Vibram shoes named in lawsuit: The danger of barefoot running

Vibram Five-finger named in lawsuit - zealousness, unfiltered advice creates more problems than it fixes

I received this link from a reader yesterday, which explains how Vibram USA Inc and Vibram FiveFingers LLC are part of a lawsuit where it is being alleged that they made "deceptive and misleading statements about the benefits of barefoot running".

It is alleged that the company, which makes the now famous Five-Finger shoe (pic on the right) have made deceptive claims about their health benefits, and this is leading to increased injuries among runners who make the switch.

The problem - the "skill" of barefoot running was not recognized

There is even some research as part of the lawsuit - the American Council of Exercise is carrying a report of this study, which finds that many people who make the switch continue to land on their heel.

Why is this potentially bad?  Well, the graph below, taken from a study on the ACE website, shows the loading rate in three conditions - barefoot (blue column), in Vibrams (purple) and in normal running shoes (green).

What should be immediately clear is that when you look at runners who land on the forefoot (shown by the cluster on the left) the loading rate is lowest when barefoot and highest when forefoot.

However, when you look at runners who land on the heel (right cluster), their loading rate goes in the other direction - here, the barefoot runners who heel strike have loading rates that are about double those of shod runners who are landing on the heel.  This is the effect of the big cushion under the heel of modern running shoes, and it serves to dampen the impact and reduce the loading rate significantly.  Vibrams lack this cushioning, on so fare only marginally better than the pure barefoot condition in heel-strikers.

Those of you who have followed this barefoot running debate will immediately recognize that this finding of impact force differences is not new at all.  In fact, it was found by Daniel Lieberman in a paper published in Nature about 2 years ago.  Lieberman's differences were even more striking - he found that if you run barefoot and land on the heel, then your impact forces are seven times higher than if you land on the heel in shoes.

The graph below is one that I redrew using Lieberman's data and put on this website when I reviewed the barefoot running phenomenon last year.

Now, having said all this, it's important to find the balanced, evidence-based view and be transparent about some "limitations" in these studies.  The first is that the link between loading rates and injuries is not as tight as many would think.  Certainly, higher loading rates have been associated with certain conditions (bone stress injuries being the main one), but the precise aetiology of how injury develops is far more complex than simply saying "if you reduce loading rate, you won't get injured".  Truth is, you might just get a different injury, especially if you start running on the forefoot because you see these graphs!

Then secondly, I'd like to see the study above published in a peer-reviewed journal, only to see the methods in a bit more detail.  Lieberman found a pretty large difference (7-fold) whereas the latest study finds a 2-fold difference between shod and barefoot runners when heel-striking.  That, plus the exact percentage of runners who continue to heel-strike, as well the 'training' they did for the two-week training period, would be of interest to me in order to understand exactly what is being measured in the laboratory.

On that note, Lieberman found that 83% of habitually shod runners were still heel-striking when barefoot.  The ACE study is saying 50% are still heel-striking, even two weeks into running with the minimalist shoes.

Now, that flies in the face of the popular literature, which tells us that when you run barefoot, you switch automatically to an apparently amazing cushioned forefoot running style.  That doesn't seem to happen, though, and the vast majority of people seem to take a lot longer to make this transition than the books (Born to Run is the main one) suggest.

The skill component

In fact, I believe this leads to the most intriguing question of all - understanding the skill of barefoot running.  The ACE study, mentioned above, had the runners do a 2-week "familiarization" period in the Vibrams, where they were asked to run for 20 minutes a day in an attempt to get them accustomed to it.  It's easy to criticize this period as too short and insufficient (all the stuff those who've already made up their mind can say - no study is perfect, remember).

But this two-week adaptation period may partly explain why Lieberman found that 83% of his shod runners were heel-striking when barefoot, whereas the ACE study found that "approximately half" were heel-striking.  Perhaps two weeks of familiarization was responsible for the shift of more runners (1 in 2 rather than 1 in 6) to a forefoot strike, as they 'learned' how to run.

The real question, however, is why the other 50% didn't make this adaptation?  And whether they would given more time? Are there some runners who would never succeed?  Who are they, and what distinguishes them from those who do succeed?  I strongly suspect that some people CANNOT adapt to barefoot running, that they don't have the necessary "skill" to improve the way they run barefoot and change what is years of shod-running-induced motor patterns.

Of course, this is an unanswered question, but I think it's the most important one that needs to be answered right now.  Just as one would not expect anyone who picks up a tennis racquet or a golf club to even become competent at playing it (especially later in life), I don't think it should be expected that simply making the transition to barefoot running will be sufficient either.  Everyone can improve, certainly.  But can they good enough to overcome or avoid what are some pretty clear "risks" associated with the transition?  Remember, in running, unlike tennis or golf, it's not good enough to simply improve over time, because if you don't improve enough, you get injured, so there is a "minimum required improvement" to make the transition to barefoot or minimalist running viable in the first place.

Coaching - sound in theory, but another risk in practice

Here, one can begin to introduce the concept of coaching, that barefoot running (or any running, for that matter) should be taught as a skill.  And certainly, this would help.  In the same way that my tennis or golf game will improve faster if I'm guided, running ability will too.  However, I don't think this will overcome what, for some people, may be a "skill deficit" that will prevent them from succeeding at barefoot or minimalist running.  Again, this is an unanswered question, at least for now.

The other issue, which I raised above, is that there is substantial risk associated with making any change in running technique.  This distinguishes running from, say golf, where wrong technique means lots of lost balls and frustration.  In running, failure to find that apparently elusive "correct running technique" equals disaster.  And what makes it even more tricky is that there's no feedback until the injury - unless you have fancy high speed cameras and force plates to analyse how you run, the first sign of the mistake is often injury.

So if you are going to advocate that people should run barefoot and then coach them so that they learn the right way to do it, then you'd better be certain that you'll make them good enough to avoid the risk - there is a minimum threshold, and if a runner fails to reach it, you've led them to injury, despite good intentions.  And it's not fair to runners to say "Run barefoot" and then blame the runner for their failures.

It's not simply about forefoot landing - even more danger lurks there

To illustrate this, the one thing that many will take out of this study is that it's the forefoot landing that will make the difference.  That is, if you land on the forefoot, you'll be fine.  And in theory, this is borne out by the evidence shown in the two graphs above.

However, in reality, it's a little more complex.  One of the authors of this ACE study is quoted as saying "Buying these Vibrams and continuing to land your heels is probably worse than wearing shoes because the Vibrams don’t have any cushioning. … People may need very explicit instruction and time spent practicing how to land on the ball of the foot. Otherwise, they may be doing themselves more harm". 

I think this is advice is probably MORE DANGEROUS than not saying anything, because as soon as you give an explicit instruction, you put the runner into the compromised situation where they are now focused on a forefoot landing. How do this achieve this?  They planar flex - point the toe away from their body, and drop more than three times their body weight down onto a contracted calf muscle in a compromised shortened position, about 400 times every kilometer.  That's a recipe for disaster, and so the most common problem associated with barefoot running is Achilles and calf related injuries.

Therefore, you can't "instruct" a runner to avoid the risk.  If anything, you instruct them into risk.  Bad idea.  The key, I believe, is to let the skill be acquired gradually, using a few drills to guide the athlete without ever changing their technique "manually", so to speak.  But here again, nobody really knows what works and what doesn't.  We don't even know what constitutes "good technique", and so to simplify it down to which part of the foot hits the ground first is also wrong.  And that's why it's reckless to advocate anything.  At this stage, everyone is learning, and so advocacy has no place, in my opinion.  It's all about education for now.

Extremism:  the media are more to blame than Vibram

Final point re "responders" and "non-responders".  Because we don't yet know who belongs to each group, I think it's reckless and irresponsible to treat them all as potential responders.  The prudent thing to do would be to assume the "worst case scenario", that everyone is a non-responder who needs serious time and intense work and lots of practice.  And then start from this point, and if a runner adapts faster, so be it, that's good news.  Instead, the media and advocates of barefoot running assume that everyone should make the switch because everyone will benefit.  And the bodies left behind will be dealt with later.  It's just too aggressive, too extreme.

And on this note, the media have propagated the myth far more even than the shoe companies like Vibram have.  Vibram are trying to sell shoes, and so they make claims as part of marketing strategies to differentiate their product from their rivals'.  That's normal.  And I can't comment on the specifics of the lawsuit - maybe they're guilty.

But I do know that the media have done a poor job of providing education on this topic.  With a few notable exceptions, they have allowed themselves to become a platform for the advocates of barefoot running without providing the necessary education.  Lieberman's paper illustrates this - he titled that research study "Foot strike patterns and collision forces in habitually barefoot versus shod runners".  The word "habitually" was in there for a reason.

But when the media got hold of that study, they reported only that barefoot running was excellent because it reduced loading rates 7-fold.  This study "proved" the benefit of barefoot running.  Quickly, the "extremists" (my pet hate in all matters of sports science) jumped on this said "It proves our point" and the study's other findings were lost in the aggressive or uninformed interpretation of the data.

This is an eerily similar thing to what happens when it comes to dietary advice.  Recently, I've been involved in debate back here in SA about paleo diets, low carb diets, high carb diets and the like.  And once again, it's a situation where people seem to become over-zealous, finding a cause for which they appoint themselves the spokesperson.  Their success, which is either isolated (1 in 100) or common (1 in 2, perhaps, but never 100%) becomes their proof, and they start telling the world there is only one way to succeed.  "Follow me to change your life" is the message, whether it's barefoot running or eating like a caveman supposedly did.  They thus make the mistake they accuse others of making, by lumping everyone into the same group.

And here, those who succeed become loud, outspoken (and dare I say, obnoxious), whereas those who fail slink away into the background and remain quiet about their failure.  So those who tried barefoot running and got injured disappear, those who succeeded often find a soapbox, write a book, and shout about it.  Those who try low carbohydrate diets and fail revert back to routine with minimal fuss, whereas those who succeed feel the need to tell the world.  They dismiss any research study finding that challenges their position as "corrupt", "incompetent" and "garbage", and so debate goes nowhere.  Once again, this happens because of aggressive advocacy, when it should be about education.

Prescribing a treatment for a condition we don't understand, without knowledge of risk or benefit

Which brings me to the final point.  The big issue, I believe, is that people have become carried away with barefoot running as a way to treat injury and potentially improve performance without really appreciating how it might work (or, importantly, that it may not).

The result then is that barefoot running has taken on the characteristics of a medicine or a drug - it is dispensed by "experts" (who often change their names to "Barefoot X") as a "treatment", but unlike drugs, there are a few key things missing:

• We don't know which conditions (injuries) the treatment will be effective for.  And by definition, this means we can't say when it will be ineffective
• We don't know what the correct dosage is
• We don't know how to phase the dosage in over time for different people
• We don't know whether the "treatment" is effective for everyone, or whether there are responders and non-responders
• We don't recognize the possible "contra-indications".  When you take a powerful drug prescribed by a doctor, he knows to check for certain conditions - pregnancy, allergies etc.  For barefoot running, nobody has thought about this
• What is the effect of other factors on the success of the 'treatment'?  For example, how does fatigue, terrain, muscle weakness, flexibility, strength etc impact on the success of the outcome?
• As a result of all of the above, we are in a very poor position to quantify the risks, and the "cost-benefit" of barefoot running.

The point is, all the answers, which are pretty important, that you can read on the package insert when you get prescription medication, are unknown for barefoot running.  Yet it is still prescribed 'recklessly'.

And for this, I completely blame the polarization of the debate that allows extremist views to develop and thrive.  It's perfect for the media and the 'zealots' who try to force their success on large groups of people without being open to the other side.  And there are some who are more moderate - I apologize for lumping everyone together.  But there are many who are not.  They base their 'prescription' of barefoot running on their own success story, or at best, a group of runners who they have succeeded with, and suddenly, the entire running community is being told to take this "drug".  It works.  Maybe.  In some people.  If they get it right.  Possibly.  That's not good enough.

And what's worse is that when it doesn't work, when they get injured, then it's their fault.  To return to the medication analogy, this is like giving a drug out to a sick patient and then hoping they get the dosage right.  And even if they follow the instructions to the letter, they may fail, and then it's their doing.  They must have done something wrong.  That's not a viable drug.  It's not a viable "product", and until that is recognized, I would caution all runners to be a little more prudent about how they advise others, and about following advice they receive.

The golden rule in science should be that polarization should be regarded as highly suspicious.  There are very few things that are known with absolute certainty, and when you're dealing with incredibly complex human physiology, the individual differences that make us who we are, what we're good at, how we run and what we eat, for example, are so vast and complex that nothing can be polarized without being wrong!  So when someone says "It's all about training, genes don't matter", they're just as wrong as someone who says "It's all about genes, training is irrelevant".

Similarly, barefoot running is not "the answer", but nor is it bad.  Carbohydrates are not evil, but nor are they the best option for some people, as evidence is now showing.  An individual approach is the only accurate way to go - it's not great for the media who love the sensation, and it's not great news for the gold-diggers who want sensation to sell books, but that's the reality.

Barefoot running - where does it leave us? Opinion and exploration

And so for barefoot running, where does that leave us?  Again, this is my opinion, based on the evidence and my own current research (I have two research studies underway, looking at various aspects of what I've discussed in this and other posts - results in a year or so!).  However, I'd say the following:

In a group of 100 runners, every single one will benefit from barefoot running as a training method.  It changes muscle activation patterns, strengthens muscles and tendons that we don't activate nearly as well in shoes, may be an effective form of rehabilitation, and it's really enjoyable.  So I would say that everyone should incorporate some barefoot running into their training programme.  Whether it's a 2 minute warm-up, an easy 30 min jog once a week, or some sprints after training, I'd say try it out and feel the difference it makes.

However, it's probably not for everyone.  Practically, theoretically, logistically and for many other reasons, some people will not take to barefoot running well enough for them to become 100% barefoot runners.  However, for others, it may well work.  It may prove to be the answer to your prayers, and the secret to injury-free running for life.  That's fantastic, and so you should embrace it and do it with enjoyment.  But don't believe that because it helped you, it must be used in the same dosages by everyone else - they may not have the same "condition" as you, they may have an entirely different history and thus set of contra-indications, and your enthusiasm, however well intended, will cause more problems than it solves.

You may sit on one of the poles - either north or south, either a responder and great barefoot runner, or a non-responder, and classic shod runner.  Which is perfect for you, but remember, between those poles, there's a world of people who are different, and so your extreme position in the complex spread of physiology shouldn't produce an extreme advocate for anything.

Ross

The 2012 red meat-mortality study (Arch Intern Med): The data suggests that red meat is protective

I am not a big fan of using arguments such as “food questionnaires are unreliable” and “observational studies are worthless” to completely dismiss a study. There are many reasons for this. One of them is that, when people misreport certain diet and lifestyle patterns, but do that consistently (i.e., everybody underreports food intake), the biasing effect on coefficients of association is minor. Measurement errors may remain for this or other reasons, but regression methods (linear and nonlinear) assume the existence of such errors, and are designed to yield robust coefficients in their presence. Besides, for me to use these types of arguments would be hypocritical, since I myself have done several analyses on the China Study data (), and built what I think are valid arguments based on those analyses.

My approach is: Let us look at the data, any data, carefully, using appropriate analysis tools, and see what it tells us; maybe we will find evidence of measurement errors distorting the results and leading to mistaken conclusions, or maybe not. With this in mind, let us take a look at the top part of Table 3 of the most recent (published online in March 2012) study looking at the relationship between red meat consumption and mortality, authored by Pan et al. (Frank B. Hu is the senior author) and published in the prestigious Archives of Internal Medicine (). This is a prominent journal, with an average of over 270 citations per article according to Google Scholar. The study has received much media attention recently.

Take a look at the area highlighted in red, focusing on data from the Health Professionals sample. That is the multivariate-adjusted cardiovascular mortality rate, listed as a normalized percentage, in the highest quintile (Q5) of red meat consumption from the Health Professionals sample. The non-adjusted percentages are 1.4  percent mortality in Q5 and 1.13 in Q1 (from Table 1 of the same article); so the multivariate adjustment-normalization changed the values of the percentages somewhat, but not much. The highlighted 1.35 number suggests that for each group of 100 people who consumed a lot of red meat (Q5), when compared with a group of 100 people who consumed little red meat (Q1), there were on average 0.35  more deaths over the same period of time (more than 20 years).

The heavy red meat eaters in Q5 consumed 972.37 percent more red meat than those in Q1. This is calculated with data from Table 1 of the same article, as: (2.36-0.22)/0.22. In Q5, the 2.36 number refers to the number of servings of red meat per day, with each serving being approximately 84 g. So the heavy red meat eaters ate approximately 198 g per day (a bit less than 0.5 lb), while the light red meat eaters ate about 18 g per day. In other words, the heavy red meat eaters ate 9.7237 times more, or 972.37 percent more, red meat.

So, just to be clear, even though the folks in Q5 consumed 972.37 percent more red meat than the folks in Q1, in each matched group of 100 you would not find a single additional death over the same time period. If you looked at matched groups of 1,000 individuals, you would find 3 more deaths among the heavy red meat eaters. The same general pattern, of a minute difference, repeats itself throughout Table 3. As you can see, all of the reported mortality ratios are 1-point-something. In fact, this same pattern repeats itself in all mortality tables (all-cause, cardiovascular, cancer). This is all based on a multivariate analysis that according to the authors controlled for a large number of variables, including baseline history of diabetes.

Interestingly, looking at data from the same sample (Health Professionals), the incidence of diabetes is 75 percent higher in Q5 than in Q1. The same is true for the second sample (Nurses Health), where the Q5-Q1 difference in incidence of diabetes is even greater - 81 percent. This caught my eye, being diabetes such a prototypical “disease of affluence”. So I entered the whole data reported in the article into HCE () and WarpPLS (), and conducted some analyses. The graphs below are from HCE. The data includes both samples – Health Professionals and Nurses Health.

HCE calculates bivariate correlations, and so does WarpPLS. But WarpPLS stores numbers with a higher level of precision, so I used WarpPLS for calculating coefficients of association, including correlations. I also double-checked the numbers with other software, just in case (e.g., SPSS and MATLAB). Here are the correlations calculated by WarpPLS, which refer to the graphs above: 0.030 for red meat intake and mortality; 0.607 for diabetes and mortality; and 0.910 for food intake and diabetes. Yes, you read it right, the correlation between red meat intake and mortality is a very low and non-significant 0.030 in this dataset. Not a big surprise when you look at the related HCE graph, with the line going up and down almost at random. Note that I included the quintiles data from both the Health Professionals and Nurses Health samples in one dataset.

Those folks in Q5 had a much higher incidence of diabetes, and yet the increase in mortality for them was significantly lower, in percentage terms. A key difference between Q5 and Q1 being what? The Q5 folks ate a lot more red meat. This looks suspiciously suggestive of a finding that I came across before, based on an analysis of the China Study II data (). The finding was that animal food consumption (and red meat is an animal food) was protective, actually reducing the negative effect of wheat flour consumption on mortality. That analysis actually suggested that wheat flour consumption may not be so bad if you eat 221 g or more of animal food daily.

So, I built the model below in WarpPLS, where red meat intake (RedMeat) is hypothesized to moderate the relationship between diabetes incidence (Diabetes) and mortality (Mort). Below I am also including the graphs for the direct and moderating effects; the data is standardized, which reduces estimation error, particularly in moderating effects estimation. I used a standard linear algorithm for the calculation of the path coefficients (betas next to the arrows) and jackknifing for the calculation of the P values (confidence = 1 – P value). Jackknifing is a resampling technique that does not require multivariate normality and that tends to work well with small samples; as is the case with nonparametric techniques in general.

The direct effect of diabetes on mortality is positive (0.68) and almost statistically significant at the P < 0.05 level (confidence of 94 percent), which is noteworthy because the sample size here is so small – only 10 data points, 5 quintiles from the Health Professionals sample and 5 from the Nurses Health sample. The moderating effect is negative (-0.11), but not statistically significant (confidence of 61 percent). In the moderating effect graphs (shown side-by-side), this negative moderation is indicated by a slightly less steep inclination of the regression line for the graph on the right, which refers to high red meat intake. A less steep inclination means a less strong relationship between diabetes and mortality – among the folks who ate the most red meat.

Not too surprisingly, at least to me, the results above suggest that red meat per se may well be protective. Although we should consider a least two other possibilities. One is that red meat intake is a marker for consumption of some other things, possibly present in animal foods, that are protective - e.g., choline and vitamin K2. The other possibility is that red meat is protective in part by displacing other less healthy foods. Perhaps what we are seeing here is a combination of these.

Whatever the reason may be, red meat consumption seems to actually lessen the effect of diabetes on mortality in this sample. That is, according to this data, the more red meat is consumed, the fewer people die from diabetes. The protective effect might have been stronger if the participants had eaten more red meat, or more animal foods containing the protective factors; recall that the threshold for protection in the China Study II data was consumption of 221 g or more of animal food daily (). Having said that, it is also important to note that, if you eat excess calories to the point of becoming obese, from red meat or any other sources, your risk of developing diabetes will go up – as the earlier HCE graph relating food intake and diabetes implies.

Please keep in mind that this post is the result of a quick analysis of secondary data reported in a journal article, and its conclusions may be wrong, even though I did my best not to make any mistake (e.g., mistyping data from the article). The authors likely spent months, if not more, in their study; and have the support of one of the premier research universities in the world. Still, this post raises serious questions. I say this respectfully, as the authors did seem to try their best to control for all possible confounders.

I should also say that the moderating effect I uncovered is admittedly a fairly weak effect on this small sample and not statistically significant. But its magnitude is apparently greater than the reported effects of red meat on mortality, which are not only minute but may well be statistical artifacts. The Cox proportional hazards analysis employed in the study, which is commonly used in epidemiology, is nothing more than a sophisticated ANCOVA; it is a semi-parametric version of a special case of the broader analysis method automated by WarpPLS.

Finally, I could not control for confounders because, given the small sample, inclusion of confounders (e.g., smoking) leads to massive collinearity. WarpPLS calculates collinearity estimates automatically, and is particularly thorough at doing that (calculating them at multiple levels), so there is no way to ignore them. Collinearity can severely distort results, as pointed out in a YouTube video on WarpPLS (). Collinearity can even lead to changes in the signs of coefficients of association, in the context of multivariate analyses - e.g., a positive association appears to be negative. The authors have the original data – a much, much larger sample - which makes it much easier to deal with collinearity.

Moderating effects analyses () – we need more of that in epidemiological research eh?

Gaining muscle and losing fat at the same time: A more customized approach based on strength training and calorie intake variation

In the two last posts I discussed the idea of gaining muscle and losing fat at the same time () (). This post outlines one approach to make that happen, based on my own experience and that of several HCE () users. This approach may well be the most natural from an evolutionary perspective.

But first let us address one important question: Why would anyone want to reach a certain body weight and keep it constant, resorting to the more difficult and slow strategy of “turning fat into muscle”, so to speak? One could simply keep on losing fat, without losing or gaining muscle, until he or she reaches a very low body fat percentage (e.g., a single-digit body fat percentage, for men). Then he or she could go up from there, slowly putting on muscle.

The reason why it is advisable to reach a certain body weight and keep it constant is that, below a certain weight, one is likely to run into nutrient deficiencies. Non-exercise energy expenditure is proportional to body weight. As you keep on losing body weight, calorie intake may become too low to allow you to have a nutrient intake that is the minimum for your body structure. Unfortunately eating highly nutritious vegetables or consuming copious amounts of vitamin and mineral supplements will not work very well, because the nutritional needs of your body include both micro- and macro-nutrients that need co-factors to be properly absorbed and/or metabolized. One example is dietary fat, which is necessary for the absorption of fat-soluble vitamins.

If you place yourself into a state of nutrient deficiency, your body will compensate by mounting a multipronged defense, resorting to psychological and physiological mechanisms. Your body will do that because it is hardwired for self-preservation; as noted below, being in a state of nutrient deficiency for too long is very dangerous for one's health. Most people cannot oppose this body reaction by willpower alone. That is where binge-eating often starts. This is one of the key reasons why looking for a common denominator of most diets leads to the conclusion that all succeed at first, and eventually fail ().

If you are one of the few who can oppose the body’s reaction, and maintain a very low calorie intake even in the face of nutrient deficiencies, chances are you will become much more vulnerable to diseases caused by pathogens. Individually you will be placing yourself in a state that is similar to that of populations that have faced famine in the past. Historically speaking, famines are associated with decreases in degenerative diseases, and increases in diseases caused by pathogens. Pandemics, like the Black Death (), have historically been preceded by periods of food scarcity.

The approach to gaining muscle and losing fat at the same time, outlined here, relies mainly on the following elements: (a) regularly conducting strength training; (b) varying calorie intake based on exercise; and (c) eating protein regularly. To that, I would add becoming more active, which does not necessarily mean exercising but does mean doing things that involve physical motion of some kind (e.g., walking, climbing stairs, moving things around), to the tune of 1 hour or more every day. These increase calorie expenditure, enabling a slightly higher calorie intake while maintaining the same weight, and thus more nutrients on a diet of unprocessed foods. In fact, even things like fidgeting count (). These activities should not cause muscle damage to the point of preventing recovery from strength training.

As far as strength training goes, the main idea, as discussed in the previous post, is to regularly hit the supercompensation window, with progressive overload, and maintain your current body weight. In fact, over time, as muscle gain progresses, you will probably want to increase your calorie intake to increase your body weight, but very slowly to keep any fat gain from happening. This way your body fat percentage will go down, even as your weight goes up slowly. The first element, regularly hitting the supercompensation window, was discussed in a previous post ().

Varying calorie intake based on exercise. Here one approach that seems to work well is to eat more in the hours after a strength training session, and less in the hours preceding the next strength training session, keeping the calorie intake at maintenance over a week. Individual customization here is very important. Many people will respond quite well to a calorie surplus window of 8 – 24 h after exercise, and a calorie deficit in the following 40 – 24 h. This assumes that strength training sessions take place every other day. The weekend break in routine is a good one, as well as other random variations (e.g., random fasts), as the body tends to adapt to anything over time ().

One example would be someone following a two-day cycle where on the first day he or she would do strength training, and eat the following to satisfaction: muscle meats, fatty seafood (e.g., salmon), cheese, eggs, fruits, and starchy tubers (e.g., sweet potato). On the second day, a rest day, the person would eat the following, to near satisfaction, limiting portions a bit to offset the calorie surplus of the previous day: organ meats (e.g., heart and liver), lean seafood (e.g., shrimp and mussels), and non-starchy nutritious vegetables (e.g., spinach and cabbage). This would lead to periodic glycogen depletion, and also to unsettling water-weight variations; these can softened a bit, if they are bothering, by adding a small amount of fruit and/or starchy foods on rest days.

Organ meats, lean seafood, and non-starchy nutritious vegetables are all low-calorie foods. So restricting calories with them is relatively easy, without the need to reduce the volume of food eaten that much. If maintenance is achieved at around 2,000 calories per day, a possible calorie intake pattern would be 3,000 calories on one day, mostly after strength training, and 1,000 calories the next. This of course would depend on a number of factors including body size and nonexercise thermogenesis. A few calories could be added or removed here and there to make up for a different calorie intake during the weekend.

Some people believe that, if you vary your calorie intake in this way, the calorie deficit period will lead to muscle loss. This is the rationale behind the multiple balanced meals a day approach; which also works, and is successfully used by many bodybuilders, such as Doug Miller () and Scooby (). However, it seems that the positive nitrogen balance stimulus caused by strength training leads to a variation in nitrogen balance that is nonlinear and also different from the stimulus to muscle gain. Being in positive or neutral nitrogen balance is not the same as gaining muscle mass, although the two should be very highly correlated. While the muscle gain window may close relatively quickly after the strength training session, the window in which nitrogen balance is positive or neutral may remain open for much longer, even in the face of a calorie deficit during part of it. This difference in nonlinear response is illustrated through the schematic graph below.

Eating protein regularly. Here what seems to be the most advisable approach is to eat protein throughout, in amounts that make you feel good. (Yes, you should rely on sense of well being as a measure as well.) There is no need for overconsumption of protein, as one does not need much to be in nitrogen balance when doing strength training. For someone weighing 200 lbs (91 kg) about 109 g/d of high-quality protein would be an overestimation () because strength training itself pushes one’s nitrogen balance into positive territory (). The amount of carbohydrate needed depends on the amount of glycogen depleted through exercise and the amount of protein consumed. The two chief sources for glycogen replenishment, in muscle and liver, are protein and carbohydrate – with the latter being much more efficient if you are not insulin resistant.

How much dietary protein can you store in muscle? About 15 g/d if you are a gifted bodybuilder (). Still, consumption of protein stimulates muscle growth through complex processes. And protein does not usually become fat if one is in calorie deficit, particularly if consumption of carbohydrates is limited ().

The above is probably much easier to understand than to implement in practice, because it requires a lot of customization. It seems natural because our Paleolithic ancestors probably consumed more calories after hunting-gathering activities (i.e., exercise), and fewer calories before those activities. Our body seems to respond quite well to alternate day calorie restriction (). Moreover, the break in routine every other day, and the delayed but certain satisfaction provided by the higher calorie intake on exercise days, can serve as powerful motivators.

The temptation to set rigid rules, or a generic formula, always exists. But each person is unique (). For some people, adopting various windows of fasting (usually in the 8 – 24 h range) seems to be a very good strategy to achieve calorie deficits while maintaining a positive or neutral nitrogen balance.

For others, fasting has the opposite effect, perhaps due to an abnormal increase in cortisol levels. This is particularly true for fasting windows of 12 – 24 h or more. If regularly fasting within this range stresses you out, as opposed to “liberating” you (), you may be in the category that does better with more frequently meals.

Gaining muscle and losing fat at the same time: Various issues and two key requirements

In my previous post (), I mentioned that the idea of gaining muscle and losing fat at the same time seems impossible to most people because of three widely held misconceptions: (a) to gain muscle you need a calorie surplus; (b) to lose fat you need a calorie deficit; and (c) you cannot achieve a calorie surplus and deficit at the same time.

The scenario used to illustrate what I see as a non-traumatic move from obese or seriously overweight to lean is one in which weight loss and fat loss go hand in hand until a relatively lean level is reached, beyond which weight is maintained constant (as illustrated in the schematic graph below). If you are departing from an obese or seriously overweight level, it may be advisable to lose weight until you reach a body fat level of around 21-24 percent for women or 14-17 percent for men. Once you reach that level, it may be best to stop losing weight, and instead slowly gain muscle and lose fat, in equal amounts. I will discuss the rationale for this in more detail in my next post; this post will focus on addressing the misconceptions above.

Before I address the misconceptions, let me first clarify that, when I say “gaining muscle” I do not mean only increasing the amount of protein stored in muscle tissue. Muscle tissue is mostly water, by far. An important component of muscle tissue is muscle glycogen, which increases dramatically with strength training, and also tends to increase the amount of water stored in muscle. So, when you gain muscle, you gain a significant amount of water.

Now let us take a look at the misconceptions. The first misconception, that to gain muscle you need a calorie surplus, was dispelled in a previous post featuring a study by Ballor and colleagues (). In that study, obese subjects combined strength training with a mild calorie deficit, and gained muscle. They also lost fat, but ended up a bit heavier than at the beginning of the intervention. Another study along the same lines was linked by Clint (thanks) in the comments section under the last post ().

The second misconception, that to lose fat you need a calorie deficit; is related to the third, that you cannot achieve a calorie surplus and deficit at the same time. In part these misconceptions are about semantics, as most people understand “calorie deficit” to mean “constant calorie deficit”. One can easily vary calorie intake every other day, generating various calorie deficits and surpluses over a week, but with no overall calorie deficit or surplus for the entire week. This is why I say that one can achieve a calorie surplus and deficit “at the same time”. But let us make a point very clear, most of the evidence that I have seen so far suggests that you do not need a calorie deficit to lose fat, but you do need a calorie deficit to lose structural weight (i.e., non-water weight). With a few exceptions, not many people will want to lose structural weight by shedding anything other than body fat. One exception would be professional athletes who are already very lean and yet are very big for the weight class in which they compete, being unable to "make weight" through dehydration.

Perhaps the most surprising to some people is that, based on my own experience and that of several HCE () users, you don’t even need to vary your calorie intake that much to gain muscle and lose fat at the same time. You can achieve that by eating enough to maintain your body weight. In fact, you can even slowly increase your calorie intake over time, as muscle growth progresses beyond the body fat lost. And here I mean increasing your calorie intake very slowly, proportionally to the amount of muscle you gain; which also means that the incremental increase in calorie intake will vary from person to person. If you are already relatively lean, at around 21-24 percent of body fat for women and 14-17 percent for men, gaining muscle and losing fat in equal amounts will lead to a visible change in body composition over time () ().

Two key requirements seem to be common denominators for most people. You must eat protein regularly; not because muscle tissue is mostly protein, but because protein seems to act as a hormone, signaling to muscle tissue that it should repair itself. (Many hormones are proteins, actually peptides, and also bind to receptor proteins.) And you also must conduct strength training to the point that you are regularly hitting the supercompensation window (). This takes a lot of individual customization (). You can achieve that with body weight exercises, although free weights and machines seem to be generally more effective. Keep in mind that individual customization will allow you to reach your "sweet spots", but that still results will vary across individuals, in some cases dramatically.

If you regularly hit the supercompensation window, you will be progressively spending slightly more energy in each exercise session, chiefly in the form of muscle glycogen, as you progress with your strength training program. You will also be creating a hormonal mix that will increase the body’s reliance on fat as a source of energy during recovery. As a compensatory adaptation (), your body will gradually increase the size of its glycogen stores, raising insulin sensitivity and making it progressively more difficult for glucose to become body fat.

Since you will be progressively spending slightly more energy over time due to regularly hitting the supercompensation window, that is another reason why you will need to increase your calorie intake. Again, very slowly, proportionally to your muscle gain. If you do not do that, you will provide a strong stimulus for autophagy () to occur, which I think is healthy and would even recommend from time to time. In fact, one of the most powerful stimuli to autophagy is doing strength training and fasting afterwards. If you do that only occasionally (e.g., once every few months), you will probably not experience muscle loss or gain, but you may experience health improvements as a result of autophagy.

The human body is very adaptable, so there are many variations of the general strategy above. In my next post, I will talk a bit more about a variation that seems to work well for many people. It involves a combination of strength training and calorie intake variation that may well be the most natural from an evolutionary perspective.

10,000 hours vs training debate: No scientific limits making it impossible for any individual to become an elite athlete with practice?

Dear Anders Ericsson...a request on behalf of sports science to stop telling people that the world is flat

The 10,000 hours vs genetic debate, and correcting Prof Ericsson's mistruths 

So last night, I was (un)fortunate enough to be involved in a radio debate with Prof Anders Ericsson on the concept of talent vs training.  For those who don't know, Ericsson is the father of the 10,000 hour concept, where he prescribes that ANY individual can become an elite athlete if they engage in the required hours of deliberate practice.  He sets that number at 10,000 hours, which is really more marketing than it is science, and I had the chance to "debate" this on air last night.

Unfortunately, the debate ended before I was able to adequately respond to some of Ericsson's claims, and so this is a post to do just that - respond, put the sports science side of the debate across.  I address the article to Ericsson somewhat tongue-in-cheek, and I don't mean to appoint myself on behalf of sports science, but the truth is that someone has to point out that the books, the popular media, and Ericsson are misrepresenting the evidence (either deliberately or ignorantly).  And besides, Ericsson did ask in the radio interview (see below).

The debate was a glorious seven minutes long (I was told it would be much longer), and it involved two opportunities for Ericsson to state his case, and two for me to try to explain the physiology of elite athletes.  Going in, I was under the impression we would debate the points, but that never really happened, mostly because I didn't think it was going to be cut short at 7 minutes.

You can listen to the podcast here.  Just click "Listen Now"  The interview portion starts at 9:00, as the section before is an interview with Chrissie Wellington (this provides some context for some of my comments in my first response).

A stunned reaction

I was, throughout the interview, stunned at what I was hearing.  And it's not as though I'm new to this particular debate - I've recently written two review articles on this topic with a colleague of mine (a geneticist, because unlike Anders Ericsson, I don't like the idea of commenting about a field that I'm not an expert in - he's a psychologist, but he was throwing physiology around with abandon, as you'll hear and read later).  These articles will be published in peer reviewed journals later this year, I'll let you know when.  There are also the two articles (PART I and PART II) that I wrote here on The Science of Sport last year, and then I presented on this at the UK Sports and Exercise Medicine conference in London last November.

I have also read the books - Bounce, Outliers, so in theory, I've heard it before.  But I was just absolutely stunned that Ericsson was saying some of the things he did - you can hear this in my reaction in the podcast as I start my response to both questions!  What he says is just ludicrous, empty and baseless, and I can only think he's misinformed, or has some other agenda to push.  Maybe he is writing a book...

Truth is, you don't even need research, you just need common sense and a tiny bit of experience with elite athletes in training groups.  For example, if any of you have ever run with a training group, you have seen and felt the reality of "individual responses" to training - you know that 1,000 hours of identical training will not produce an identical result in ten different people.  There are examples all over the place that show that practice is not sufficient for elite performance, and there are as many examples of athletes who have succeeded on far, far less than this (there are even cases in chess, where, dare I say it, performance is a little less complex because there's no risk of overtraining, injury, etc)

Also, Ericsson's theory that it is the training done during the adolescent years that matters is not only wrong (look how many talented young athletes fail at senior level despite accumulating far more hours than their peers by the age of 18, and how many endurance athletes only take up the sport in their 20s and become world class in a few years despite zero training when adolescents), it's also very irresponsible, because it compels parents, teachers and coaches to start training young athletes too soon and that's detrimental to the person (see Cote et al for review).

The statements - no scientific evidence showing that genes or physiology limit performance?

In his second response in the podcast, Ericsson makes the following statement in response to my argument that the scientific evidence suggests without doubt that elite athletes and champions are BORN AND MADE:

"I would argue here, and reading all the reviews, and we've had reviews where every scientist from the exercise physiology field and sports psychology.  And I find it kind of remarkable that Ross is making these claims because I've never seen them made in print in any peer-reviewed publication" - 13:55 in the podcast

He goes on to say the following:

"I have to say that I'd be very interested to see Ross finding any scientific studies that support the kind of claims that he was making at the beginning of the programme" - 15:01 in the podcast

Outside the scope of knowledge - don't tread where you shouldn't unless you have a guide

Before I continue, just have to mention that I have provided a list of peer reviewed publications as references at the end of this post - they are both review articles (Ericsson made the claim that he's read ALL the reviews - clearly he's missed these ones), and they are original research studies that show the importance of genetic factors and physiological variability to training.  Clearly, he's never read these either.  I'd excuse this on the basis that Anders Ericsson is a psychologist, so one would not expect him to have a firm grasp of sports science, performance,  physiology and the genetic literature, but the fact of the matter is that he's making claims in those fields, so therefore it's fair-game to challenge his knowledge and understanding of the literature and the sports science performance fields.

And I must just make this point - I don't for a second think we should create intellectual "silos" where you can ONLY comment on your field.  I think that would be foolish because it's the process of thinking, the scientific approach to a question that matters more than the actual content.  And I'd like to think that the biggest advances in our understanding often come from thinking outside the "constraints" of what we know, and by integrating research from different fields by different experts.

In other words, someone may be trained as a physiologist, but it's their application of the scientific approach, allied to some small physiological understanding, that may allow them to contribute to the field of biomechanics of barefoot running, for example.  Key to this are two things:  a)  you must be dilligent about doing your research, and b) find someone who IS an expert to assist.  That's why when in writing review articles on talent vs training and elite performance, I partnered with a geneticist (Malcolm Collins) who does understand the field at the depth that is required to put scientific statements out there.  Similarly, I'm now doing barefoot running research, where my interest is the physiology, but we have a team that includes an engineer and biomechanist, so that I don't have to tread where I'm not capable.

Responding to Ericsson - one example of "limited" physiological response to training

In any event, during the debate, I tried to respond to Ericsson, and there are four things that I think are essential to understand here:

1.  It is true that genetic "proof" has yet to be provided.  But elite sporting performance is too complex, and genetic factors too varied to ever "prove" the link Ericsson seems to require.  Consider this:  height is a pretty straightforward characteristic, and it's known to be highly heritable (tall parents = tall children).  In fact, 80% of the variance in height is known to be genetic.  However, studies have found that it takes an astonishing 300,000 genetic variants to account for only 45% of this variance.  That's just height - how much more then would it take to explain something as complex as sports performance? 
   
   The reality is that the field of genetics is young, and with time, more evidence will emerge.  But there's a massive difference between something being "proven" (where I agree with Ericsson) and saying that it is absent (which is what he implies).  Genetic evidence is not absent - most physiological factors that are known to limit performance have been associated with genes (including injury risk, aerobic capacity, muscle fiber type), and others can be easily related to heritable factors (think height for basketball, limb proportion, bone mass etc).  When Ericsson suggests there is no evidence, it is because he is ignorant of the evidence.
2.  Ericsson's own work disproves his theory - his studies have tried to explain performance level as a function of training, yet research he has been involved in shows that only a very small part of performance can be explained by practice.  Only 28% of the variance darts performance is explained by the number of hours practiced!  That's astonishingly low, and it means that time spent in practice is a very poor predictor for performance.  The question you should be asking is what accounts for the other 72%, and could some of it be innate?  It's definitely enough to throw out the deliberate practice, 10,000 hour theory, because Ericsson is clearly predicting that most (or all, in some of his articles) of performance is explained by training.
3. You cannot prove that practice is necessary AND sufficient to produce champions or elite performers based on retrospective studies.  They're weak, because there are so many other ways to explain the findings.  For example, Ericsson's famous violin study showed that the expert performers did the most practice, and he concluded that the practice turned them into experts.  However, it's equally possible, in this study design anyway, that the children with the innate violin ability were encouraged by others and their own success to practice more.  Retrospective studies are poor ways to show that practice makes perfect.  You have to do prospective studies.
4. Prospective studies have been done.  Most notably, Bouchard published a study in 2011 (reference below) in which he found that the response in VO2max (a measure of aerobic capacity and adaptation to training, and ultimately performance) of a large cross-section of the population to a standardized training programme was enormously varied.  Some individuals improved by less than 5%, others improve by 30%.  And here's the key point - it is possible, using genetic techniques, to identify which genetic polymorphisms (think of them as variants of genes) are responsible for this huge difference. 
   
   It turns out that Bouchard's work has provided some pretty important findings:
• About 50% of an individual's starting VO2max and 50% of the "trainability" in VO2max is heritable
• 21 Genetic polymorphisms have been associated with 50% of the training response to VO2max
• If a person carries NINE OR FEWER of these genetic variants, then they are low responders and improve VO2max by only 200 ml/min.
• If a person carries NINETEEN OR MORE of these variants, then they are high responders and improve VO2max by over 600 ml/min

In other words, genetic factors very clearly impact on what we start with, they impact on how we adapt to training, and therefore, by extension, they impact on where we get to.  Our physiology has a ceiling, and it is in part, genetically determined.  This is clear for VO2max, and it's clear for other factors that are known to affect performance.  Skeletal muscle, for example, is known to be BOTH heritable and trainable.  Running economy differs enormously between individuals as a function of factors such as height, limb proportions, muscle mass, and other factors that are known to be genetically determined.  And so unless you have the right skeletal structure, height, limb proportions, you cannot have the running economy required to run a 2:08 marathon.  It's physiology, limiting performance, and related to factors that we are born with.  To deny this is to say that the world is flat when you are staring out of a spaceship window at the globe.

Further, as one of you commented on Facebook yesterday, biomechanical factors such as the muscle's moment arm exert huge effects on performance, and so characteristics that we are born with determine the level of performance that we can attain.  I would point out the most obvious example of this is basketball, but there are countless others.

A pointless polarization of the debate

Ultimately, however, the idea that elite sporting performance can be explained by one factor is foolish.  That's why when Ericsson makes the claims he does, in the field of physiology, it's so absurd, and potentially damaging because people believe it at face value, and they implement sports systems and strategies that buy into this flawed concept.   It's quite clear, from what we observe in athletes, what we study in laboratories, what we know from geneticists, that there is a significant contribution of all kinds of factors to performance.  Physiology matters, but so does practice.  Psychological factors are crucial, but so too are financial and economic considerations.

The dominance of Kenyan runners, for example, will never be found to be due to ONE factor.  Those who are looking solely at genes are doomed to failure, but so are those who want to say that it's purely an altitude, diet, socio-economic, lifestyle, or incentive-driven phenomenon.  All these factors contribute, and the environment interacts with the genes to produce a champion.  I've said this before, but training should be defined as the realization of genetic potential.

Every single person improves as a result of training - some, as Bouchard has shown, improve by very little in a variable like aerobic capacity.  Perhaps they are better suited to skill-based sports.  Some improve enormously, and those who do are more suited to endurance sport.  Then there is injury - this is vital and completely overlooked.  We know that certain genes are associated with different performance characteristics, and there are genes that are associated with injury.  Some people will never even reach 10,000 hours because they are susceptible to injury at five hours per week of training and cannot do more - they'd need 40 years to get good enough if that's all it took.

So the point I'd like to conclude with, before I list some more points for Anders Ericsson to consider, is that we should not polarize the debate.  We should recognize that there are many paths to elite performance, and that a one-size or one-number fits all approach is foolish.  We should learn what we can from those who succeed, including that they are dedicated and practice a lot, which is obvious.  And we should learn why people fail.  And we should avoid generalizations and simplifications that help us sell books to motivate people.

Training is the realization of genetic potential - practically, that means that every single one of you reading this, discussing this, can improve through training.  That's the motivation. But will we all become Olympic caliber athletes in any sport we choose?  Keep dreaming.  The world is not flat, Prof Ericsson.  Please stop telling people it is...

Ross

By way of an "Appendix", here is a little more on Ericsson's views, because I don't want to take him out of context in a 7 minute radio interview...

Ericsson's first entry into this field was his work looking at skill acquisition in activities such as music - his seminal study of violinists showed that expert performers engaged in at least 10,000 hours of training whereas those violinists judged merely as "good" or "average" did about 8,000 and 5,000 hours respectively.

But then Ericsson moved beyond education and skill acquisition and began to tackle sport.  He wrote a review article in the New York Academy of Sciences Journal in 2009, in which he states the following:

"the distinctive characteristics of exceptional performers are the result of adaptations to extended and intense practice activities that selectively activate dormant genes that are contained within all healthy individuals’ DNA." - Ericsson et al, NYAS, 1172: 199-217, 2009

So in other words, he is now going to tackle genetics.  He is saying (and I want to be careful here about taking this out of context), that exceptional performers become exceptional because they practice, and this training activates dormant genes, and these genes are present in ALL healthy individuals' DNA - his word, my emphasis.

Right, so this is fine, if he sticks to "performance" in skill-based activities.  I would disagree with him - studies on chess show clearly that some people get good very quickly, others never improve to Master level no matter what they do.  The same is true of darts, tennis, golf, any activity.  But nevertheless, let's assume that he is referring to his study on musicians and things like mathematical ability.

But he doesn't stop there. He then tackles physiology, and writes the following in the same paper:

"From this evidence it would appear that VO2max/kg (aerobic capacity) would not be a good candidate for a factor that was constrained by heredity"

This comes from a section in the paper where Ericsson, a psychologist, tackles the PHYSIOLOGY of elite performance and comes to this incredible conclusion that there is no evidence that aerobic capacity is constrained by genetic factors.  If you read the study, you will discover that Ericsson arrives at this conclusion based on THREE studies - one review, and two other studies, one of which actually finds the opposite to what he concludes. 

I have explained above the recent work that shows clearly that genetic factors influence VO2max, and admittedly, this review precedes that series of studies.  But there were still others that had found a) huge inter-individual differences between people in response to the same training and b) accounted for large parts of VO2 as being heritable.

Ericsson's approach to the physiology side of this argument is simply not good enough when physiologists can cite dozens of physiological systems or factors that are known to affect performance, and when geneticists can show associations between these systems and our genes.

And yes, I agree that this area is not yet developed - it's so "young" a field that it will take time to understand the genetic complexity.  But even here, there's a difference between something being absent and something being proven.  Neither side will "prove" their argument, but I think it's pretty clear that evidence shows conclusively that BOTH genes and training make champions.

And finally, here are some references that Ericsson may have missed:

Duffy L, Baluch B. Dart performance as a function of facets of practice amongst professional and amateur men ana women players. Int J Sport Psychol. 2004;35:232-245.

Vaeyens R, Güllich A, Warr CR et al. Talent identification and promotion programmes of Olympic athletes. J Sports Sci. 2009;27:1367-80.

Elferink-Gemser MT, Jordet G, Coelho-E-Silva MJ et al. The marvels of elite sports: how to get there? Br J Sports Med. 2011;45:683-4.

Phillips E, Davids K, Renshaw I et al. Expert performance in sport and the dynamics of talent development. Sports Med. 2010;40:271-83.

Huijgen BC, Elferink-Gemser MT, Post WJ et al. Soccer skill development in professionals. Int J Sports Med. 2009;30:585-91.

Gobet F, Campitelli G. The role of domain-specific practice, handedness, and starting age in chess. Dev Psychol. 2007;43:159-72.

Gibbons T, Hill R, McConnell, A. et al. The path to excellence: A comprehensive view of development of U.S. Olympians who competed from 1984-1998 United States Olympic Committee. 2002.

Baker J, Côté J, Deakin J. Expertise in Ultra-Endurance Triathletes Early Sport Involvement, Training Structure, and the Theory of Deliberate Practice. J Appl Sport Psychol. 2005;17:64-78.

Oldenziel K, Gagne F. Factors affecting the rate of athlete development from novice to senior elite: How applicable is the 10-year rule. Athens 2004: Pre-olympic Congress Sport Science Through the Ages: Challenges in the New Millennium. Athens. 2004.

Hodges NJ, Starkes JL. Wrestling with the nature of expertise: A sport specific test of Ericsson, Krampe and Tesch-Römer’s (1993) theory of “deliberate practice”. Int J Sport Psychol. 1996;27:400-24.

Helsen WF, Starkes JL, Hodges NJ. Team sports and the theory of deliberate practice. J Sport Exerc Psychol. 1998;20:12-34.

Bullock N, Gulbin JP, Martin DT et al. Talent identification and deliberate programming in skeleton: ice novice to Winter Olympian in 14 months. J Sports Sci. 2009;27:397-404.

Roescher CR, Elferink-Gemser MT, Huijgen BC et al. Soccer endurance development in professionals. Int J Sports Med. 2010;31:174-9.

Vaeyens R, Lenoir M, Williams AM et al. Talent identification and development programmes in sport : current models and future directions. Sports Med. 2008;38:703-14.

Tucker R, Collins M. Athletic performance and risk of injury - Can genes explain all? Dialog Cardiovasc Med. In Press.

Collins M, Raleigh SM. Genetic risk factors for musculoskeletal soft tissue injuries. Med Sport Sci. 2009;54:136-49.