Conditioning Research

Mountain Trail Walking Study

noreply@blogger.com (Chris) — Tue, 14 Feb 2012 07:49:00 +0000

I suppose this one is for Hillfit? Nothing very exciting - walking in the mountains is hard work and neither BCAA nor arginine supplementation have much impact.

Energy expenditure during 2-day trail walking in the mountains (2,857 m) and the effects of amino acid supplementation in older men and women

We compared relative exercise intensity and active energy expenditure (AEE) on trail walking in the mountains, with those of daily exercise training, and whether branched-chain amino acid (BCAA) and arginine supplementation attenuated the release of markers indicating muscle damage and declines in physical performance. Twenty-one subjects (~63 years) were divided into two groups: amino acid (AA, 51 g of amino acids and 40 g of carbohydrate, male/female = 6/4) or placebo (PL, 91 g of carbohydrate, male/female = 6/5) supplementation during 2 days of trail walking in the mountains. We measured heart rate (HR), AEE, fatigue sensation, water and food intake, and sweat loss during walking. In addition, we measured peak aerobic capacity (VO2peak) and heart rate (HRpeak) with graded-intensity walking, vertical jumping height (VJ) before and after walking. We found that average HR and AEE during uphill walking were ~100% HRpeak and ~60% VO2peak, while they were ~80 and ~20% during downhill walking, respectively. Moreover, average total AEE per day was sevenfold that of their daily walking training. VJ after walking remained unchanged compared with the baseline in AA (P > 0.2), while it was reduced by ~10% in PL (P < 0.01), although with no significant difference in the reduction between the groups (P > 0.4). The responses of other variables were not significantly different between groups (all, P > 0.2). Thus, trail walking in the mountains required a high-intensity effort for older people, while the effects of BCAA and arginine supplementation were modest in this condition.

It is all getting epigenetic now

noreply@blogger.com (Chris) — Mon, 13 Feb 2012 22:46:00 +0000

Reading through a few abstracts today I was noticing how lots of research is looking at epigenetics - how environmental factors affect the status of genes - which ones are turned on or off to over simplify things. Here is a typical one

Effects of mild-exercise training cessation in human skeletal muscle

Stoppage of endurance exercise training leads to complete loss of maximal oxygen uptake (VO2max) gain but not submaximal exercise blood lactate concentrations. However, the detailed mechanisms are still unknown. Thus, we investigated the effects of exercise-training cessation at lactate threshold (LT) intensity on physiological adaptations and global mRNA expressions in human skeletal muscle. The VO2max, muscle capillaries density and global gene expression were measured after 12 weeks of LT training, and after 12 weeks of detraining. Twelve weeks of detraining reversed the effect of 12 weeks LT training on VO2max and VO2 at LT intensity, although the later value was higher than the pre-training level. Moreover, the training cessation did not affect the number of capillaries around type I fiber, which was increased by training. The training modulated 243 characterized transcripts, in which 77% showed a significant reversible effect by detraining. However, the transcripts most-induced by the training were still elevated after the same period of detraining. The pathway and network analysis revealed that these genes were related to oxidative phosphorylation (OxPhos), calcium signalling and tissue development. Therefore, these physiological and transcriptional changes suggest improved oxygen supply and OxPhos in the skeletal muscle, which may contribute to the incomplete loss of absolute VO2 at LT intensity after training cessation. The present study does not only demonstrate, for the first time, sustained effects of training after detraining at the transcriptional level, but also indicates the possible signalling pathways.

The researchers are no longer just looking at what the exercise or cessation of exercise does directly to the body. Beyond that they are looking at how exercise changes gene expression. In this case, exercise seems to have long lasting impacts on the genes that enhance oxidative phosphorylation (OxPhos), calcium signalling and tissue development. These changes persist even when people stop training.

It is really fascinating. Exercise changes what your genes set you up for.

Muscle and cancer - It is not getting old that is the problem, it is getting weaker!

noreply@blogger.com (Chris) — Fri, 10 Feb 2012 07:45:00 +0000

I saw this get picked up in a few places but no one was linking to the actual study. The takeaway message is that building and maintaining muscle strength is vital to all for overall health and this extends to surviving cancer. It is not getting old that is the problem, it is getting weaker!

Researchers studied patients with advanced melanoma to understand the illness as it related to muscle strength. They looked at CT scans of the psoas muscle in order to measure core muscle density. The authors then correlated the core muscle density with the risk of metastasis, or spreading of the cancer.

Patients with higher muscle density were found to have significantly better survival rates and less metastasis. The authors concluded that decreased muscle density was an important predictor in the outcome of the disease. Furthermore, they stated that “frailty, not age, was associated with decreased disease-free survival.”

Here is theabstract

Sarcopenia as a Prognostic Factor among Patients with Stage III Melanoma.

Abstract

BACKGROUND: Several hypotheses proposed to explain the worse prognosis for older melanoma patients include different tumor biology and diminished host response. If the latter were true, then biologic frailty, and not age, should be an independent prognostic factor in melanoma.

METHODS: Our prospective institutional review board (IRB)-approved database was queried for stage III patients with computed tomography (CT) scans at time of lymph node dissection (LND). Psoas area (PA) and density (PD) were determined in semi-automated fashion. Kaplan-Meier (K-M) survival estimates and Cox proportional-hazard models were used to determine PA and PD impact on survival and surgical complications.

RESULTS: Among 101 stage III patients, PD was significantly associated with both disease-free survival (DFS) (P = 0.04) and distant disease-free survival (DDFS) (P = 0.0002). Cox multivariate modeling incorporating thickness, age, ulceration, and N stage showed highly significant association with PD and both DFS and DDFS. DDFS was significantly associated with Breslow thickness (P = 0.04), number of positive nodes (P = 0.001), ulceration (P = 0.04), and decreasing muscle density (P = 0.01), with hazard ratio of 0.55 [95% confidence interval (CI) 0.35-0.87]. PD also correlated with surgical complications, with odds ratio (OR) of 1.081 [95% CI 1.016-1.150, P = 0.01].

CONCLUSIONS: Decreased psoas muscle density on CT, an objective measure of frailty, was as important a predictor of outcome as tumor factors in a cohort of stage III melanoma patients. On multivariate analysis, frailty, not age, was associated with decreased disease-free survival and distant disease-free survival, and higher rate of surgical complications.

A bit more barefooting

noreply@blogger.com (Chris) — Thu, 09 Feb 2012 07:45:00 +0000

Marc from Feel Good Eating pointed me towards this one from yesterday's NY Times:

Does Foot Form Explain Running Injuries?

But, says Mr. Daoud, who was himself an oft-injured heel-striker during his cross-country racing days, "if you have experienced injury after injury and you're a heel-striker, it might be worth considering a change." (If you're unsure of your strike pattern, have a friend videotape you from the side as you run, he suggests, then use slow motion to watch how your foot hits the ground.)

If you do decide to reshape your stride, proceed slowly, he cautions. Many people who abruptly switch to barefoot running or a forefoot running form get hurt in the process, he says. The body's tissues adapt to the forces generated by long-term heel striking. Change your form, and the forces will affect different parts of the leg, leading to soreness and, potentially, injury.

Try landing on the ball of your foot "for five minutes at first at the end of a run," Mr. Daoud suggests. Work up to longer periods of forefoot landings as your body adjusts and only if you do not notice significant, continuing soreness.

In his own case, Mr. Daoud now runs consistently with a forefoot landing style, but the transition was not seamless. "I broke a metatarsal while running my first marathon after transitioning a bit too quickly and expecting a bit too much from my body too soon," he says. So fair warning to those considering making the transition to forefoot landings: "Give your body time!"

I think I had mentioned this research before but it is good to see it getting broader readership

Keep off the antioxidant supplements

noreply@blogger.com (Chris) — Thu, 09 Feb 2012 00:34:00 +0000

This one has been brewing for a while but now it seems fairly solid - antioxidant supplements are, at the least, useless. Stumptuous would like it (beware of the bad language).

This is an amazing letter

TO THE EDITOR: In a recent paper by Higashida et al. (5), the authors report that very large doses of antioxidant vitamins do not prevent the exercise-induced adaptive responses of muscle mitochondria, GLUT4, and insulin action to exercise. As clearly stated in the paper, their data disagree with those reported by three independent research groups from Germany (14), Australia (17), and Spain (4).

Using a significantly different experimental protocol regarding exercise training intensity and duration, antioxidant supplementation (doses and types of antioxidants), and molecular parameters analyzed (mRNA vs. protein levels), Higashida et al. compared their data with ours and came to exactly the opposite conclusions, i.e., that antioxidant vitamin supplementation does not have an inhibitory effect on the adaptive responses of skeletal muscle to exercise. Regarding our study published in the American Journal of Clinical Nutrition (4), we found a very significant increase (∼186%) in endurance time in rats after training (6 wk), which was dramatically blunted when the animals were supplemented with vitamin C (∼26% increment). Endurance capacity is directly related to mitochondrial content, which is why we decided to determine the mitochondrial biogenesis cascade in skeletal muscle in our animals, and we found that it was significantly hampered. Although we found a dramatic effect of vitamin C on endurance time in animals, we did not find the same effect on V̇O2 max in either the animal study or the human study. This is clearly stated and discussed in the introduction, results, and discussion sections of our paper. However, Higashida et al. did not run any performance tests in their study; moreover, they misquoted a few times the results obtained in our human study. Training studies, including the data published by Higashida et al., conducted to determine whether antioxidant vitamins improve exercise performance, have generally shown that supplementation is useless (3, 7, 13, 18, 20). However, recent evidence shows that they can be worse than useless. Several studies suggest that antioxidants may have detrimental effects on performance. As early as 1971, it was shown that vitamin E supplementation (400 IU/day for 6 wk) caused unfavorable effects on endurance performance in swimmers (15). The authors concluded: “There is no evidence here to suggest that vitamin E has any beneficial effect on endurance performance. Indeed the evidence, if anything, suggests that the vitamin has an unfavourable effect.” Malm and coworkers (10, 11) showed, in two consecutive studies, the deleterious effects of ubiquinone-10 supplementation on the performance of humans after a high-intensity training program. In 2002, it was shown that supplementation of racing greyhounds with 1 g vitamin C/day for 4 wk significantly slowed their speed (12). Moreover, in a human study, the negative effects of ascorbic acid supplementation on the adaptive responses of endogenous antioxidant enzymes and stress proteins were demonstrated (8). Furthermore, it has been shown that supplementation with ascorbic acid to prevent delayed-onset muscle soreness after exercise does not preserve muscle function but hinders the recovery process, thereby being detrimental to future performance (2). Finally, in our animal study, we found that vitamin C supplementation decreases training efficiency because it prevents exercise-induced mitochondrial biogenesis (4). Similar conclusions have been recently achieved by a US-based research group (6). The authors found that inhibition of a free radical-generating enzyme (xanthine oxidase) by allopurinol severely attenuates exercise activation of the mitochondrial biogenesis pathway in skeletal muscle. Thus, in our opinion and contrary to the considerations of Higashida et al., there is growing evidence of the negative effects of antioxidant supplementation in exercise performance in both animal and human studies.

The evidence on the detrimental effects of antioxidant supplementation when given to patients and healthy people (non athletes) is, if possible, more robust. In 2007, Bjerlakovic et al. looked at data from sixty-seven studies on antioxidant supplements and they concluded that beta carotene, vitamin A, and vitamin E supplementation seemed to increase the risk of death (1). This data confirmed previous reports showing that long-term vitamin E supplementation may increase the risk for heart failure in patients with vascular disease or diabetes mellitus (9). When a 6-wk aerobic exercise training program was applied in patients with hypertension, supplementation of antioxidants (vitamins C and E and α-lipoic acid) led to an enhancement of blood pressure and an inhibition of exercise-induced flow-mediated vasodilatation (19). Finally, one of us (M. Ristow) showed that antioxidant supplementation with vitamins C and E prevents the induction of molecular regulators of insulin sensitivity and endogenous antioxidant defense by physical exercise (14).

A significant number of both healthy and sick individuals are taking antioxidant supplements in the belief that these will improve their health and prevent or ameliorate diseases (1). Moreover, a large proportion of athletes, including elite athletes, take vitamin supplements, often large doses, seeking beneficial effects on performance (16). The complete lack of any positive effect of antioxidant supplementation on physiological and biochemical outcomes consistently found in human and animal studies raises questions about the validity of using oral antioxidant supplementation in both health and disease.

The vast majority of experimental evidence clearly advises against this supplementation. Thus, we unreservedly confirm the conclusions derived from our previous research (4, 14) and disagree with Higashida et al. In our opinion, antioxidant supplements are, at the least, useless.

fasting ...cancer...we have heard this before?

noreply@blogger.com (Chris) — Thu, 09 Feb 2012 00:23:00 +0000

Fasting Weakens Cancer in Mice

Man may not live by bread alone, but cancer in animals appears less resilient, according to a study that found chemotherapy drugs work better when combined with cycles of short, severe fasting. Even fasting on its own effectively treated a majority of cancers tested in animals, including cancers from human cells.

The full study is here, well the abstract anyway

A Birthday dinner

noreply@blogger.com (Chris) — Thu, 09 Feb 2012 00:03:00 +0000

OK, so today I am 44. I am not going to give one of those daft macho posts about how I will kick old age in the arse. It is coming to us all and we cannot stop it. I am sure we can delay and cut the risk of disease, but believe me one day you will be old and disabled or you will be dead. Today is what you have. NOW! Live it right now and prepare for eternity.

Bah

Anyway tonight was a meal to celebrate my birthday and we went to Wedgewood on the Royal Mile, my favourite Edinburgh restaurant. The dining room has been redecorated and refreshed recently and it has made a difference to the feel of the place. (I'd recommend this place or Le Sept to a visitor to Edinburgh. Le Sept is my regular lunchtime haunt, while Wedgewood is for special occasions) It was - as ever - well presented. It all tasted fantastic too.


the amuse bouche

Rabbit terrine with piccalilli and sweetcorn ice-cream

Salmon, mash, shrimp, some green stuff

goats cheese demifrio and this wierd red onion balsamic sorbet

Fantastic stuff t

Hills not Pills

noreply@blogger.com (Chris) — Wed, 08 Feb 2012 07:35:00 +0000

My article in this month's TGO is called Hills not Pills and looks at the psychological benefits of exercise in the outdoors. (some references for the piece are here) Others have written about this recently - like Chris Kresser - but one of the things that prompted me to write was learning just how many people rely on antidepressants. It is true here in the UK but also across the world as this graphic shows.

Created by: Medical Billing and Coding Online

Just go outside for a walk

our genome is not prepared for grains

noreply@blogger.com (Chris) — Tue, 07 Feb 2012 23:38:00 +0000

More on social stress

noreply@blogger.com (Chris) — Tue, 07 Feb 2012 21:59:00 +0000

I had a post up the other day on the inflammatory effects of social stress. Here is another one for your consideration.

Comparing yourself to others can have health impacts
although this one just indicates that things are...complicated (as ever)

the slow middle finger....

noreply@blogger.com (Chris) — Tue, 07 Feb 2012 21:46:00 +0000

No, this is not about an obscene gesture.

Rather I just wanted to point to this fascinating report of a study that I saw today. The role of the brain in movement is fascinating and I've become increasingly interested in the whole area of neuroplasticity. Todd Hargrove continuously writes compelling and intriguing material on the role of the bran and nervous system in movement and through him I've been reading around Feldenkrais. Z Health and its ideas about proprioception and the arthokinetic reflex are another area that I would like to lose myself in with study if I had the time. Then there is the work of Tim Anderson with Becoming Bulletproof and Pressing Reset which give practical prescriptions for work to enhance this set of skills and senses, thinking about how movement is at the root of all of who we are.

I always find it interesting that in Christian theology there is no place for disembodied spirits. We are body, soul and spirit. We need a body to be human. It is through the body that we interact and influence the world. The Bible talks of the resurrection of the body so that in eternity we have bodies....not just spirits floating around. But what ever your own personal spirituality, right now we are in bodies and movement is fundamental to what they are and to their health.

Anyway enough of that, this study looked at the nature of our plastic brain, a brain that changes and develops in reaction to how we move, to the skills that we develop.

Why the middle finger has such a slow connection

Thumb and little finger are the quickest

The researchers set subjects a simple task to measure the speed of decision: they showed them an image on a monitor that represented all ten fingers. If one of the fingers was marked, the subjects were to press a corresponding key as quickly as possible with that finger. The thumb and little finger were the fastest. The middle finger brought up the rear. "You might think that this has anatomical reasons or depends on the exercise" said Dr Dinse, "but we were able to rule that out through further tests. In principle, each finger is able to react equally quickly. Only in the selection task, the middle finger is at a distinct disadvantage."

Computer simulation depicts brain maps

To explain their observations, the researchers used computer simulations based on a so-called mean-field model. It is especially suited for modelling large neuronal networks in the brain. For these simulations, each individual finger is represented by a group of nerve cells, which are arranged in the form of a topographic map of the fingers based on the actual conditions in the somatosensory cortex of the brain. "Adjacent fingers are adjacent in the brain too, and thus also in the simulation", explained Dr. Dinse. The communication of the nerve cells amongst themselves is organised so that the nerve cells interact through mutual excitation and inhibition.

Inhibitory influences from both sides slow down the middle finger

The computer simulations showed that the longer reaction time of the middle finger in a multiple choice task is a consequence of the fact that the middle finger is within the inhibition range of the two adjacent fingers. The thumb and little finger on the other hand only receive an inhibitory effect of comparable strength from one adjacent finger each. "In other words, the high level of inhibition received by the nerve cells of the middle fingers mean that it takes longer for the excitement to build up – they therefore react more slowly" said Dr. Dinse.

Targeted reduction of the inhibition through learning

From the results of the computer simulation it can be concluded that weaker inhibition from the neighbouring fingers would shorten the reaction time of the middle finger. This would require a so-termed plastic change in the brain – a specialty of the Neural Plasticity Lab, which has been studying the development of learning protocols that induce such changes for years. One such protocol is the repeated stimulation of certain nerve cell groups, which the laboratory has already used in many experiments. "If, for example, you stimulate one finger electrically or by means of vibration for two to three hours, then its representation in the brain changes" explained Dr. Dinse. The result is an improvement in the sense of touch and a measurable reduction of the inhibitory processes in this brain area. This also results in the enlargement of the representation of the finger stimulated.

Second experiment confirms the prediction

The Bochum researchers then conducted a second experiment in which the middle finger of the right hand was subjected to such stimulation. The result was a significant shortening of the reaction time of this finger in the selection task. "This finding confirms our prediction" Dr. Dinse summed up. Thus, for the first time, Bochum's researchers have established a direct link between the so-called lateral inhibitory processes and decision making processes. They have shown that learning processes that change the cortical maps can have far-reaching implications not only for simple discrimination tasks, but also for decision processes that were previously attributed to the so-called "higher" cortical areas.

It is this idea that you can get better at a skill through practice and that this practice changes the brain that fascinates and amazes me. It is a motivation to move and to keep growing.

That massage study

noreply@blogger.com (Chris) — Mon, 06 Feb 2012 20:45:00 +0000

Like everyone else I was quick to jump on the abstract of that massage study at the weekend. Paul at Save Yourself is a lot more considered and his analysis is first rate. Nothing against massage - it is good and it works for certain things - but we need to be careful about the science. Paul's stuff is always well thought out and well researched. He puts me to shame.

Take the time to read his analysis of the study and the way it has been reported:

Massage reduces inflammation and promotes mitochondria?

Some interesting new scraps of basic biology evidence are scientific miles away from proof of therapy

Muscle Heat Stress - grows new mitochondria

noreply@blogger.com (Chris) — Sun, 05 Feb 2012 20:00:00 +0000

This is an interesting study. It is a bit of a cliche, but everyone talks about the mitochondria being the powerhouse of the cell. They are where ATP, the energy currency of the cell is produced. The more mitochondria you have the more fuel you will be able to generate in your muscles. (OK I am over simplifying)

Studies into interval training have found that high intensity training can induce mitochondrial biogenesis - i.e. grow new ones.

This new study indicates that the heat generated by exercise in muscles could be responsible for generating new mitochondria.

Mild heat stress induces mitochondrial biogenesis in C2C12 myotubes

During endurance exercise, most (≈75%) of the energy derived from the oxidation of metabolic fuels and ATP hydrolysis of muscle contraction is liberated as heat, the accumulation of which leads to an increase in body temperature. For example, the temperature of exercising muscles can rise to 40°C. Although severe heat injury can be deleterious, several beneficial effects of mild heat stress (HS), such as the improvement of insulin sensitivity in patients with type 2 diabetes, have been reported. However, among all cellular events induced by mild HS from physical activities, the direct effects and mechanisms of mild HS on mitochondrial biogenesis in skeletal muscle are least characterized. AMP-activated protein kinase (AMPK) and sirtuin 1 (SIRT1) are key energy-sensing molecules regulating mitochondrial biogenesis. In C2C12 myotubes, we found that 1 h mild HS at 40°C upregulated both AMPK activity and SIRT1 expression, as well as increased the expression of several mitochondrial biogenesis regulatory genes including peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) and transcription factors involved in mitochondrial biogenesis. In particular, PGC-1α expression was found to be transcriptionally regulated by mild HS. Additionally, after repeated mild HS for 5 days, protein levels of PGC-1α and several mitochondrial oxidative phosphorylation subunits were also upregulated. Repeated mild HS also significantly increased mitochondrial DNA copy number. In conclusion, these data show that mild HS is sufficient to induce mitochondrial biogenesis in C2C12 myotubes. Temperature-induced mitochondrial biogenesis correlates with activation of the AMPK-SIRT1-PGC-1α pathway. Therefore, it is possible that muscle heat production during exercise plays a role in mitochondrial biogenesis.

Hillfit Manifesto

noreply@blogger.com (Chris) — Sun, 05 Feb 2012 18:19:00 +0000

I've added a new page to the Hillfit Website - the Hillfit Manifesto. The aim is to explain what it is all about, to summarise the drive behind the book.

Check it out and let me know what you think

Bad social experiences promote inflammation

noreply@blogger.com (Chris) — Sat, 04 Feb 2012 18:56:00 +0000

This is fascinating - the impact of stress from competitors and general social interactions can promote inflammation.

Negative and competitive social interactions are related to heightened proinflammatory cytokine activity

These findings suggest that daily social interactions that are negative and competitive are associated prospectively with heightened proinflammatory cytokine activity.

It is all about environment.....but that is not just diet, social interactions, other stresses are important too. Getting your stress under control - work, relationships etc - is as vital as diet. You can get diet and exercise dialed in but if you are chronically stressed from other things then you will still suffer.

I am like this at the moment from work and family pressures

There is a good commentary here.

Stability and Mobility for natural running

noreply@blogger.com (Chris) — Sat, 04 Feb 2012 17:55:00 +0000

Excellent stuff from the Natural Running Centre

Lots of good stuff here on posture, gait, mobility and stability

thanks to Jim Hansen for pointing this out

You have a brain so you can move

noreply@blogger.com (Chris) — Sat, 04 Feb 2012 13:10:00 +0000

This came via a very good post from Marc Keys. He talks about skill development. As we have said before strength is one thing, skill development is another. Get strong and then apply it to your chosen skill, something I talk about in Hillfit

Natural Messiah had a great discussion of this video a few months ago

Exercise is good for older brains

noreply@blogger.com (Chris) — Sat, 04 Feb 2012 12:22:00 +0000

Continuing the theme of keeping older brains healthy....I've had stuff before on how exercise increases insulin sensitivity (which we saw was a good thing) and how resistance training benefits older people. Now this study which sees better brain performance in the elderly following intense exercise.

Acute moderate exercise enhances compensatory brain activation in older adults.

Insulin Resistance and brain health

noreply@blogger.com (Chris) — Sat, 04 Feb 2012 09:04:00 +0000

Watching my Dad's dementia, brain health is becoming a real interest. Here is a study which shows that reduced insulin sensitivity is linked to smaller brain size and deteriorated language skills in the elderly.

"We found that in elderly whose insulin sensitivity was still high, the brains were larger, and they had more grey matter in regions that are important for language skills, compared with those who had diminished insulin sensitivity. We also observed that higher insulin sensitivity was associated with better scores on the language test. Our findings offer a possible explanation for why methods that improve insulin sensitivity, such as exercise, are promising strategies for counteracting cognitive aging late in life," says Christian Benedict.

Of course insulin resistance is complex - not just about eating too many carbs - and Stephan's series is a great outline of the issues. Again, environment, genetics, gut flora are all kicking around but a real food diet, rest, exercise and reducing stress all help keep you sensitive to insulin.

Epigenetics again

noreply@blogger.com (Chris) — Sat, 04 Feb 2012 08:59:00 +0000

At the moment everything seems to be about epigenetics, mitochnodria or the microbiome.

Here is one about epigenetics - turning genes on or off:

Scientists at the University of California, San Francisco (UCSF) have identified nearly 200 genes in the healthy prostate tissue of men with low-grade prostate cancer that may help explain how physical activity improves survival from the disease.

Vigorous exercise linked to gene activity in prostate

Less Stuff.....

noreply@blogger.com (Chris) — Fri, 03 Feb 2012 21:39:00 +0000

Grip Work

noreply@blogger.com (Chris) — Fri, 03 Feb 2012 21:12:00 +0000

Massage post exercise reduces inflammation, builds mitochondria

noreply@blogger.com (Chris) — Fri, 03 Feb 2012 07:41:00 +0000

I've mentioned before that I get a regular session of bodywork from my pal Colin at Edinburgh Deep Tissue Massage. I enjoy the chat, he sorts out any strains or spasms that are going on and he also gives me some good coaching in general on posture, movement and exercise.

It seems that there are real clinic benefits to all this too. I spotted this report of a new study on massage which explains :

While massage is well accepted as a therapy for relieving muscle tension and pain, the researchers delved deeper to find it also triggers biochemical sensors that can send inflammation-reducing signals to muscle cells.

In addition, massage signals muscle to build more mitochondria, the power centres of cells which play an important role in healing.

"The main thing, and what is novel about our study, is that no one has ever looked inside the muscle to see what is happening with massage, no one looked at the biochemical effects or what might be going on in the muscle itself," said Crane.

"We have shown the muscle senses that it is being stretched and this appears to reduce the cells' inflammatory response," he said. "As a consequence, massage may be beneficial for recovery from injury."

Really interesting stuff - cellular effects from massage which extend to generating more mitochondria.

As ever of course, Alex at Sweat Science got here first and has a much more detailed analysis of the research.

Cosmetics and Chemicals

noreply@blogger.com (Chris) — Fri, 03 Feb 2012 07:24:00 +0000

This was interesting

Created by: Cosmetology School

Curing ITB pain

noreply@blogger.com (Chris) — Thu, 02 Feb 2012 22:35:00 +0000

a nice technique....from Martha Peterson