feedback” is a saying that Arthur De Vany likes to use regarding his perspective on the lack of failure in life. I got stronger than I ever had been overall in my upper body and not a new pound of lean mass to show for it. This information is actionable and so we’ll see the result in another 4 months or so. Onward!

Update: 4/24/2012

James asked this in the comments:

I’d be interested to know what the inter and intra day reliability of your individual bodpod unit is. We have a bodpod and as part of our lab accreditation we had to perform a reliability study on it and although I can’t remember the coefficients of variation of the top of my head I do recall it was higher than expected. Bodpods better than most body composition measures, but far from perfect.

This is a great question that I don’t have an answer for but I can tell you that it was the reason I got the Dexa done to “check” the accuracy of the Bodpod. Halfway through the interval of this experiment, on 12/13/2011, I had a Bodpod done: same administer, same time of day, same status (17 hours fasted, no liquids since 8pm the night before). The results were as follows:

• Body Weight: 175.04 lbs
• Lean Body Mass: 151.437 lbs
• Fat mass: 23.603 lbs
• Body fat: 13.5%

So it might be off slightly day to day, it seems to be consistent enough to track long term changes, at least as consistent as hydrostatic weighing. That seemed to work for Clarence Bass, so I figure it’s OK for me for a very accurate directional accuracy.

Strength Training and its Effects on the Biomarkers of Aging

Skyler Tanner

April 4, 2012

Texas State University – San Marcos

Aging is inevitable but a simple look around will show that people age at different rates regardless of their biological age. In 1992 researchers William Evans, PhD, and Irwin H. Rosenberg (11) professors of nutrition and medicine, respectively, at Tufts University USDA Human Nutrition Research Center on Aging (HNRCA) determined 10 biomarkers of aging. Biomarkers are things that tell how old you would be if you didn’t know how old you were in years. These biomarkers are:

1)      Muscle Mass

2)      Strength

3)      Basal Metabolic Rate

4)      Body Fat Percentage

5)      Aerobic Capacity

6)      Blood-sugar Tolerance

7)      Cholesterol/HDL Ratio

8)      Blood Pressure

9)      Bone density

10)  Ability to regulate Internal Temperature

Somewhat radical for the time Evans and Rosenberg found that strength training was the intervention that most positively affected all of the biomarkers. This is a review of the research that has occurred in the past 2 decades, focusing on the physical biomarkers: strength, muscle mass, blood pressure, bone density, cardiometabolic health, and metabolic syndrome.

Muscle Mass and Strength

Muscle mass and strength loss with age are associated with reduction in health status. This loss of muscle is referred to as Sarcopenia, which literally means “poverty of flesh.” Whether it is the goal of a practitioner to improve health status or functional abilities, steps should be taken to reduce risk factors by preventing disability and decreasing disease progression. While common interventions attempt to improve markers of cardiovascular and metabolic functions, strength alone is independently associated with functional ability in the elderly (17,18). Since steady-state aerobic training has not been shown to improve muscular force output in the elderly (22), muscular strength may become a more limiting factor in daily activities than cardiovascular function in elderly individuals. As a result ST may be the training intervention of choice, as loss of muscular ability has been shown to at least be partially responsible for reduced function in the elderly (12,13,19).

Understanding this, specialized measurements have been proposed when dealing with an elderly population in order to determine a reduction of function. Han et al (15) have proposed that a “Lean Mass Index” be used with the elderly in place of the traditionally used “Body Mass Index.” By differentiating between total mass and lean mass, clinicians can more accurately determine the rate of muscle wasting and act accordingly. Further indicators of muscle wasting and reduced function include balance, which is also an indication not only of reduced function but also reduced strength (27), as balance is a combination of central nervous system ability and muscle’s strength-producing ability.

The rate of muscle and strength loss has been investigated. Hughes et al (16) found during a 12 year longitudinal study that knee and elbow flexors and extensors lost 20 to 30% strength between the ages of 55 and 65 years. In addition to this, the cross-sectional area (CSA) of all of the thigh muscles reduced by 14.7%. Researchers also found that the stronger the person was during the initial measurement the stronger they were during the measurement 9 years later. To a certain extent this is confirmed in a recent study by Wroblewski et al (35). This study examined the lean muscle mass of master athletes, those aged 40 to 81 years. Researchers found that those training 4 to 5 days per week did not show a significant decrease in strength with age, no loss in total lean mass, and no loss in the CSA of the mid-thigh area. The researchers concluded that “This study contradicts the common observation that muscle mass and strength decline as a function of aging alone. Instead, these declines may signal the effect of chronic disuse rather than muscle aging,” and that “This maintenance of muscle mass and strength may decrease or eliminate the falls, functional decline, and loss of independence that are commonly seen in aging adults.”

While some muscle and strength loss does occur with aging, the rate of muscle and strength loss can be severely truncated with a properly-designed ST program. Rhodes et al (28) found that one year of ST improved by the strength of elderly women by up to 29% with a similar increase in bone mineral density at the hip and back. Lemmer et al (23) demonstrated that elderly individuals are able to gain a significant amount of strength through training, 28% on average, and that these 50% of this improvement is maintained after 31 weeks of detraining.

Osteoporosis

Osteoporosis is the age-related reduction in bone mineral density (BMD), leading to a reduction in bone mass and thus increased risk for bone breaks. While osteoporosis is most prevalent in postmenopausal women, and thus a greater health concern for women, the prevalence of osteoporosis also increases with age in men. The loss of BMD in postmenopausal women results in a 200% increase of hip fracture risk every 5 years past age 50, with one-third of 80-year-old women having a hip fracture and one third of those will have had 2 hip fractures (5).

The loss of BMD is correlated with strength reductions in women and has promising implications as a measurement for determining the loss of BMD before true osteoporosis is diagnosed (36). It is well understood that physical activity improves BMD while also improve strength and muscle mass in elderly women (28), indicating that sarcopenia and osteoporosis are related. Recent studies suggest that serum osteocalcin, which is secreted during bone remodeling, is correlated with activity and inversely related to fat mass and plasma glucose in elderly men (20). Also of note that ST improves biochemical markers of bone turnover in both elderly men and women, indicating that high osteocalcin levels indicate a sufficient level of physical activity to minimize or stop losses in BMD during aging (34).

While ST has been shown to improve BMD, it is important to note that most studies indicate that it would take an increase of at least 20% to reduce the risk of fracture from a fall in the elderly (6). With this in mind, ST over a lifetime would maintain sufficient BMD to reduce fracture risk but protection in the elderly from a ST intervention would likely occur due to reduction in falls rather than a reduction in fractures after a fall has occurred.

Metabolic Syndrome

Increases in LBM lead to an overall favorable shift in body composition away from that which precedes metabolic syndrome. An increase in fat mass, specifically in the abdominal region, is thought to be the first step in events that lead to hypertension, glucose intolerance, insulin resistance, and abnormal lipoprotein-lipid profiles. These are concurring risk factors are often referred to as syndrome X or metabolic syndrome (8).

ST improves body composition in men and women, both in studies where calories are controlled for (30,31), and studies where they are not (34).  Especially important about this is the reduction of visceral adipose tissue (VAT) seen in both studies. As mentioned above, increase in abdominal fat precedes metabolic syndrome and the majority of this fat is VAT (10). ST has shown to reduce VAT in both elderly men (33) and elderly women (32).

The loss of fat-free mass (FFM) and an increase in fat mass is associated with aging. The loss of FFM is accompanied with a reduction in resting metabolic rate (RMR), which can lead to obesity. While previous studies have shown heavy ST increases FFM and RMR in elderly men and women (3), Campbell et al concluded that the increase in RMR was due to an increase in the metabolic activity of the lean tissue, rather than the increase in FFM, as in their study much of that was reported to by body water. However, as demonstrated by Wroblewski et al (35), chronic exercise preserves FFM and RMR in master athletes, thus making it reasonable that ST over a sufficient period of time would not only improve functional ability but maintain an elevated RMR, thus leading to reductions in obesity risk.

Blood Pressure

The increase in resting blood pressure (BP) is referred to as hypertension. Hypertension is a major risk factor for heart disease which increases throughout the aging process. By 60 to 70, approximately 50% of men and women are hypertensive and this remains a risk factor for heart disease until a person is over the age of 85 (20).

Studies regarding the effects of ST on hypertension are mixed. Cononie and Graves (4) studied the effects of a 6 month moderate ST on resting BP in normal to moderately high BP 70-to 79-year-old men and women. Researchers observed no changes following ST in either systolic blood pressure (SBP) or diastolic blood pressure (DBP).  A more recent study challenges the conclusion, showing that heavy ST can reduce resting BP in 65- to 73-year-old men and women with high normal resting BP (24). The reductions in blood pressure were seen up to 48 hours post-exercise and the mean BP values shifted from high normal into the normal range.

While these studies indicate contradictory results, there is emerging evidence that different genotypes respond differently to ST with regards to BP reduction in the elderly.  Delmonico et al (7) indicate that elderly men and women with a specific gene expression see a greater decrease in BP compared to those with a different gene expression. To quote the authors, “The AGT A–20C and AGTR1 A1166C genotypes may influence resting BP response to ST, such that C-allele carriers at each of these loci reduce their resting BP in response to ST to a greater extent than A homozygotes.” Clearly more research is needed to determine at ST dose to elicit BP improvements.

Cardiometabolic Health

Cardiovascular fitness, as assessed by treadmill test, is an important risk factor for all-cause mortality. It also indicates mortality and morbidity associated with coronary heart disease (CHD) in both men and women. As noted by Blair et al, ““Higher levels of physical fitness appear to delay all-cause mortality primarily due to lowered rates of cardiovascular disease…(2).” In addition to reductions in cardiovascular disease, improved cardiometabolic health by way of physical activity shows a reduction in relative risk (RR) for a variety of other ailments. The RR of developing CHD from being physically inactive (RR=1.9) is similar to the RR associated with cigarette smoking (2.5), hypertension (2.3) and hypercholesterolemia (2.1) (26).

It is well understood that aerobic exercise training leads to improvements in cardiovascular fitness, but the effects of ST have been somewhat controversial. Ades et al. found that 12 weeks of ST increased treadmill walking endurance at 80% VO2max by 38% in 65- to 79-year-old women, even though their VO2max did not change (1). These improvements were correlated with improvements in leg strength. Parker et al showed that 16 weeks of ST with 60- to 77- year-old women decreased heart rate, blood pressure, and rate pressure product significantly during a weight-loaded treadmill walking test (25). Thus cardiovascular endurance may increase due to ST in spite of little or no change in VO_2max.

When comparing aerobic exercise to ST, neither training modality improved plasma lipoprotein-lipid profiles significantly (32). Improvements shown in studies on younger individuals are thought to occur due to bodyweight loss rather than ST or aerobic exercise (9). Rhea et al (29) showed that 16 weeks of heavy ST in obese postmenopausal women, aged 50 to 69 years, did not elicit positive changes in lipoprotein levels regardless of bodyweight loss.

There is evidence to suggest that different genotypes respond differently to aerobic activity may be an important determinant as to whether aerobic exercise training improves lipoprotein-lipid profiles (14). It is conceivable that the same is true for lipoprotein-lipid responses to ST but no evidence exists at present time.

Conclusions and Criticisms

The effects of ST on biomarkers of aging are as follows:

(1)   Decades of strength and muscle mass losses can be regained very quickly with heavy resistance ST.

(2)   Substantial changes in VO_2max do not occur due to ST but endurance performance can be improved due to ST.

(3)   While recent research suggests that there is potential for ST to improve lipoprotein-lipid profiles in certain genotypes, there is no supporting this at present time.

(4)   Evidence shows that ST can normalize BP in the high normal category but no evidence exists that demonstrates ST can reduce BP in elderly hypertensives.

(5)   Reductions in body fat and VAT have been shown but diet cannot be ruled out as the cause of this reduction.

(6)   Evidence for improvements in BMD due to ST is mixed. There is good evidence for ST as a means of preventing BMD loss due to aging however ST by itself has yet to have been shown to replace BMD sufficiently enough to prevent breaks due a fall. There is, however, strong evidence that ST reduces several risk factors for falls.

Research continues to show the benefit of strength training on the biomarkers of aging. While it is clear that more research is needed to determine specific protocols that address the specific circumstances of elderly individuals, what is clear is that strength training is of benefit for all persons of any age. The research is clear: intelligently prescribed strength training can improve the quality of life for elderly individuals.

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these men must choose to eat AND train to get bigger, with VERY specific meal times, protein servings every three hours or so, abundant rest/recovery/sleep, and pre/peri/post workout supplementation to exaggerate the insulin/amino acid uptake cycle for maximal anabolic response. Unfortunately, I don’t see a lot of men willing to follow this because they have chosen a dietary lifestyle (like Paleo or IF) for health reasons, and it may not be an optimal one for maximal hypertrophy. If you want a specific goal, you have to go after it with your ENTIRE lifestyle, not just training protocol selection.

And here was my response:

Brandon,

Martin of the Leangains fame has shown that you don’t need to eat every 3 hours (or whatever) to drive muscle gain, just like you don’t need to eat every 3 hours to drive fat loss.

Which causes me to question: how can eating every 3 hours be both good for fat burning and good for muscle gain, 2 polar opposite outcomes? It can’t and it doesn’t.

That said, you’re right about being actively eating for hypertrophy, being consistent to get enough when it is appropriate, and matching a training program that provides a sufficient stimulus for growth. Most guys simply don’t eat enough to maximize their gain but that gain on average is very small. Simply put the nutrient signals that we all like about an ancestral health type of diet (controlled insulin, adequate protein, high satiety signaling) are the opposite of what tends to promote growth (high insulin, more protein, less satiety to help get enough calories).

Much like fat loss and muscle gain are opposite ends of the spectrum, a diet that promotes growth promotes aging while a diet that promotes health and longevity doesn’t. There is a great read by Michael Rose called “The end of aging: Why life begins at 90″ that lays this out.

The link to Michael Rose’s article is found here.

Upon reading my response again, it makes it seem like I disagree with what Brandon has proposed but that isn’t the case. I only took umbrage with the eating every 3 hours bit; everything else is very correct. When it is spelled out, it makes it seem more complicated than it is however, again citing leangains, the “pre/peri/post” workout is taken care of by aminos before the workout and your largest meal after the workout. There is even more recent research to suggest that what really matters is the amount of calories and nutrients ingested. Quoting an interview with Alan Aragon:

Alan: The post-exercise “anabolic window” is a highly misused & abused concept. Preworkout nutrition all but cancels the urgency, unless you’re an endurance athlete with multiple glycogen-depleting events in a single day. Getting down to brass tacks, a relatively recent study (Power et al. 2009) showed that a 45g dose of whey protein isolate takes appx. 50 minutes to cause blood AA levels to peak. Resulting insulin levels, which peaked at 40 minutes after ingestion, remained at elevations known to max out the inhibition of muscle protein breakdown (15-30 mU/L) for 120 minutes after ingestion. This dose takes 3 hours for insulin & AA levels to return to baseline from the point of ingestion. The inclusion of carbs to this dose would cause AA & insulin levels to peak higher & stay elevated above baseline even longer.

So much for the anabolic peephole & the urgency to down AAs during your weight training workout; they are already seeping into circulation (& will continue to do so after your training bout is done). Even in the event that a preworkout meal is skipped, the anabolic effect of the postworkout meal is increased as a supercompensatory response (Deldicque et al, 2010). Moving on, another recent study (Staples et al, 2010) found that a substantial dose of carbohydrate (50g maltodextrin) added to 25g whey protein was unable to further increase post-exercise net muscle protein balance compared to the protein dose without carbs. Again, this is not to say that adding carbs at this point is counterproductive, but it certainly doesn’t support the idea that you must get your lightning-fast post-exercise carb orgy for optimal results.

Something that people don’t realize is that there’s no “magic anabolic window” that’s open for a short period of time near the workout & then rapidly disappears. As a result of a single training bout, the receptivity of muscle to protein dosing can persist for at least 24 hours (Burd et al, 2011).

Or to sum it up:

The Primary Laws of Nutrient Timing

• The First Law of Nutrient Timing is: hitting your daily macronutrient targets is FAR more important than nutrient timing.
• The Second Law of Nutrient Timing is: hitting your daily macronutrient targets is FAR more important than nutrient timing.

Here might be why paleo + milk makes people grow like gangbusters assuming they get enough calories. What I’m taking here is Dan’s summing up of Pedro Bastos’ (Sup, Bastos?) presentation at the Ancestral Health Symposium:

• How can milk lead to rapid growth? Maybe insulin.
• Insulin response is 5x higher than expected for glycemic index. Doesn’t matter if it’s skim or whole.
• The good: Whey can increase muscle protein synthesis and glutathione, one of the major endogenous antioxidants the body.
• Betacellulin – Another growth factor in milk. Survives pastorization. Found in cheese.
• IGF-1 in bovine milk is identical to human IGF-1. Not high amounts in bovine milk.

But there’s a downside, from the same article:

• Increasing height associates with increasing risk for epithelial cell cancers.
• Milk may promote premature puberty, a risk factor for breast cancer.
• Prostate cancer shows a high correlation with milk intake.
• Milk may be protective against colon cancer.
• Milk seems to promote acne, at least in people who have insulin resistance.

So you want to promote muscle growth but not cancer growth. Milk calories are cheap and, assuming no gut or lactose issues, easily digested.

In the “I can’t yet prove it but I highly suspect it” category, I suspect that there is a peak anabolism in our lifetime. What I mean is that there is a peak muscle mass for our genetics and a closing window in which to reach it. If you reach it, your ceiling is set high for the rest of your life…you’ve reached your “10″ level. But if you start training after that critical point, you’ll never get to “10,” maybe a maximum of “8″ on that same scale. Here is why I think that; first let’s look at a slide of lifetime bone mineral density to illustrate my previous point:

See how the peak hits around age 35 and maintains before a decline? Also note that lifestyle (read: physical loading) is the main reason why the peak densities are different between the lines. The second and third lowest line, upon reaching their max around 35, can never drive their BMD up to that of the first line. Now let’s look at some muscle evidence:

This muscle mass curve is from the book “Bending the Aging Curve” by Joseph Signorile and it is a visual of the data presented in the study “Variability in muscle fibre areas in whole human quadriceps muscle: effects of increasing age.” The bent muscle curves, while not from the same study, are shown in other studies. Check out the MRI from the master athletes in the study “Chronic Exercise Preserves Lean Mass in Master Athletes:”

Fairly compelling visual evidence, in my opinion, to just how much lean mass we can build and maintain. Different life stages prime us for different outcomes, which leads me to…

Putting it together

I didn’t intend for this to be as long as it has become but in conclusion

1. Maximizing muscle growth requires adequate nutrition, smart strength training, and adequate time.
2. Nutrient timing for strength and mass gain is far less important than getting enough calories in during the 24 hours after a workout.
3. A proper diet, nearly ancestral in its framework, can effective “stop” aging around 35.
4. Milk promotes growth above and beyond its caloric value. Good for muscle, bad for cancer.
5. Muscle, like bone, seems to have a “peak” value that can be achieved. There are studies that suggest this occurs in and around our 5th decade (which, like centuries, means the value 1 number below the number actually listed, so our 40′s)
6. So if you want to maximize muscle growth milieu while minimizing the negative implications of a growth-promoting environment, follow a paleo+milk-type diet with plenty of calories up until around the age of 35. Note that I’m suggesting adding milk only after a workout, the amount will vary depending on your size and goals.  After that I would suggest dropping the milk and ramping up calories by way of shakes like those suggested by Dallas in his “Clean Mass Gain” while also understanding that you’ve likely reached a high percentage of your potential anyway. You’re unlikely to add more than 2lbs/year at this point so the calories you need won’t be very much above baseline. If you maintain 12-13% bodyfat, you’re eating enough to support whatever muscle you’re likely to have in your genetic tank.

I hope this helps some of you regarding the balance between longevity and maximum muscle. The latter helps the former, generally, and there seems to be a “best time frame” to maximize this.

If you can’t answer in an enthusiastically positive manner, let me make a suggestion: simplify your routine to big, joint-neutral exercises and focus on adding a small amount of weight week after week. Don’t look for novelty, don’t view this as an intervention. This isn’t a 3 month event; you need to train until you die precisely so you can live until you keel over. Slow down, make steady progress, don’t hurt yourself, and find other things to do with your time rather than trying to find the perfect routine or the perfect diet. Good enough, done consistently, blows away 2 months of perfect.

The lipid hypothesis is completely valid. Once something reaches the statud (sic) of a theory it has enormous evidence. Cholesterol is a major contributor to cornary (sic) artery disease. The studies are clear on PubMed.

You should never have anymore than about seven eggs per week, if that. Harvard says up to seven eggs a week is harmonious with health. Seven eggs in a single day is terrible for your heart and vasuclar (sic) system. Chris M. is a crank. He knows very little about cholesterol, and chooses to cherry pick studies.

You don’t want to be the smartest man in the cemetery. The American Heart Association. Did you ever hear of it? You Weston A. Price cranks will be sorry you did not listen to Dr. Caldwell Esselstyn. If he is a good enough doctor to advise coronary heart disease patient , former president Bill Clinton, than he is a good enough doctor for anybody.

Mind you this was in a post regarding egg protein availability, which had nothing to do with cholesterol levels. But sure, I’m game, I’ll play.

The problem with lab studies

I have having a discussion with Dallas of the Whole 9 last week regarding how, in some circles, epidemiology gets pissed all over because there aren’t controls. By its very nature it’s not double-blind, condition-controlled study. However, for free living humans, it’s the best thing we have (unless an ethics committee somewhere decides that we can grow a person in a cage and control everything from cradle to grave).

Don’t misunderstand me: lab studies are great for something what happens to the changes in a diet but not necessarily the diet itself. Que? Yes, due to the nature of most studies a person’s free-living diet is being altered via some sort of intervention: high carb becomes high fat, low protein becomes high protein, fat people become less fat, etc. Lab values change as a result of the intervention but these changes do not reflect how the diet might actually react, as far as blood chemistry and a host of other factors are concerned, when maintained for a long period of time in the real world. Its the change in the diet that we see in the results, not of the diet itself.

This is the reason why we must take theory to practice and see how these things pan out in the real world. So with regards to egg consumption let’s take a look at big, fat, stupid Americans and their (apparently, this election cycle) mortal enemy: Mexicans.

Incredible Edible Egg Data

After Michael flew off half-cocked, I investigated a bit of his point in the real world. If you believe the lipid hypothesis (saturated fat and cholesterol intake drive blood cholesterol drives heart disease) then the logical things to look at are:

1. Who eats the most eggs per year?
2. What is their rate of heart disease?

Michael was adamant that nobody, under any circumstance, should eat more than 7 eggs per week because it is “harmonious with health.” Now the definition of harmonious is “forming a pleasing whole” but I assume that Michael wanted to say that it is harmful to health. So if that’s true than somebody eating more than 7 eggs per week should really be in trouble: health epidemic, people dying in the streets with exploding hearts-kind of trouble. So who eats the most eggs per year? It turns out its Mexico:

Mexico’s National Poultry Institute (INA) announced that Mexicans consume the most eggs worldwide, an average of 438 eggs per year per person.

Awesome, nearly 100 more eggs per year than days in a year! So if all of this cholesterol is truly killing the shit out of the Mexican population, they should lead the world in heart disease right? Well…:

Those patterns mirror the trend past studies have shown in Mexico’s rate of death from heart disease, which nearly doubled between 1970 and 2000. The current rate — about 56 heart disease deaths per 100,000 people…

THAT NUMBER IS HUGE! EPIDEMIC! LOCUS RAINING FROM THE SKY!… wait, there’s no context. Let’s compare that data to us. The United States population consumes, on average, 243.6 eggs per year. So basically half as many eggs per year. And what is our rate of heart disease?

(Mexico) is still lower than that of the U.S., where the rate in 2006 was 135 per 100,000.

So they consume twice as many eggs as we do and yet they have 59% less heart disease? No entidendo!

The Moving Parts

Now I’m not saying that Michael is wrong and I’m right…no that’s exactly what I’m saying. The problem is that there are a lot of moving parts to heart disease and cholesterol intake is one piece of the puzzle. Mexico’s heart disease is on the rise in large part because smoking is on the rise, not because of egg intake.

When you’re in an culture that over-consumes junk at the expense of real, nutritious food reducing cholesterol intake may reduce blood cholesterol numbers which may reduce risk. Maybe. But what about if you’re stressed out and overworked? That minor reduction in cholesterol isn’t going to make up for all those elevated inflammatory cytokines, which are hugely correlated with heart disease, perhaps more directly even. Still smoke? Egg reduction isn’t going to save you from that. Ditto for being overfat or obese. Lots of cardiovascular activity? You’re in trouble and probably avoiding eggs because it’s “healthy.” See the problem with targeting one metric as the shepard of good health?

Mexico is a country of more traditional food preparations, meaning more micronutrients per calorie, thus more satiety per calorie. It also helps that they’re relatively poor meaning eating isn’t done because they’re bored. I also suspect that easily accessible junk taking up a larger chunk of their daily calorie intake is partially to blame for the increase in cardiovascular disease.

For a theory to be valid it must work 100% of the time. When it doesn’t, it is modified to fit new evidence or, if that cannot happen, abandoned to the dustbin of history. There can be no such thing as a “paradox” that refutes the theory; the “paradox” needs to be used to modify your theory. Instead the lipid hypothesis uses “paradox” as a title for “things that ruin our pet theory so we’ll try to ignore them by calling them paradoxes.” France, Iceland, and Mexico are all places that have epidemiological data that makes them fly in the face of the theory. Their existence means the needs to be adjusted or abandoned all together. Being that its easier to build anew than have loads of disjointed, ill-fitting theories coddled together, I suggest a restart.

Don’t believe me? Take a look at this graph and tell me that your pet theory still functions (click to enlarge):

Anyone who says that 1 single thing is THE factor for health and disease is unaware of how little they know. Certain things give greater returns on time invested but no one thing is the main cog in the wheel when it comes to optimizing health and longevity. Context of the population being dealt with, especially their hysteresis, matters. Immensely.

Go get you some cage-free anarchy chickens and worry a little less.

1. “What in my life is worth attending if not for PaleoFX?”
2. “How did my life spiral out of control to the extent that I cannot attend the PaleoFX?”

Well friend I have good news! Keith Norris and I will be presenting a post-PaleoFX workshop: Leveraging Technology for Ancestral Wellness. Here we will wax poetic about tools, techniques, and technology that allows maximum wellness with no time wasted. The workshop will be Saturday, March 17th, from 3 to 6 PM at Efficient Exercise’s Rosedale location.  $95 will get you a front row seat to an event that will have your mind and body spinning for days with new ideas that you can implement right nowinto your own lifestyle to achieve new levels of health and vitality.

If you want to avoid more feelings of guilt, sign up today for this amazing workshop!

“I have to admit that, objectively, my paleo way is a little more than an absorbing hobby.”

That’s a quote from Keith Thomas in an interview over at Conditioning Research. I think to a certain sense this is true; in fact I think most of the health and fitness pursuits that we engage in add up to little more than a hobby. First, let’s define hobby:

A hobby is a regular activity or interest that is undertaken for pleasure, typically done during one’s leisure time…Engaging in a hobby can lead to acquiring substantial skill, knowledge and experience. However, personal fulfillment is the aim.

I think that sums it up nicely. I make no bones with my own clients that I got into what I do because I enjoyed it first and foremost: it had to be of benefit to me before it would be of benefit to them. Part of what might be cognitive dissonance with regards to so much of the paleophere nonsense, which is no different than any other part of the health and fitness sphere or hell anything in life sphere, is that people have differing aspects that they find enjoyable about the pursuit. Sure there are some people who are amazing marketers and sales people, the Mark Sissons of the world, but I find that rather frustrating. No other hobby do we attempt to market why we find it valuable to us and why it might be valuable to others. I’m not on the bus trying to convince the person next to me that they should take up basketball because I find it enjoyable and it will increase the expression of their Type IIAC muscle fibers. I’m also not on the bus.

I think this is maybe why Art De Vany went behind a pay wall: there is a huge amount of religious/woo nonsense involved in all of this and it’s much less frustrating to be an attractor than a promoter. To me, a pay wall is a way of saying “here’s what I do and if you want to learn more you can come find out,” rather than attempting to convince people through marketing day after day. Promoting T’s you up for people looking to troll; being an attractor allows more of your mental energy to go toward why you started this whole thing: the selfish pursuit of very specific things that are directly interesting to you. If you are able to help people who seek more information, all the better!

Got myself just over a pound of pork belly at Whole Paycheck and proceeded to come up with a cure similar to the recipe here.

It went into the refrigerator looking pretty much like this (even though this is after the next steps):

After 12 hours overnight, I pulled the pork out, rinsed off the salt, sealed it in a bag, and sous vided (its a verb now, damnit) the thing at 144*F for 40 hours. After the 40 hour mark I cooled it between weighted cookie sheets because you don’t want it to curl. When I removed it from the fridge, it looked near as makes no difference to what you see above.

After cooling, I had to scrape off the tasty tasty fat, so the dull knife edge and some scraping left my dogs very happy and a pork belly looking pretty limp:

So the belly when back in a bag into a 140*F bath to warm up. All the while I had carrots in the sous vide at 183*F with butter oil and 21 calories of DEADLY WHITE SUGAR! THROW ME OFF PALEO ISLAND! Also I made a gastrique with a tasty little ingredient:

Likely not good enough for Richard

After the carrots were done, the belly went into a pan with high oleic sunflower oil, was browned on all sides, and plated. Thus we ended up with this:

So what I did for the blob of pork was cut a chunk of the pork belly off, fork shredded it, and whipped it. Could have used a bit more shredding and cooling. but it’s called a rillette.

Anyway Sarah couldn’t tell me enough times how much she loved it; I thought it came out pretty good, certainly up to par with the pork belly I had earlier in the week…perhaps better. The carrots came out really nice as well; the butter oil worked really well and didn’t cause Sarah any problems (she has a dairy allergy).

It seems like a hell of a lot of work but I really only “cooked” for about an hour. It was pretty f’n rico, if I do say so myself.