alex – Page 16 – Sweat Science

October 23, 2011October 23, 2011

Stress fractures: is it weak bones or muscles?

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My new Sweat Science columns are being published at www.outsideonline.com/sweatscience. Also check out my new book, THE EXPLORER'S GENE: Why We Seek Big Challenges, New Flavors, and the Blank Spots on the Map, published in March 2025.

- Alex Hutchinson (@sweatscience)

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A new study from researchers at the University of Calgary, published in the November issue of Medicine & Science in Sports & Exercise, looks at bone quality and leg muscle strength in a group of 19 women who have suffered stress fractures in their legs, and compares them to a group of matched controls. The basic results:

the women who got stress fractures had thinner bones;
at certain key locations, the quality of the bone was lower in the stress fracture group;
the stress fracture group also had weaker leg muscles, particularly for knee extension (lower by 18.3%, statistically significant) and plantarflexion (lower by 17.3%, though not statistically significant).

Now, this sounds very similar to the results of a University of Minnesota study published a couple of years ago. Here‘s how I summed up the conclusions reached by those researchers:

What’s interesting, though, it that the bone differences were exactly in proportion to the size of the muscles in the same area, and there was no difference in bone mineral density. What this suggests is that the best way to avoid stress fractures is to make sure you have enough muscle on your legs — presumably by doing weights and (it goes without saying) eating enough.

What I don’t understand is that, in the new Calgary study, even though they mention the Minnesota study repeatedly in their discussion, they don’t discuss at all this idea that it’s the lower muscle strength that dictates the reduced bone size and thus the stress fracture risk — even though that was the primary conclusion of the Minnesota study. Instead, they say “the role of muscle weakness in [stress fractures] is unclear from previous studies,” and suggest that weaker knee extension might change running form to produce a “stiffer” running stride or somehow alter the direction of forces on the bone during running — both of which seem like unnecessarily complex and speculative ideas compared to the straightforward link between muscle strength and bone strength.

It’s entirely possible that I’m missing something here, because the paper is quite complex. But what I take away from it is, once again, that strengthening your legs is likely (though not yet proven in a prospective trial) to reduce your stress fracture risk.

October 20, 2011October 20, 2011

Good diet trumps genetic risk of heart disease

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- Alex Hutchinson (@sweatscience)

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I posted last week about “epigenetics” — the idea that, while the genes you’re born with are unchangeable, environmental influences can dictate which of your genes are turned “on” or “off.” A few days later, I saw a mention of this PLoS Medicine study in Amby Burfoot’s Twitter feed. It’s not an epigenetic study, but it again reinforces the idea that the “destiny” imprinted in your genes is highly modifiable by how you live your life.

The study mines the data from two very large heart disease studies, analyzing 8,114 people in the INTERHEART study and 19,129 people in the FINRISK prospective trial. They looked at a particular set of DNA variations that increase your risk of heart attack by around 20%. Then they divided up the subjects based their diet, using a measure that essentially looked at either their raw vegetable consumption, or their fresh veg, fruit and berry consumption. Here’s what the key INTERHEART data looked like:

Breaking it down:

The squares on the right represent the “odds ratio,” where the farther you are to the right (i.e. greater than one), the more likely you are to have a heart attack.
The top three squares represent the people who ate the least vegetables, and the bottom three squares are those who ate the most vegetables.
Within each group of three, GG are the people with the “worst” gene variants for heart attack risk, AG are in the middle, and AA are the people with the least risk.

So if we look at the top group first, we see exactly what we’d expect: the people with the bad genes are about twice as likely to suffer a heart attack as the people with the good genes. But if you look at the middle group (i.e. eat more vegetables), the elevated risk from bad genes is down to about 30%. And in the group eating the most vegetables, there’s essentially no difference between the good and bad genes.

How does this work? The researchers don’t know — partly because no one’s even sure exactly how the bad gene variants cause higher risk. (There are some theories, e.g. that it affects the structure of your veins and arteries.) But the practical message is pretty clear: if you eat your veggies, you don’t have to worry about this particular aspect of your genetic “destiny.”

October 19, 2011

How quickly is water absorbed after you drink it?

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- Alex Hutchinson (@sweatscience)

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I’ve always been curious about this. Sometimes, after drinking a big glass of water, it seems like I pee it all out literally just a few minutes later. Is this just in my head, or is ingested fluid really processed that quickly? A new study by researchers at the University of Montreal, published online in the European Journal of Applied Physiology, takes a very detailed look at the kinetics of water absorption and offers some answers.

The study gave 36 volunteers 300 mL of ordinary bottled water, “labelled” with deuterium (an isotope of hydrogen than contains a proton and a neutron instead of just a proton) to allow the researchers to track how much of that specific gulp of water was found at different places in the body. They found that the water started showing up in the bloodstream within five minutes; half of the water was absorbed in 11-13 minutes; and it was completely absorbed in 75-120 minutes.

Here’s what the data looks like:

On the left, it shows how quickly the water was absorbed in the first hour, measured in the blood. On the right, it shows the gradual decay of deuterium levels over the subsequent 10 days, measured from urine samples. This, of course, shows that when I pee after drinking a glass of water, I’m not peeing out the same glass of water! Within ~10 minutes, fluid levels in my blood will have risen sufficiently to trigger processes that tell me to pee — but, according to this data, it takes about 50 days for complete turnover of all the water in your body.

The other wrinkle in this data is that the subjects showed two distinct absorption patterns (shown on the bottom and top), with about half in each group. In the top group, the water is very rapidly absorbed into the blood (possibly because these people get water out of the stomach and into the small intestine very quickly) before running into a slight bottleneck as the water is then distributed throughout the body to all the extremities. The second group, on the other hand, doesn’t hit this bottleneck: the flow of water out of the stomach and into the small intestine is slow enough that extra water doesn’t have a chance to build up in the blood before being distributed throughout the body.

So what does this all mean? I don’t have any particular practical applications in mind — I just thought it was kind of cool.

October 18, 2011October 19, 2011

Stretching doesn’t prevent or reduce muscle soreness

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- Alex Hutchinson (@sweatscience)

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[UPDATE: Welcome Reddit Running and Running Times folks! In answer to the question on the Running Times homepage, 11 of the 12 studies in this review used static stretching, while one used PNF stretching.]

The British Journal of Sports Medicine just published an analysis of the most recent Cochrane Review on stretching to prevent or reduce muscle soreness. The title says is all: “Stretching before or after exercise does not reduce delayed-onset muscle soreness.” This isn’t a surprise — while the exact mechanism that leads to DOMS is still up for debate, it’s pretty clear that it involves microscopic damage to muscle fibres and the subsequent repair process. Once those muscle fibres are damaged, no amount of post-exercise stretching can magically undamage them!

The analysis incorporated 12 studies, including one very large randomized trial with 2,377 participants. There was no difference between pre-exercise and post-exercise stretching in the effect on soreness. Of the 12 studies, 11 used static stretching and one used PNF stretching. Here’s a forest plot of some of the results, from the BJSM summary:

As the Cochrane Review notes, people generally stretch for one of three reasons:

reduce the risk of injury;
enhance athletic performance;
reduce soreness after exercise.

There’s plenty of evidence that the second point is misguided: stretching actually seems to harm athletic performance in many contexts. Now this Cochrane Review reaffirms that the third point is misguided too — and the BJSM reviewers make it clear that, in their opinion, this isn’t one of those tentative findings that might be modified by future research:

The best available evidence indicates that stretching does not reduce muscle soreness. These findings were consistent across settings (laboratory vs field studies), types and intensity of stretching, populations (athletic or untrained adults of both genders) and study quality. As such, they are unlikely to be changed by further studies.

That leaves the first point — reducing injury. There’s still a little wiggle room here. Numerous studies have failed to find any reduction in injuries following stretching, but it’s certainly a complicated topic. In particular, I’m open to the possibility that individually tailored stretching targeted at specific areas of weakness, inflexibility or imbalance could help people avoid or treat certain injuries.

October 17, 2011

Beliefs vs. science for vitamin supplements

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- Alex Hutchinson (@sweatscience)

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Marion Nestle has an interesting blog post about the two most recent studies that fail to find benefits from taking vitamin supplements. (One study followed 38,772 women for 22 years, and found that those taking multivitamins or certain single vitamins were slightly more likely to die than those not taking any supplements; the other was a placebo-controlled trial of 35,533 men, which found that taking 400 IU per day of vitamin E increased the risk of prostate cancer during a 12-year follow-up.)

The reason I’m posting this isn’t that I think vitamins will kill you — the effects were small, and for the most part I think supplements tend to do nothing, rather than have big effects either way. Personally, I suspect that the most negative effect of vitamin supplements is the feeling of false healthiness they provide, which then allows you to justify making other, less healthy choices throughout the day.

Anyway, what I found most interesting in Nestle’s post was her explanation of two very different ways of looking at research into nutritional supplements — both of which rely on a collection of “true” statements, but reach opposite conclusions:

For example, on the need for supplements, a belief-based approach rests on:

Diets do not always follow dietary recommendations.

Foods grown on depleted soils lack essential nutrients.

Pollution and stressful living conditions increase nutrient requirements.

Cooking destroys essential nutrients.

Nutrient-related physiological functions decline with age.

A science-based approach considers:

Food is sufficient to meet nutrient needs.

Foods provide nutrients and other valuable substances not present in supplements.

People who take supplements are better educated and wealthier: they are healthier whether or not they take supplements.

I’m not sure I quite agree with her labels (“belief-based” and “science-based”), but I definitely see these patterns of thinking in discussions of pretty much all areas of health and exercise research. The first set of statements makes a strong case that it’s plausible that supplements could improve health — but it leaves out the final step, which is to show that they do improve health. Similarly, the second set of statements explains why we shouldn’t be surprised if supplements don’t improve health, but doesn’t prove it. So to me, neither of these two approaches is satisfying — because the debate should be settled empirically.

Of course, research is complicated, and in many health debates it’s difficult to agree on what constitutes empirical evidence. That’s less and less true in the case of vitamin supplements, though. Study after study fails to find any benefits, so the hypotheses of the “belief-based” approach seem emptier and emptier to me.