K Starr on the push up

What I also like is Kelly's effortless squat

Don't take it sitting down

I think we've heard this before now|:

Stand Up: Your Life Could Depend On It

ScienceDaily (Mar. 27, 2012) — Standing up more often may reduce your chances of dying within three years, even if you are already physically active, a study of more than 200,000 people published in Archives of Internal Medicine shows. The study found that adults who sat 11 or more hours per day had a 40% increased risk of dying in the next three years compared with those who sat for fewer than four hours a day. This was after taking into account their physical activity, weight and health status.

Good Science

 

 

In response to my Pale(Br)o Science post Sol pointed to his (?) website Examine.com which I have been checking out. 

Examine.com is a science-focused compendium on supplements, nutrition, fitness, and health.  Akin to Wikipedia, we are a site that allows people to contribute to the site. Unlike Wikipedia, we have editors that oversee and approve all content.

There is all sorts of stuff on there, well referenced and researched and well worth reading and referring to.

Movement Lectures - Good Listening.....

I just wanted to point to this new resource:

I am getting a bit bored with the podcasts that I have been listening to recently - I think that most things that can be said about paleo have now been said - so I was checking out these little mp3s

So far I've listened to Tim Anderson on crawling and Tom Furman on the ability to move.  Both were really well produced, explained the topic well and came with a pdf transcript.

Good stuff.

Climbing....is natural

Someone shared this on Facebook the other day.  While you might wonder about the safety of the kid - that is a big fall - it is amazing to watch pure natural movement

Abdominal/lumbar musculature and pelvic stabilisation

Colin has posted a really good article on the role of the abs and lumbar musculature in pelvic stabilisation:

Abdominal/lumbar musculature and pelvic stabilisation

Pale(br)o Science

BroScience is a term used by some bodybuilding communities:

Broscience is the predominant brand of reasoning in bodybuilding circles where the anecdotal reports of jacked dudes are considered more credible than scientific research.

A sarcastic term implying that the time tested, muscle building wealth of knowledge developed and utilized by successful, experienced bodybuilders is inferior to the continually shifting hypotheses of articulate, textbook-savvy 155lb. chemists with little or no real world first-person experience to substantiate their conclusions. The term "Broscience" is oft repeated on bodybuilding and fitness oriented internet forums in an attempt to demonstrate online dominance as a substitution for success in the arena of actual bodybuilding.

There is even a site called Broscience.com  which highlights how science conflicts with popular myth in the bodybuilding world.

I think there is some similar stuff in the paleo world.....Palebro science perhaps.  People like Kurt Harris and Matt Lalonde are key in fighting the myths with science.

Lay off the antioxidants

I think I've had stuff up before warning you off antioxidant supplements.  Here is another  study -  a Cochrane Review - which says that  current evidence does not support the use of antioxidant supplements.  Indeed certain of them seem to increase mortality.

The abstract is below:

Background:
Our systematic review has demonstrated that antioxidant supplements may increase mortality. We have now updated this review.

Objectives:
To assess the beneficial and harmful effects of antioxidant supplements for prevention of mortality in adults.

Search strategy:
We searched The Cochrane Library, MEDLINE, EMBASE, LILACS, the Science Citation Index Expanded, and Conference Proceedings Citation Index-Science to February 2011. We scanned bibliographies of relevant publications and asked pharmaceutical companies for additional trials.

Selection criteria:
We included all primary and secondary prevention randomised clinical trials on antioxidant supplements (beta-carotene, vitamin A, vitamin C, vitamin E, and selenium) versus placebo or no intervention.

Data collection and analysis:
Three authors extracted data. Random-effects and fixed-effect model meta-analyses were conducted. Risk of bias was considered in order to minimise the risk of systematic errors. Trial sequential analyses were conducted to minimise the risk of random errors. Random-effects model meta-regression analyses were performed to assess sources of intertrial heterogeneity.

Main results:
Seventy-eight randomised trials with 296,707 participants were included. Fifty-six trials including 244,056 participants had low risk of bias. Twenty-six trials included 215,900 healthy participants. Fifty-two trials included 80,807 participants with various diseases in a stable phase. The mean age was 63 years (range 18 to 103 years). The mean proportion of women was 46%. Of the 78 trials, 46 used the parallel-group design, 30 the factorial design, and 2 the cross-over design. All antioxidants were administered orally, either alone or in combination with vitamins, minerals, or other interventions. The duration of supplementation varied from 28 days to 12 years (mean duration 3 years; median duration 2 years). Overall, the antioxidant supplements had no significant effect on mortality in a random-effects model meta-analysis (21,484 dead/183,749 (11.7%) versus 11,479 dead/112,958 (10.2%); 78 trials, relative risk (RR) 1.02, 95% confidence interval (CI) 0.98 to 1.05) but significantly increased mortality in a fixed-effect model (RR 1.03, 95% CI 1.01 to 1.05). Heterogeneity was low with an I2- of 12%. In meta-regression analysis, the risk of bias and type of antioxidant supplement were the only significant predictors of intertrial heterogeneity. Meta-regression analysis did not find a significant difference in the estimated intervention effect in the primary prevention and the secondary prevention trials. In the 56 trials with a low risk of bias, the antioxidant supplements significantly increased mortality (18,833 dead/146,320 (12.9%) versus 10,320 dead/97,736 (10.6%); RR 1.04, 95% CI 1.01 to 1.07). This effect was confirmed by trial sequential analysis. Excluding factorial trials with potential confounding showed that 38 trials with low risk of bias demonstrated a significant increase in mortality (2822 dead/26,903 (10.5%) versus 2473 dead/26,052 (9.5%); RR 1.10, 95% CI 1.05 to 1.15). In trials with low risk of bias, beta-carotene (13,202 dead/96,003 (13.8%) versus 8556 dead/77,003 (11.1%); 26 trials, RR 1.05, 95% CI 1.01 to 1.09) and vitamin E (11,689 dead/97,523 (12.0%) versus 7561 dead/73,721 (10.3%); 46 trials, RR 1.03, 95% CI 1.00 to 1.05) significantly increased mortality, whereas vitamin A (3444 dead/24,596 (14.0%) versus 2249 dead/16,548 (13.6%); 12 trials, RR 1.07, 95% CI 0.97 to 1.18), vitamin C (3637 dead/36,659 (9.9%) versus 2717 dead/29,283 (9.3%); 29 trials, RR 1.02, 95% CI 0.98 to 1.07), and selenium (2670 dead/39,779 (6.7%) versus 1468 dead/22,961 (6.4%); 17 trials, RR 0.97, 95% CI 0.91 to 1.03) did not significantly affect mortality. In univariate meta-regression analysis, the dose of vitamin A was significantly associated with increased mortality (RR 1.0006, 95% CI 1.0002 to 1.001, P = 0.002).

Authors' conclusions:
We found no evidence to support antioxidant supplements for primary or secondary prevention. Beta-carotene and vitamin E seem to increase mortality, and so may higher doses of vitamin A. Antioxidant supplements need to be considered as medicinal products and should undergo sufficient evaluation before marketing.

The Runner's High - you are destined to enjoy exercise

I saw this report pass over my Google Reader today, based on a study just published in the Journal of Experimental Biology:

Wired to run: exercise-induced endocannabinoid signaling in humans and cursorial mammals with implications for the ‘runner’s high’

Humans report a wide range of neurobiological rewards following moderate and intense aerobic activity, popularly referred to as the ‘runner’s high’, which may function to encourage habitual aerobic exercise. Endocannabinoids (eCBs) are endogenous neurotransmitters that appear to play a major role in generating these rewards by activating cannabinoid receptors in brain reward regions during and after exercise. Other species also regularly engage in endurance exercise (cursorial mammals), and as humans share many morphological traits with these taxa, it is possible that exercise-induced eCB signaling motivates habitual high-intensity locomotor behaviors in cursorial mammals. If true, then neurobiological rewards may explain variation in habitual locomotor activity and performance across mammals. We measured circulating eCBs in humans, dogs (a cursorial mammal) and ferrets (a non-cursorial mammal) before and after treadmill exercise to test the hypothesis that neurobiological rewards are linked to high-intensity exercise in cursorial mammals. We show that humans and dogs share significantly increased exercise-induced eCB signaling following high-intensity endurance running. eCB signaling does not significantly increase following low-intensity walking in these taxa, and eCB signaling does not significantly increase in the non-cursorial ferrets following exercise at any intensity. This study provides the first evidence that inter-specific variation in neurotransmitter signaling may explain differences in locomotor behavior among mammals. Thus, a neurobiological reward for endurance exercise may explain why humans and other cursorial mammals habitually engage in aerobic exercise despite the higher associated energy costs and injury risks, and why non-cursorial mammals avoid such locomotor behaviors.

They basically found that that exercising mammals release pleasurable endocanabinoids in response to exercise.

Having suggested that natural selection used the endocanabinoid system to motivate endurance exercise in humans and other animals that walk and run over long distances, Raichlen adds 'These results suggest that natural selection may have been motivating higher rather than low-intensity activities in groups of mammals that evolved to engage in these types of aerobic activities'.

There is some more background at Eureka here.

The team publish their discovery that animals that evolved for endurance exercise benefit from endocanabinoids while animals that did not don't experience the pleasures, leading them to propose that natural selection used the endocanabinoid system to motivate endurance exercise in humans.

Given that we do experience the runners' high, the implication is that we evolved for endurance....or were designed for endurance. 

It is also interesting from the perspective of motivation and the ideas of Samuele Marcora that I mentioned here.

keep squatting....and eating coconut oil

I spent the weekend visiting my parents.  My Dad has dementia and is currently in a hospital ward.  His mental state oscillates, but when he is well he is still funny, loving, caring and sharp.  It is just the dislocation from reality that is difficult to witness.

Anyway, I was struck again by how basic and essential it is to be able to stand up from a chair.  There is balance involved, but so much more is the need for basic strength in the hip extensors, back and thighs.  Occupational therapy is fine, but it would be fantastic if we could get them on a leg press a couple of times a week.

I have got my Mum to start giving him coconut oil each day now, especially after listening to this podcast.  Podcast #13: How To Upgrade Your Brain with Coconut Oil & Ketones

Breastfeeding and Strength

This looks like a fascinating study.  The longer that men were breastfed as babies, the stronger they were as old men.  

Muscle Strength in Older Community-Dwelling Men Is Related to Type of Milk Feeding in Infancy.

BACKGROUND:
There is a growing literature that links greater duration and exclusivity of breastfeeding to beneficial effects on adult health outcomes. Muscle growth in the neonatal period may be very sensitive to variations in early nutrition, but little is known about long-term effects of infant feeding on muscle strength.
METHODS:
In 2,983 community-dwelling older men and women born 1931-1939, we examined the relationship between their type of milk feeding in infancy and their muscle strength in adult life. Information about milk feeding for each participant was abstracted from their infant record; grip strength was measured using a Jamar dynamometer.
RESULTS:
Sixty percent (1,783) of the participants were breastfed only, 31% (926) were breast- and bottle-fed, and 9% (274) were bottle-fed only. There were no differences in type of milk feeding between men and women or according to social class at birth. Among the men studied, grip strength was related to the type of milk feeding, such that greater exposure to breast milk in infancy was associated with greater grip strength in adult life (p = .023). This association remained after adjustment for the effects of a range of confounding influences (birthweight, infant growth, height, age at measurement, adult diet, and level of physical activity). In contrast, the type of milk feeding in infancy was not related to grip strength among the women studied (p = .807).
CONCLUSIONS:
These data suggest that in men, differences in nutritional exposure in the early postnatal period may have lifelong implications for muscle strength.

Extreme Mountain Biking

This is scary to watch



via Mud and Routes

Work is murder

Ok, this one is a bit overblown but it will justify your dislike of work....

>

Your epigenetics make you fat

I think I have remarked before on this Trinity of sexy themes at the moment in research in health and fitness:

• Microbiome
• Mitochondria
• Epigenetics

This is one for the epigenetics thread:  remember you have genes but the key thing is which of those genes are turned on  and which are turned off.  You are not programmed by you DNA, it is far more complex than that - you have a complex set of switches that react to your environment.

And that applies to your obesity.  You are not programmed to be fat.  Even if you have certain genes that are associated with fatness, they can be overridden.  The environment, epigenetic factors, the signals that you send to your cells,  are so much more important.  So to the study:


Getting Active Blunts Fat Genes

Physical activity appears to dampen the effect of fat-increasing genes, while inactivity allows the genetic disposition to unfold, a longitudinal study found.

Each additional gene variant linked with increasing body mass index (BMI) was associated with a mean gain of 0.13 kg/m2 in BMI, according to Qibin Qi, PhD, from Harvard School of Public Health in Boston, and colleagues.

However, individuals who were most physically active saw a blunted genetic effect, with a mean increase of 0.08 kg/m2, while those watching more than 40 hours of TV per week had an accentuated effect, with a mean increase of 0.34 kg/m2.

Although the genetic effect on BMI was most pronounced at each extreme, it was less so with more benign lifestyles, researchers reported at the American Heart Association's Epidemiology and Prevention/Nutrition, Physical Activity and Metabolism (EPI/NPAM) meeting in San Diego.

For those in the lowest quintile of physical activity, the mean increase in BMI was 0.15 kg/m2 -- a number slightly higher than the reference mean gain associated with each gene variant.

For those who watched up to only one hour of TV per week, the mean gain in BMI was 0.08 kg/m2, the same as in the highest quintile of activity.
 

 You do not have to be fat.  Get up and move about a bit.

Placebo's evil twin....in the gym

Today I came across this new and very interesting study: Preventing motor training through nocebo suggestions

Here is the abstract:

Although placebos have repeatedly been shown to increase physical performance and endurance, much less is known about the effect of their negative counterpart, nocebos. Here, we employ negative suggestions and a sham electrical stimulation as a nocebo conditioning procedure in healthy subjects performing a leg extension exercise to total exhaustion. Using two different protocols, we analyze the contribution of expectation alone or the combination of conditioning and expectation to the nocebo effect evaluated as the change of work performed and rate of perceived exertion. We find that it is possible to negatively modulate the physical performance in both cases, and we argue that this effect can effectively offset the outcome of training programs.

The discussion in the paper is instructive:

The main finding of this study is that it is possible to negatively modulate the performance of subjects carrying out a muscle exercise to volitional maximum effort by employing discouraging suggestions and negative conditioning.

I do find this study absolutely fascinating.  The whole idea of the power of belief in health and healing is realitively well known - we have all heard of the placebo.  But what is less well known is the nocebo - the idea that rather than positive benefits, there can be negative impacts from certain contexts and expectations: you can get worse.

What is interesting here is how nocebo effects extend to exercise performance - hearing negative suggestions can impact how well you perform.

All this stuff about the impact of the mind is so important and could potentially trump all other effects - diet, exercise whatever.  If you think it is doing you good it will.  If you think it is harmful, then it will be.    It is like Samuele Marcora's work on the psychobiological model of fatigue - the impact of perception is so important.

By the way, coincidentally, Chris Kresser had a great podcast on this this week with a full transcript here: The Placebo Effect and The Power of Belief in Healing

In some ways this is all like epigenetics - the impact of environment, in this case perceptions and expectations, outweigh what seem to be the bigger more obvious factors.

The search for the perfect diet or exercise routine may be pointless.....the most important element to either is what you believe  about the diet or training regime.

Dr Kurt Harris has a good post on placebo here.

Busy

Sorry that the blog is quiet at the moment.  My work is busy so when I get home I am tired and have no had the time or space to post much.   I will keep posting whatever I find of interest as I get the time.

Work is busy and as someone said in an email to me the other day, it always takes more from us than we give.  But I keep smiling through it and have started to walk in and back for the space and to avoid the bus.

Early birth and health....what about the obvious?

I meant to blog about this last week, but didn't get round to it.   There were lots of new stories a couple of  weeks ago that  babies born even a couple of weeks early have more health problems.

Babies born a few weeks early 'suffer health risks'

Babies born just a few weeks early have a higher risk of poor health, including asthma, than those born later, research suggests.

I think they missed a big confounding factor in this analysis - caesarian birth.    Lots of those early births are due to C sections and that brings us back to microbiota.  Babies born by C section miss out on being exposed to a bunch of healthy bacteria from the birth canal......maybe that is causing the health problems?

Babies delivered via cesarean section show different microbial profiles than those born vaginally—whereas vaginally delivered infants are colonized at first by fecal and vaginal bacteria from the mother, infants born through cesarean section are exposed initially to bacteria originating from the hospital environment and health care workers. 

The runner's high

An interesting piece in Scientific American on the runner's high which looks at different explanations for why it happens - interestingly scientists seem to be in the dark on this one.....

It hurts so good: the runner’s high

Jez Bragg on trail running

Jez is an amazing athlete

Your Child’s Brain on Television

Via: Online Courses News

Stretching again

Another study that says dynamic stretches rather than static stretches are appropriate for use before exercise.

Relative static stretch-induced impairments and dynamic stretch-induced enhancements are similar in young and middle-aged men.

Thoughts on self defence from the Daily Prep

this is from the Daily Prep

So is this congruent?

I will return to my notes on Congruent Exercise soon, but I just thought I'd post this.  I am all for making exercise accessible and part of your day, but really.....

From Nano Workout -

Itchy feet is a good exercise to do during the day if you work in an office and get back pain after long hours in front of the computer and need to stretch your back.

Lean forward and grab on to your left foot with your right hand. Arch your back and pull upwards to stretch the right side of your back. Switch sides.

Rugby Giants

There is an interesting story on the BBC news website today about the way in which rugby players are getting bigger and bigger and the impact it is having on the tactics of the game.

If we combine those figures to give us the average weight and height of an England player, the trends are even clearer.

Someone who pulls on the white shirt in 2012 is on average almost three stone heavier and three inches taller than their predecessors of 50 years ago. They are well over a stone heavier and an inch taller than the XV which completed a second successive Grand Slam in 1992 and have 4.5lbs and almost an inch on the team of 2002 that went on to win the World Cup 18 months later.


1962: 85.7kg, 1.80 m
1972: 90.7kg, 1.85 m
1982: 89.9kg, 1.82 m
1992: 96.8kg, 1.85m
2002: 101.9kg, 1.86m
2012: 104kg, 1.88m

"Some of the collisions are like car crashes," he says. "When you get George North running flat out into a Manu Tuilagi, the forces involved are incredible. You get some horrific injuries from contact. You can hear half the impacts from the touchline."
After the last Lions tour, the squad's vastly experienced doctor James Robson - also Scotland's team doctor - warned that the size of players was forcing rugby towards a "watershed" moment.

"People are trying to run through the opposition, rather than around them," he said. "My hope is that coaches recognise that and we get a little bit smaller and faster and more skilful - that players win the space rather than the collision."

What the article doesn't explain is why they are now so big?  Is it jstu a general population who are bigger, are they better trained - they are certainly very well muscled now - better nutrition?

Back to the microbiota - impact of the type of dietary fat

So back to another sexy term.  Not epigenetics this time but the microbiome.  There are studies out there that show that the gut midrobiome of the obese differs from that of the lean (and fecal transplants from lean to obese can make them lose fat).   This study seems to show that saturated fats shift gut microbiota profiles toward those typical of obese individuals, and that dietary fatty acid saturation influences shifts in gut microbiota independently of changes in body mass.

Oh noes, don't tell me that my saturated fat bias is being challenged?

Gut bacteria profiles of Mus musculus at the phylum and family levels are influenced by saturation of dietary fatty acids.

Make you vaccination more effective with intense exercise!

Vaccination response following aerobic exercise: Can a brisk walk enhance antibody response to pneumococcal and influenza vaccinations?

A brisk walk does not do what high intensity exercise can

Exercise and telomere length

You might need to go and look up telomeres to get this.  (There is a simple explanation here:  Telomeres are relatively short sections of specialized DNA that sit at the ends of all chromosomes. One of the Nobel Prize winners, Elizabeth Blackburn, Ph.D., of the University of California at San Francisco, has compared telomeres to the plastic tips at the ends of shoelaces that prevent the laces from unraveling.  Each time a cell divides, its telomeres erode slightly and become progressively shorter with each cell division. Eventually, telomeres become so short that their host cells stop dividing and lapse into a condition called cell senescence. As a result, vital tissues and important organs begin to fail and the classical signs of aging ensue.)

So longer telomeres protect from aging.

This study showed that long-term exercise altered telomere dynamics, slowing age-related decreases in telomere length in cardiac and liver tissue but contributing to shortening in exercised skeletal muscle.

So the heart and liver seemed to benefit while the muscles were aged....It is never simple


Chronic Exercise Modifies Age-Related Telomere Dynamics in a Tissue-Specific Fashion.

you need more sleep.....

Of course you need more sleep.  I wrote a piece for TGO last month on the importance of sleep.  This infographic puts it all well:

Created by: MedicalBillingAndCodingCertification.net

How does having weak muscles affect walking?

This study looks interesting.  We often tell people that strength will let them do al things better, being stronger makes everything easier (well I say that in Hillfit anyway)

This abstract is of a study that wanted to test the impact of weak muscles on gait.   They did it through various simulations, but it is still instructive.  Note that you can apparently get away with weak hip and knee extensors but when the plantar flexors (feet), hip abductors, and hip flexors get weak then your walking will be in trouble. 

Think about elderly people if we just got them doing some basic training for these muscles to strengthen them then we could really get their function up. 

How robust is human gait to muscle weakness?

Abstract
Humans have a remarkable capacity to perform complex movements requiring agility, timing, and strength. Disuse, aging, and disease can lead to a loss of muscle strength, which frequently limits the performance of motor tasks. It is unknown, however, how much weakness can be tolerated before normal daily activities become impaired. This study examines the extent to which lower limb muscles can be weakened before normal walking is affected. We developed muscle-driven simulations of normal walking and then progressively weakened all major muscle groups, one at the time and simultaneously, to evaluate how much weakness could be tolerated before execution of normal gait became impossible. We further examined the compensations that arose as a result of weakening muscles. Our simulations revealed that normal walking is remarkably robust to weakness of some muscles but sensitive to weakness of others. Gait appears most robust to weakness of hip and knee extensors, which can tolerate weakness well and without a substantial increase in muscle stress. In contrast, gait is most sensitive to weakness of plantarflexors, hip abductors, and hip flexors. Weakness of individual muscles results in increased activation of the weak muscle, and in compensatory activation of other muscles. These compensations are generally inefficient, and generate unbalanced joint moments that require compensatory activation in yet other muscles. As a result, total muscle activation increases with weakness as does the cost of walking. By clarifying which muscles are critical to maintaining normal gait, our results provide important insights for developing therapies to prevent or improve gait pathology.

The neurology of computer games

I've had a fair bit of stuff on this blog about neuroplasticity - the way in which our brains change in response to how we use them, what we call on them to do.  This infographic looks at the way in which computer games affect the brain and that includes neuro plastic changes:

Clink on it to make it bigger if you like


Via: Online Universities Blog

A couple on Alzheimer's / Dementia

My Dad has dementia and anything I see about it has special impact. 

First off, Vitamin D looks like it has potential here as often elsewhere:

• How Vitamin D Boosts Amyloid Beta Removal From Brain - which points to this at Eureka : scientists pinpoint how vitamin D may help clear amyloid plaques found in Alzheimer's

the early findings show that vitamin D3 may activate key genes and cellular signaling networks to help stimulate the immune system to clear the amyloid-beta protein.

Previous laboratory work by the team demonstrated that specific types of immune cells in Alzheimer's patients may respond to therapy with vitamin D3 and curcumin, a chemical found in turmeric spice, by stimulating the innate immune system to clear amyloid beta. But the researchers didn't know how it worked.

 Then this one which I don't fully understand (but thanks to Colin for sending it on)

• Antibodies that block the process of synapse disintegration in Alzheimer's disease have been identified, raising hopes for a treatment to combat early cognitive decline in the disease  - 

neurons that were exposed to the antibody remained healthy, with no synaptic disintegration.

Dr Salinas said: "Despite significant advances in understanding the molecular mechanisms involved in Alzheimer's disease, no effective treatment is currently available to stop the progression of this devastating disease."

She added: "This research identifies Dkk1 as a potential therapeutic target for the treatment of Alzheimer's disease."
 

Our plastic muscles....coffee and exercise

Back to our sexy themes...this time it is epigenetics:

Acute Exercise Remodels Promoter Methylation in Human Skeletal Muscle

Highlights

• Transient promoter methylation occurs after an acute exercise
• Ex vivo muscle contraction mimics exercise-induced hypomethylation
• Caffeine mediates DNA hypomethylation in myocytes, implicating a role for Ca2+ release
• Summary

DNA methylation is a covalent biochemical modification controlling chromatin structure and gene expression. Exercise elicits gene expression changes that trigger structural and metabolic adaptations in skeletal muscle. We determined whether DNA methylation plays a role in exercise-induced gene expression. Whole genome methylation was decreased in skeletal muscle biopsies obtained from healthy sedentary men and women after acute exercise. Exercise induced a dose-dependent expression of PGC-1α, PDK4, and PPAR-δ, together with a marked hypomethylation on each respective promoter. Similarly, promoter methylation of PGC-1α, PDK4, and PPAR-δ was markedly decreased in mouse soleus muscles 45 min after ex vivo contraction. In L6 myotubes, caffeine exposure induced gene hypomethylation in parallel with an increase in the respective mRNA content. Collectively, our results provide evidence that acute gene activation is associated with a dynamic change in DNA methylation in skeletal muscle and suggest that DNA hypomethylation is an early event in contraction-induced gene activation.

 Exercise is an environmental factor that affects gene-expression, i.e., which genes are made active.  Exercise itself has immediate impacts on your DNA.   The wierd thing about this study though is that caffeine also has similar impacts.  Again it is an environmental factor that affects gene expression.

The New Scientist explains it this way:

Now there is no excuse to avoid the gym: just one hour of exercise instantly changes your genes to boost the breakdown of fat.

Juleen Zierath and Romain Barrès at the Karolinska Institute in Stockholm, Sweden, and colleagues looked for epigenetic changes – the addition of a methyl group to genes – in muscle cells during strenuous exercise. To do so, the team collected biopsies from the thigh muscles of eight men who led relatively sedentary lives, both before and after an hour of exercise.

Several genes involved in fat metabolism that were methylated before the exercise lost their methyl group. Such demethylation allows genes to more easily make proteins, which suggests that more proteins involved in the breakdown of fat are being made after exercise, says Zierath.

The group was surprised to see these effects happen so quickly. They think calcium, produced in muscle cells during exercise, may be involved since subjecting the same biopsies to caffeine – which also increases calcium in muscles – caused the same demethylation.

Unfortunately, you would get caffeine intoxication before gaining the same effects from coffee as an hour-long workout, says Zierath.

Here is how Science Daily explained the story:

The new study shows that the DNA within skeletal muscle taken from people after a burst of exercise bears fewer chemical marks (specifically methyl groups) than it did before exercise. Those changes take place in stretches of DNA that are involved in turning "on" genes important for muscles' adaptation to exercise.

When the researchers made muscles contract in lab dishes, they saw a similar loss of DNA methyl groups. Exposure of isolated muscle to caffeine had the same effect.
Zierath explained that caffeine does mimic the muscle contraction that comes with exercise in other ways, too. She doesn't necessarily recommend anyone drink a cup of joe in place of exercise. It's nevertheless tempting to think that athletes who enjoy a coffee with their workout might just be on to something.

Broadly speaking, the findings offer more evidence that our genomes are much more dynamic than they are often given credit for. Epigenetic modifications that turn genes on and back off again can be incredibly flexible events. They allow the DNA in our cells to adjust as the environment shifts.

sleep or die

via fitbomb


Via: YourLocalSecurity.com

The nature of fatigue

I've been doing some reading for an article that I am writing on the nature of fatigue and the Brain's role in exhaustion.

Once the article has been published I'll post some of it here, but for now I just wanted to point to the work of Samuele Marcora

There is a good interview with him here - Perception is everything

and his key studies are 

·      The limit to - Marcora SM, Staiano W. Eur J Appl Physiol. 2010 Jul;109(4):763-70. Epub 2010 Mar 11.

·      Mental fatigueMarcora SM, Staiano W, Manning V. J Appl Physiol. 2009 Mar;106(3):857-64. Epub 2009 Jan 8.

·      The face of fatigue de Morree HM, Marcora SM. Biol Psychol. 2010 Dec;85(3):377-82. Epub 2010 Sep 9.

In his model, fatigue is a psychological issue, not a physical one.  When the perception of effort excedes the reward from that effort we give up.  The key is in modifying our perceptions.

Chins in a silly place

you sort of get the impression that these guys must be drunk?



Thanks to James Steele

Exercise and Food Reward

Given all the current interest in the Food Reward theories of obesity (check out Richard's post with a phenomenal number of comments), I thought I'd just point to this study that popped across my screen this morning:

Aerobic exercise reduces neuronal responses in food reward brain regions

Exercise reduced neuronal responses in brain regions consistent with reduced pleasure of food, reduced incentive motivation to eat, and reduced anticipation and consumption of food. Reduced neuronal response in these food reward brain regions after exercise is in line with the paradigm that acute exercise suppresses subsequent energy intake.

If Food Reward is an issue and I think it obviously is then we also need to think about exercise.

UK: The Public Bodies, (Sustainable Food) Bill

From The Weston A Price Foundation London Chapter:

ACTION ALERT - Government moves to enforce their dietary guidelines upon schools, prisons, hospitals and all other public bodies. Please lobby your local MP and interest groups. Details below.

The Public Bodies, (Sustainable Food) Bill has just passed its second reading in the Houses of Commons.

This bill will force all public bodies, i.e. schools, prisons and hospitals to comply with the government's low fat, low salt, nutrient deficient dietary guidelines. This will bring Britain in-line with USA, where Federal Funding is dependent on compliance with the USDA's dietary guidelines which have caused so much harm. That drive is coinciding with corporations having their food certified as being one of your five a day. So we see baked beans and pizza being certified in order that they gain catering contracts if this legislation is passed.

PLEASE CIRCULATE MY RESPONSE TO THE BILL TO YOUR LOCAL MP AND INTEREST GROUPS: http://files.meetup.com/1463924/Sustainable%20Food%20Bill%20Response.doc

If this bill is passed, parents will only be able to provide nutrient dense foods if they provide a packed lunch and will be banned from lobbying their school to introduce nutrient dense foods. We have even seen in some American States, schools telling parents what to put in school lunches and Chicago has banned packed lunches to stop Parent's circumventing the dietary guidelines.

This bill is one step towards a tax on fat, saturated fat and sugar, which Prime Minister David Cameron has voiced support for this in the recent "Conservative" Party Conference. We are even against a tax on sugar because it will encourage artificial sweeteners.

Philip Ridley
01442 384451
westonaprice.london@gmail.com

westonaprice.org/london

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Gut Microbiome and metabolic health

This is another study that points to the the relevance of your gut microbes to health.  The finding is that certain strains of microbe in the gut are associated with obesity-related Metabolic disorders.

Women With and Without Metabolic Disorder Differ in Their Gut Microbiota Composition

sitting around and diabetes

I have had stuff up here before about the dangers of being too sedentary.  Here is a new one about its link to diabetes

Diabetes Risk from Sitting Around

 "This study provides important new evidence that higher levels of sitting time have a deleterious impact on insulin resistance and chronic low-grade inflammation in women but not men and that this effect is seen regardless of how much exercise is undertaken. This suggests that women who meet the national recommendations of 30 minutes of exercise a day may still be compromising their health if they are seated for the rest of the day.

Lieberman on Obesity

Vitamin D and muscle

I am not even going to pretend that I have read this, but I spotted it earlier today and just wanted to get it out there

It is a review article on Vitamin D, but focussing on the way in which it impacts muscle and performance.  The abstract is below and the whole thing is available as a pdf.


VITAMIN D AND ATHLETIC PERFORMANCE: THE POTENTIAL ROLE OF MUSCLE

Vitamin D deficiency is a worldwide epidemic, with well known impacts on calcium metabolism and bone health, but increasingly recognized associations with chronic health problems such as bowel and colonic cancer, arthritis, diabetes and cardiovascular disease. In recent years in the Sports Medicine literature, there has been an increased focus on the potential impact that inadequate Vitamin D levels may have on athletic performance.

     In the early 20th Century, athletes and coaches felt that ultraviolet rays had a positive impact on athletic performance, and while remaining limited, evidence is accumulating to support this view. Muscle structure and function is recognised to play a key role in athletic performance, and both cross-sectional and longitudinal studies allude to a functional role for Vitamin D in muscle. The identification of the Vitamin D receptor in muscle tissue provides a direct pathway for Vitamin D to impact upon Skeletal Muscle structure and function. This review focuses on the current understanding of the action of Vitamin D within skeletal muscle tissue, and the potential impact on performance.

CLINICAL RECOMMENDATIONS

•    Athletes should have their (25-Hydroxy) Vitamin D levels measured regularly throughout the year.
•    Vitamin D deficient or depleted Athletes should be advised on appropriate UVB exposure or supplemented as required.
•    Optimal levels of Vitamin D remain controversial, but levels of 25-Hydroxy Vitamin D of 30ng/ml may be considered safe.

Work is killing you

stress....sitting......and more


Created by: Online University

Just take the exercise pill

Can we just make drugs which remove the need to exercise?  Perhaps, but I hope not.

"No one can deny that the human body was meant to move, and to move often," said Gerald Weissmann, M.D., Editor-in-Chief of the FASEB Journal, "but the reality is that many of us don't move enough, whether because of disease, injury, or simply a busy schedule. This discovery is another important step towards the treatment of muscle wasting in cancer, severe infection or aging – or to maintain our muscle mass to help face the slings and arrows of outrageous fortune."

The abstract is here

Marathons are dangerous?

Maybe.  But maybe particularly if you are not used to running.

Post-Exercise Cardiac Troponin Release is Related to Exercise Training History

Average miles run per week in the last 3 years, a marker of total training experience, encompassing training volume and duration, was negatively associated with post-marathon cTnI release (p<0.001).