Archive for March, 2011

Who’s the mystery man with the 90.6 VO2max?

March 30th, 2011

Interesting riddle posed by a case report in the European Journal of Applied Physiology (third post from that journal this week — I need to check it more often!): who is the mystery cross-country skier who appear to have one of the highest VO2max readings ever recorded, at 90.6 ml/min/kg?

Here are the clues:

  • The test was performed at the University of Innsbruck in Austria.
  • The subject was “a young elite cross country skier,” male, 22 years old.
  • The test took place 4 years before the skier won an Olympic gold medal.

Austria didn’t have any gold medalists in XC skiing in 2010 (and none of the winners are the right age anyway). Same with 2006. They had a gold medalist in 2002 (Christian Hoffmann), but he’s two years too old. They did win the 2006 men’s team event in Nordic combined, and one of the team members — Michael Gruber — would have been 22 years old in 2002, four years earlier. But come on… are you telling me that the man with one of the highest VO2max readings in history was a part-time ski-jumper?! If so, that’s a pretty good reminder that VO2max isn’t everything…

So what is the ultimate highest value? The paper notes an “anecdotal report” in a 2003 textbook by Astrand of someone testing 94 ml/min/kg (anyone know who that was?). They also discuss some measurements on cyclists in the 1990s by Randy Wilber (who is a co-author of this paper) at the US Olympic Training Center. The 1997 paper they cite is a comparison of 10 mountain bikers with 10 members of the US Cycling Federation National Road Team, but they also cite some unpublished data on “American elite male road cyclists who had won individual stages (and the General Classification) of the Tour de France.” There aren’t many of the latter around, are there? Anyway, a few of these cyclists tested at over 80 ml/kg/min at 1860 metres, which they argue equates to 85-86 at sea level, and roughly comparable to about 90-91 if they were doing arm-and-leg exercise (like skiing) rather than just leg exercise (cycling).

But that’s a lot of approximations. I’ve never seen a peer-reviewed report over 90 until this one. Anyone else?

Walking in a forest reduces blood pressure

March 29th, 2011

I present this research half in jest, and half seriously. There have been a bunch of studies lately purporting to show the magical benefits of spending time with nature, most of which qualify as pretty soft science. Still, even if the studies are full of uncontrolled variables and confounding factors, I like to think there’s a kernel of truth in the basic premise. So here are the details of this latest one, published in the European Journal of Applied Physiology by researchers at the Nippon Medical School in Tokyo.

They took 16 volunteers, and took them on two day trips a week apart. In one, they walked for two hours in a forest; in the other, they walked for two hours in “an urban area of Tokyo.” At 8 a.m., 1 p.m. and 4 p.m. on each of the days, the researchers took a boatload of measurements, including blood and urine samples. The simplest and clearest result was in blood pressure, shown here:

As you can see, blood pressure was lowered significantly by the forest walk compared to the urban walk. Why is this? The researchers suggest that the forest works its magic “by lowering the activity of the sympathetic nerve and increasing the activity of the parasympathetic nerve.” In support of this idea, they found that noradrenaline in the urine samples — a marker of sympathetic nerve activity — was lower after forest walking. So far as good. But how do forests do this?

We speculated that phytoncides (wood essential oils) from trees may have beneficial effects on blood pressure. Dayawansa et al. (2003) reported that cedrol (cedar wood oil) inhalation induced significant reductions in systolic and diastolic blood pressure compared to blank air together with an increase in parasympathetic activity and a reduction in sympathetic activity in humans.

Well… I suppose that could be the mechanism. But on the other hand, a far simpler possibility is that walking in a quiet, peaceful forest is more relaxing than battling the cars and pedestrian mobs of downtown Tokyo. It seems to me that the first order of business for this apparently burgeoning field of study is to look into some of these more obvious variables: noise levels, crowds, the chance of being flattened by a wayward bus. Until it’s clear that there’s some phenomenon that can’t be explained by these obvious factors, I don’t think we need to spend too much time pursuing magic tree oils.

(I suppose this is where I point out that the study was funded, with no apparent irony, by Japan’s Forestry and Forest Products Research Institute.)

What’s the ideal running stride to avoid injury?

March 27th, 2011

This week’s Jockology column in the Globe revisits a familiar question:

The question

Is there an ideal running stride, and can I learn it?

The answer

You may think running has more in common with day-to-day functions like breathing and eating than with more technical sports like golf or swimming: As kids, we learn how to run with no special instruction, just as our ancestors have for millennia. The result?

“Most people run very badly,” says Blaise Dubois, a Quebec City physiotherapist whose multi-day course on the prevention of running injuries has been drawing sellout crowds of health professionals, coaches and running enthusiasts around the world… [READ THE REST OF THE COLUMN]

I had a really interesting interview with Blaise Dubois for this article. We spoke for nearly 90 minutes — so of course, only a tiny fraction of the discussion made it into this article. Hopefully I’ll have time at some point in the next few weeks to go through my notes and write a blog post about some of the other things we talked about. Hat tip once again to this post from Pete Larson’s blog that convinced me to get in touch with Blaise.


How fast can you start putting on muscle?

March 25th, 2011

The traditional view is that it takes at least 6-8 weeks of hard resistance training before your muscles start getting bigger. You’ll see strengths gains long before that, the theory goes, but they come from neural factors (basically the “contract” signal from your brain gets the message to your muscle fibres more effectively). In the last few years, though, that orthodoxy has been challenged by a few studies that claimed to see muscle increases after just a few weeks of training. A new study from the University of Oklahoma, published in the European Journal of Applied Physiology, should help settle the debate. They set out to do a study with three key characteristics:

  1. Hard training: the subjects trained three times a week for eight weeks. The program was leg press, leg extension and bench press. Each exercise was three sets to failure with two minutes rest, with the weight chosen so that failure occurred after 8 to 12 reps in each set.
  2. Frequent testing: instead of just doing before-and-after measurements, the testers measured strength and muscle cross-sectional area every week for eight weeks.
  3. Sensitive measurement: a tape measure won’t cut it. They used a CT scanner to measure the muscle cross-sectional area at the midpoint of the thigh.

Here’s what they found:

The top line is muscle size, bottom is strength. The first two data points are the pre-training baseline measurements. It’s possible that the initial jump in muscle size after the first week (i.e. after just two training sessions) is predominantly due to swelling associated with muscle soreness. But the soreness had totally dissipated by week 3, so by then we’re unquestionably dealing with actual hypertrophy. By the end of the eight weeks, the total increase in muscle size (CSA) was 9.6%. Two comments. First, I was curious as to why they included bench press when all the measurements are on the legs. In discussing why an earlier study failed to see gains quite this early, the researchers note that

subjects only performed one exercise (leg extensions), so the training stimulus was not as great as that in the present study.

Does this mean that upper-body training can contribute to lower-body hypertrophy, perhaps by tweaking anabolic hormone levels and ramping up whole-body protein synthesis? I’m not sure — if anyone can clarify, please do so in the comments section. Second, this training program is hard. Three times a week, three sets of three exercises may not sound that tough — but every set is to failure (much like the controversial low-weight approach advocated by Stu Phillips, actually). If you really want to put on muscle quickly, you have to work hard.

“Cardio causes heart disease”: misinterpreting science for fun and profit

March 22nd, 2011

There’s an article by “paleonutrition” advocate Kurt Harris, posted on the Psychology Today website, that is currently making the rounds, in which he argues that aerobic exercise causes heart disease.  The study he’s talking about was published in Radiology back in 2009 by a German group led by Frank Breukmann and Stefan Möhlenkamp. They compared 102 marathon runners between the ages of 50 and 72 with 102 age-matched controls, and used cardiac MRI with late gadolinium enhancement to look for evidence of permanent heart damage. Five of the runners had evidence of past heart attack, and another seven had heart damage not associated with a heart attack, for a total prevalence of 12%. Among the controls, two had evidence of past heart attack, and another two had other damage, for a total prevalence of 4%.

The difference between the two groups wasn’t statistically significant. This doesn’t matter to Harris:

I am obliged to point out that by the conventional arbitrary criteria used in biomedical publishing, the difference was “not statistically significant”… Stop doing what you are told and read the statistics without letting the authors or editors tell you what is “significant”.

That’s certainly a convenient approach: if you already think you know what the right answer is, then you don’t need to worry about little details like statistical significance.

Still, the results are  very much worth considering. Harris wonders why the study was ignored by the “nutrition and fitness” blogosphere, and takes a shot at the New York Times:

[I]t’s published in Radiology, which is not exactly Gina Kolata territory.

Actually, the Times ran a Bloomberg article on the early results from this study cohort way back in 2006. And Runner’s World interviewed cardiologist Paul Thompson, a co-author of the most recent results from the study, in January. Thompson points out some important caveats about the study group:

[H]is marathon group includes a number of former smokers and others who might have been quite unhealthy before they began running…

The key issue with Möhlenkamp’s runners is that their cardiac risk scores are compared using their present cholesterol, blood pressure, and other health numbers. They might have had terrible numbers before they started running, so when their coronary calcium is compared with folks who are not athletes, but had good risk numbers all their lives, it looks like the runners had more calcium, ie, more atherosclerosis than predicted by their risk factors… Many of the runners “got religion” when they turned 40 or so.

To his credit, Harris acknowledges that 50% of the runners in the study had a history of smoking, compared to just 42% of the controls — but immediately dismisses the possibility that this (and any other underlying factors that differ between the two groups) could play a role. Again, why worry about statistics and the possibility of confounders when you already know the right answer?

Let me perfectly clear: it’s entirely possible that repeated marathon running (the runners in the study had completed an average of 20 marathons) produces damage to the heart. By all means we should continue to study this, and find out. Despite Harris’s snide comments about aerobic exercise not producing immortality, we’ve known that aerobic exercise doesn’t grant immunity from heart disease for decades. In fact, very first time noted iconoclast Tim Noakes made a splash in scientific circles was way back in 1976, with a paper about heart attacks in veteran marathon runners.

Of course, there’s a difference between running marathons and “aerobic exercise” as practiced (or not) by the vast majority of the population. I’m a lifelong runner, but if someone asked me: “What’s the optimal exercise routine for cardiac health?” I wouldn’t necessarily recommend running marathons. I’d probably suggest something like an hour a day, with two to three days a week devoted to shorter, faster interval workouts. And of course, I would also recommend doing some resistance training — and I wouldn’t take, for example, a study showing that competitors in the World’s Strongest Man competition die early as evidence that “resistance training is bad for you.”

That’s basically what Harris is doing here: concluding, on the basis of this one study of a fairly extreme group of outliers, that aerobic exercise in general is as bad for you as boxing or football. The only sensible exercise, he argues, is resistance training:

I still find no grounds at all to believe that high levels of “cardio” protects your heart or makes you live longer. Certainly not “the more the better” which is what we’ve been led to think since the 1970s running craze.

The reason he finds no grounds, of course, is that he’s never looked. In his article, he waxes philosophic about the fact that “the picture or the test result is not the patient or even the disease.” Then, on the basis of a test result, he concludes that running will kill you. But what if we look at “the thing itself,” and find out whether runners die less from heart attacks — and whether “the more the better” holds up.

Paul Williams did this study and published it back in 2009. He followed 35,402 runners for 7.7 years, during which time 467 men reported heart attacks, angina or had to have bypass surgery, while another 54 died of heart disease. The risks of all these symptoms, including death, decline with every additional kilometre run. Those running more than 9 km/day “produced risks 65% lower for angina, 29% lower for nonfatal CHD, and 26% lower for fatal and nonfatal CHD” compared to those running fewer than 3 km/day (the level corresponding to national physical activity guidelines for adults).

I’ve rambled on a bit here, so let me finish by repeating one simple point. Even if you take the results of Möhlenkamp’s study at face value (which I don’t, as explained above), the conclusion you can draw is that running a large number of marathons may damage your heart. To go from this to arguing that 20 minutes on the elliptical is bad for you requires a Beamon-esque leap of logic, along with a cheerful disregard of literally hundreds of epidemiological studies.

Muscle cramps risk factors: tapering, stretching and pacing

March 22nd, 2011
Comments Off on Muscle cramps risk factors: tapering, stretching and pacing

I’ve written a few times now about the “new” theory of muscle cramping advanced by Martin Schwellnus of the University of Cape Town and his colleagues, most recently last month. In a nutshell, he argues that muscle cramps have nothing to do with dehydration or electrolyte depletion, but result from “altered neuromuscular control” (for an more detailed explanation, see this article).

Schwellnus and his colleagues have just published a new study online at the British Journal of Sports Medicine — a prospective study of 49 runners at the 2009 56K Two Oceans marathon. And it produced some very interesting results. Twenty of the runners reported cramps during or within six hours after the race, compared to 29 non-crampers. The two groups were statistically identical in many important respects: age, weight, height, BMI, sex, training history, recent and all-time personal best times, finishing times during the race. But they differed in a few key areas:

  • Pacing: Even though the two groups had similar best times and similar pre-race goals, the group that ended up cramping split the halfway mark 13 minutes faster than the non-crampers on average (144 minutes versus 157 minutes).
  • Tapering: In the three days prior to the race, the crampers trained 1.1 hours on average, while the non-crampers trained 0.6 hours on average. This despite the fact that the non-crampers actually did marginally more training overall in the final week (31.8 km versus 26.5 km).
  • Muscle damage: Perhaps related to the inadequate taper, the eventual crampers had higher levels of creatine kinase before the race, indicating the presence of muscle damage. They were also more likely to report soreness in their hamstrings.
  • Stretching: 92.9% of the crampers reported stretching before exercise, while just 54.6% of the non-crampers reported stretching. Of course, this could simply be because those prone to cramp are more likely to stretch.

Does this settle the cramping debate? Nope, but it should provide a little more fuel for the fire!

Athletes have superior street-crossing abilities

March 21st, 2011

How’s this for a compelling reason to take up sports, from the conclusions of a newly published University of Illinois study:

Compared to non-athletes, collegiate Division I athletes showed higher street crossing success rates, as reflected by fewer collisions with moving vehicles.

It’s actually an interesting study, though it’s hard not to snicker while reading it. Researchers assembled 18 D1 athletes from a variety of sports (baseball, XC, gymnastics, soccer, swimming, tennis, track, wrestling) and 18 non-athlete controls matched for age, gender, height, weight, GPA and video-game experience, then had them all try to successfully cross a busy street in a 3-D virtual environment, while walking on a manual self-paced treadmill. The results: athletes made it to the other side without getting splatted 72.05% of the time, while non-athletes only made it 55.04% of the time.

The purpose of the study was to find out whether sports training improves multitasking ability:

An ability to efficiently process information is said to improve multitasking performance. That is, if information passes through the bottleneck efficiently and quickly, more information can be processed in a shorter time frame and performance can be maximized.

The athletes also outperformed the non-athletes in a simple test of reaction time — that difference alone is enough to account for the difference in street-crossing success. Of course, there’s a glaring cause-and-effect question here, which the researchers acknowledge:

We speculate that athletes are faster multitaskers than non-athletes, but it is also possible that successful virtual reality street crossers with fast processing speed are more likely to excel at sports.

It’s by no means obvious to me which direction the arrow of causality runs here. I suspect it’s a bit of both. Interestingly, these researchers are also part of the group that has been publishing some very encouraging findings about the effects of aerobic exercise on the brain. Just last month, they published a Proceedings of the National Academy of Sciences paper showing that aerobic exercise increases the size of the hippocampus by 2% in older people, reversing the effects of 1-2 years of age-related decline. In this case, cause and effect were clear.

Bottom line: sports skills may help you cross the street successfully, but if you want to remember how to get home again, make sure you’re doing some aerobic exercise.


How evolution keeps you on the couch

March 19th, 2011

Mark Fenske, a neuroscientist at the University of Guelph, has an interesting article in the Globe and Mail about how evolutionary forces on our brains affect our motivation to exercise. His basic argument is that we’re wired to avoid wasting energy, since our ancestors needed to make sure they’d have enough energy to find food or flee from danger. And recent neuroimaging studies (he’s not specific about which studies, by whom, and under what conditions) offer some support for this idea:

When subjects were considering whether to perform a given action, neural activity within one part of the striatum, the putamen, was found to decrease with the amount of physical effort the action would require… By helping to produce an aversion to unnecessary physical activity, the striatum may be partly to blame for the growing number of couch potatoes in Western societies.

Seems fairly intuitive — it would be surprising if we hadn’t evolved some such mechanism. But does this mean we’re incapable of overcoming this barrier to exercise? Of course not:

A number of studies indicate that increasing the reward associated with an effortful action can lead to its being chosen over an easier option. And brain scans show that the size of such a reward is associated with activity in the nucleus accumbens, which is another part of the striatum linked to motivation.

Again, this is quite painfully obvious on an intuitive level, though it’s interesting that scientists are zeroing in on which specific parts of the brain are responsible for these drives. The real pay-off, and the reason I’m linking to the article, comes in Fenske’s conclusion. We can trick the brain and tip the balance in favour of exercise, he says, by reminding ourselves of the well-established mental and physical benefits of exercise:

[B]y learning and thinking about exercise-related rewards we can strategically increase the incentive value of physical activity. This may explain why being reminded of such benefits, and how I always feel better after running than before, is so effective at getting me out the door.

To some extent, that’s what this blog is all about! The more we learn about all the different ways exercise benefits us, the easier it is to get out the door.

(And there’s a postscript too: exercise leads to physical changes in parts of the basal ganglia related to cognitive control. So the more you exercise, the better you get at overcoming your ancient brain’s aversion to “needless” effort.)

Exercise and poop

March 16th, 2011

You may want to skip this post if you’re about to eat…

Swedish scientists just published a delightful and highly detailed study comparing the gastrointestinal characteristics of a group of 15 elite orienteering during a week of heavy training, and again during a week of rest. (I don’t generally keep up to speed on the Scandinavian Journal of Gastroenterology, so thanks to Amby Burfoot for the tip-off!) Most people won’t be surprised to learn that, during the heavy training week, subjects had more bowel movements (1.5 per day versus 1.3) and looser stools (4.2 versus 3.9 on the Bristol Stool Form Scale, which rates stools from a hard, nut-like 1 to a watery 7).

The study also delved into much greater detail, using “radiopaque markers” whose progress could be followed through the digestive system using fluoroscopic imaging (essentially a real-time X-ray). Throughout the week, the subjects ate 10 little ring-shaped markers with breakfast each day; then on the final day, they ate 20 little spherical markers with breakfast, and were imaged every half-hour for the next eight hours. The spheres were used to track progress out of the stomach and through the small intestine (where most nutrient absorption occurs), which is measured in hours. The number of ring-shaped markers still in the body allowed the researchers to calculate how long food was taking to travel through the colon, which is measured in days.

The key results: gastric emptying (how quickly food left the stomach) was not significantly different during the two weeks (average of 1.8 hours during the resting week, 2.4 hours during the exercise week). Transit through the small intestine was significantly quicker during the training week (3.7 hours versus 6.9 hours on average). Transit through the colon wasn’t significantly different (1.2 days during training, 1.4 during rest).

So what does it all mean? Well to me, this is one of those “Am I normal?” studies: without going into excessive detail, it’s nice to see that my personal observations match up with typical patterns. One of the questions that remains unanswered is: are athletes in training less efficient at absorbing nutrients from their food since they’re forcing the food through their small intestine more quickly?

Artificial intelligence, the Singularity, and Robert J. Sawyer

March 15th, 2011

Totally off-topic here, but I just wanted to highlight an essay of mine that appears in next month’s Walrus magazine (and is now available online). Using Robert J. Sawyer‘s WWW trilogy (whose final volume is about to be released) as a jumping off point, it explores some of the issues surrounding computers whose intelligence is beginning to approach human-like levels:

If you’ve got any spare change, the Lifeboat Foundation of Minden, Nevada, has a worthy cause for your consideration. Sometime this century, probably sooner than you think, scientists will likely succeed in creating an artificial intelligence, or AI, greater than our own. What happens after that is anyone’s guess — we’re simply not smart enough to understand, let alone predict, what a superhuman intelligence will choose to do. But there’s a reasonable chance that the AI will eradicate humanity, either out of malevolence or through a clumsily misguided attempt to be helpful. The Lifeboat Foundation’s AIShield Fund seeks to head off this calamity by developing “Friendly AI,” and thus, as its website points out, “will benefit an almost uncountable number of intelligent entities.” As of February 9, the fund has raised a grand total of $2,010; donations are fully tax deductible in the United States… [READ THE REST OF THE ESSAY]

And for the record, I wrote this before Watson beat the puny humans on Jeopardy!