Archive for April, 2011

Sports fans and their heroes in the wired age

April 27th, 2011

A quick plug for an essay of mine that appeared in Maisonneuve a few months ago (the full text has just been made freely available online), about the changing relationship between sports fans and athletes in the wired age. It’s a long piece that mixes some personal history with sociology and (inevitably, as a runner!) some discussion of the Letsrun message boards:

A CBC video clip of the 1996 Canadian Olympic Track and Field Trials recently surfaced online. You can watch, in grainy low definition, the twelve finalists in the men’s 1,500 metres step to the line under starter’s orders. A momentary pause, as the runners crouch in anticipation—then the gun fires. Eleven runners explode down the track. The twelfth, inexplicably, stays frozen on the starting line for a brief instant, then snaps out of it and takes off after his competitors. He never quite catches up, and finishes last.

A surprising number of people have stumbled on this clip and emailed it to me, along with some variation of the question, “What the hell happened there?”… [READ ON]

More on Taubes, Lustig and toxic sugar

April 26th, 2011

A quick post with a couple of links for those interested in reading more about the Taubes/Lustig “toxic sugar” debate. To hear more from Taubes, check out his answers to numerous reader questions at the NYT site. And to read David Katz’s response to Taubes/Lustig (hat tip to Yoni Freedhoff at Weighty Matters), click here. A peek at Katz’s conclusion:

As dietary guidance, the vilification of one nutrient at a time has proven as flighty as hummingbirds, propelling us from one version of humbug to another. My advice is to grasp firmly your common sense, and stay grounded.

The hummingbird stuff makes more sense if you read the whole post, but it’s generally a Pollan-esque argument rather than a research-y one. Still, it’s about where I come down. Taubes’s response to that point:

This is a common argument over the years, that reductionism in nutrition research misses the point. Michael Pollan makes this argument in “In Defense of Food.” The counter argument is that this is, indeed, a science and one way sciences make progress is by reducing problems down to their basics. This can often be misleading, and Suzanne’s point (as with Michael Pollan’s) that it has been in the past is very true.

I’ve been a strong journalistic opponent of the belief that salt causes hypertension or that dietary fat or saturated fat causes disease and in doing so I’ve attacked the bad science behind some of these reductionist arguments. But just because over the years one single nutrient after another has been singled out as harmful doesn’t mean that one single nutrient isn’t harmful. It only means that the research is poor and some of the beliefs about how research should be done in these fields are also misconceived.

Does vitamin C block gains from training?

April 24th, 2011

The traditional theory goes like this: strenuous exercise produces “reactive oxygen species” (ROS), which cause damage to cells and DNA in the body. Taking antioxidant supplements like vitamins C and E helps to neutralize the ROS, allowing the body to recover more quickly from workouts.

The new theory, in contrast, goes like this: strenuous exercise produces ROS, which signal to the body that it needs to adapt to this new training stress by becoming stronger and more efficient. Taking antioxidant supplements neutralizes the ROS, which means the body doesn’t receive the same signals telling it to adapt, so you make smaller gains in strength and endurance from your training.

So which is true? Back in 2009, a German study found that vitamins C and E did indeed block gains in insulin sensitivity — a key adaptation to exercise — in a group of sedentary volunteers. But in January 2010, a study of cyclists found no difference in fitness parameters like maximal oxygen consumption, power output, lactate threshold and so on between a placebo group and a vitamins C/E group. But then last December, a study with rats found that vitamin E did block gains in mitochondria, a key adaptation to endurance training.

Which brings us to the most recent study, published in March in the International Journal of Sports Physiology and Performance. A total of 17 recreational runners did a four-week training program consisting of four interval workouts a week (5x3min hard with 3min jog recovery — a bit of an odd program, but it succeed in significantly boosting VO2max, running economy, 10K time trial performance, etc.). Half the subjects took 1 gram of vitamin C every morning, while the other half took a placebo; the trial was double-blinded, so no one knew who was in which group. The results: no significant differences between the groups.

So where does this leave us? I’m not really sure. The paper discusses a couple of possible explanations. One is that antioxidants do block some training gains but that this study was too small to detect them. With nine subjects in one group and eight in the other, that’s certainly possible. For example, the subjects ran two  “YoYo Intermittent Recovery Tests” with slightly different parameters. In the first one, the vitamin C group improved 22% while the placebo group improved only 16%; in the second one, it was the other way around, with the placebo group improving 10% and the vitamin C group improving only 5%. This doesn’t give me a whole lot of confidence in the test-retest variability, or the ability to detect subtle differences in adaptation.

Another possibility relates to the initial fitness of the subjects. The 2009 German study used sedentary, unfit subjects, who thus would be expected to produce very high levels of ROS in response to the unfamiliar stress of exercise. In these subjects, one might expect antioxidant supplements to make a bigger difference to training adaptations. The new study, on the other hand, used subjects with higher initial aerobic fitness (“recreationally active,” not trained athletes). As the saying goes, “exercise is the most powerful antioxidant we have.” So it’s possible that fit subjects already have reasonably effective natural antioxidant defenses in place, so taking additional antioxidant supplements doesn’t make as much (or any) difference.

All of this leaves us with no firm answer — as usual, more studies are needed. My guess (thinking back to my last post about the pros and cons of training on empty) is that we’ll eventually conclude that the answer is “it depends.” Perhaps antioxidant supplements will be helpful during extremely heavy training blocks, but should be avoided as you approach competition. Or perhaps it’s the other way around: let the ROS run wild during heavy training blocks, but take antioxidants to ensure full repair as competition approaches. The latter approach fits with a Portugese study that found that antioxidants may delay muscle repair after heavy workouts, but could allow muscles to actually work harder in the heat of competition. It’s too soon to know for sure.

Training without breakfast?

April 21st, 2011

Training on “empty” — i.e. with low carbohydrate stores — is one of the hot topics in sports nutrition these days. (I’ve posted on it a few times, for example here and here.) Louise Burke of the Australian Institute of Sport has a good summary of the current thinking in the ACSM’s Sports Medicine Bulletin.

Traditionally, athletes have approached their daily workouts to train as hard as possible, using strategies that promote good performance, just as they would in a race or match. In many sports, these strategies involve fueling up with carbohydrates before, during and between workouts to sustain the capacity to produce power. Recently, however, scientists have proposed an alternative approach…

I won’t bother trying to summarize the whole thing, because Burke is already compressing a lot of information into a small space — if you’re interested in the topic, it’s worth a read. A couple of minor points to highlight, though:

While some publicity surrounding this study suggests otherwise, the outcomes from [training low] weren’t achieved by following a low carbohydrate diet.

This is about having low carb stores for a short period of time, for instance by depleting carbs with a prior workout, not being in a chronically low-carb state. And a very interesting point:

It makes sense that sessions completed at lower intensity or at the beginning of a training cycle are best suited for, or perhaps least disadvantaged by, [train low] strategies. Conversely, quality sessions done at higher intensities or in the transition to peaking for competition might best be undertaken with better fuel support.

In other words, nutrition should be periodized. What you eat — and how you think about the relationship between your food and your performance — should be different in base phase than it is come competition time.

Cardio or Weights book tour: first stop Vancouver

April 19th, 2011

BMO Vancouver marathon posterJust over a month until the release of Cardio or Weights, and plans are starting to come together for some talks and appearances. First order of business: Vancouver people, please spread the word! I’ll be giving a free Science of Running talk on Saturday, April 30 at 12 p.m. at the BMO Vancouver Marathon’s Brita Sports Expo (at Concord Place). The talk will be about 30 minutes, focusing on practical tips for runners based on recent research, followed by plenty of time for Q&As.

While I’m in Vancouver, I’ll also be speaking at the Forerunners clinic on Wednesday evening, and I’ll be hanging around the Canadian Running magazine booth at the marathon expo on Thursday, Friday and Saturday. Please drop by to say hello when you pick up your number, and feel free to hit me up with any sports science questions (or tell me why I’m wrong or crazy or both!). If all goes well, I’ll also have some advance copies of Cardio or Weights with me (they should be back from the printers any day now).

One other note: I’ve set up a Sweat Science Facebook page (there’s also a link at the top right of this page). For simplicity, I’m going to keep the updated list of upcoming events on that page, under the Events tab. That’s also where I’ll post news about upcoming interviews and other book-related stuff, to avoid cluttering this blog up too much. For instance, I’ve posted a short video Q&A I just did with my publisher. Please check out the Facebook page (and perhaps even click “Like!”) if you have a chance — thanks!

The more you run, the less your diet affects your weight

April 19th, 2011

Another month, another neat paper from Paul Williams’ prolific National Runners’ Health Study, online at Medicine & Science in Sports & Exercise. With his sample of >100,000 runners, Williams took two well-established correlations — those who eat more meat tend to weigh more, as do those who eat less fruit — and checked to see whether these links between diet and weight were affected by how much exercise the subjects did.

The first thing to emphasize: don’t get hung up on whether or why meat and fruits are “good” or “bad.” That’s not what this study is about. It’s just a cross-sectional study, so individual dietary markers (like meat and fruit consumption) may simply be markers of other behaviours. But whatever the reason for these correlations, they’re well established. The question is: if you do lots of exercise, are you less likely to get fat from whatever dietary patterns are associated with high meat and low fruit intake?

The answer is yes:

Specifically, compared to running < 2 km/d, running >8 km/d reduced the apparent BMI increase per serving of meat by 43% in men and 55% in women, and reduced the apparent BMI reduction per serving of fruit by 86% in men and 94% in women.

Williams suggests two possible explanations for this effect:

  • Aerobic exercise trains your body to burn a higher percentage of fat rather than carbohydrate for fuel. In contrast, people who burn a lower percentage of fat compared to carbohydrate are thought to be at higher risk of gaining weight.
  • Exercise improves “coupling between energy intake and expenditure.” In effect, researchers have found that people who exercise more tend to develop stronger appetite cues that tell them when they’re hungry or full. There have been some neat studies of this, where subjects were fed “disguised” drinks that had either high or low energy content. As a later meal, regular exercisers unconsciously adjusted by eating more or less (depending on which drink they’d received) compared to sedentary people.

So why is this important? It goes back to the never-ending “diet versus exercise” debate for weight loss, a false dichotomy if there ever was one. Williams notes that a recent review of epidemiological studies looking for links between reported levels of physical activity and prospective weight gain concluded that they “generally failed” to show any links. This contrasts sharply with Williams’ own findings, which clearly show that “running attenuates age-related weight gain prospectively in proportion to the exercise dose, and that increasing and decreasing exercise produces reciprocal changes in body weight.” He speculates that the difference arises because running is relatively vigorous. It’s also easy to quantify compared to vague epidemiological studies that have subjects estimate how much time they spend playing soccer or mowing the lawn, at what subjective level of effort.

Whatever the mechanism, it’s a good reminder that exercise can play a role in weight control. It certainly doesn’t give you a free pass on your diet — but if you do enough, it seems to give you a little more wiggle room.

XC skiing and arthritis

April 18th, 2011

To be perfectly honest, I wasn’t thrilled to see the results of this study (tweeted by Amby Burfoot). But data is data*, and if you report the good news you can’t ignore the bad. Swedish researchers did a very cool analysis of 54,000 men and women who competed in the famous 90 km Vasaloppet classic-style nordic ski race between 1989 and 1998 (full text available here). What’s fascinating is that Sweden keeps meticulous records of all its citizens, including all the in-patient health care they receive, linked to a 10-digit identification number. So the researchers were able to link the names and finishing times of all the racers with their health records, census data (to check confounders like education, occupation and income), death records and emigration records.

The basic question they looked at was: does exercise (as represented by the number of times subjects raced the Vasaloppet in the 10-year window, and their fastest finish) correlate with severe osteoarthritis later in life (as indicated with having a knee or hip replacement due to arthritis). The answer, unfortunately, was yes. For example, those who completed five or more races and had a fast finish time were 2.73 times more likely to need a joint replacement in the following ~10 years than those who participated only once and had a slow finish time.

The results contrast with a string of recent studies that found that, if anything, longtime runners are less likely to develop arthritis than non-runners. So there are a few questions here. Does the skiing motion have some unique effects on joints, causing more stress and cartilage damage? Or is it more a question of degree: “moderate” exercise is good for the joints, but 90 km ski races (which took between four and 13 hours to finish) are a bit too extreme? I don’t know, but I suspect the latter is a factor.

One point worth noting. Compared to similar studies of the general population, the skiers as a group had exactly the same risk for knee replacement, and a slightly higher risk of hip replacement. That suggests that, while the elite athletes at the front of the pack were worse off than the general population, the “casual” exercisers toward the back of the pack were in fact better off than the general population (though “casual” isn’t really the right term for someone doing a 90 km ski race).

And a last point: the same group has made several other studies of the characteristics of Vasaloppet finishers. Even if their knees get creaky, they do live longer than their sedentary peers; and the more races they do, the longer they live. So that’s something, I guess!

[* I know, “data” is supposed to be plural. Hopefully people will overlook this transgression… :)]

Relative injury risk of cycling, walking, driving and motorcycling

April 15th, 2011

Monday’s post on whether helmets encourage risky behaviour sparked a rather spirited discussion in the comments section. One of the louder claims was that, by choosing to write an article about bike helmets, I was making an implicit and unwarranted assumption that biking is more dangerous than, say, walking.

It’s an interesting question: is cycling more any more dangerous than walking? I went to look for some data. This is the first paper I found on Pubmed. I don’t know if it’s representative; I didn’t do a comprehensive search, and I’m under no illusion that this data will change anyone’s mind. Nonetheless, it’s data, from a paper published last fall in BMC Public Health. Researchers examined records from New Zealand’s Mortality Collection and National Household Travel Surveys to determine the incidence of injuries for several different survey periods. Here’s what they found for the most recent period, 2003-7 (the full paper is freely available at the link above, if you want to see the rest of the data):

Activity / Total injuries per year / Injuries per million hours spent travelling

Cyclists / 682 / 30.74

Car/van driver / 1714 / 2.10

Car/van passenger / 1086 / 2.89

Motorcyclist / 784 / 107.64

Pedestrian / 471 / 2.38

[UPDATE April 19: I’ve closed comments on this post, as I think we’ve reached a point of diminishing returns. Thanks to everyone for their contributions!]

Gary Taubes on “toxic” sugar

April 14th, 2011

A friend just forwarded the new Gary Taubes NYT Magazine article on Robert Lustig’s claims that sugar is “toxic.” It’s an interesting article, worth a read, and Taubes is reasonably circumspect in acknowledging the uncertainties in the current evidence. He starts with this acknowledgment:

The viral success of [Lustig’s] lecture, though, has little to do with Lustig’s impressive credentials and far more with the persuasive case he makes that sugar is a “toxin” or a “poison,” terms he uses together 13 times through the course of the lecture, in addition to the five references to sugar as merely “evil.”[…]

His critics argue that what makes him compelling is his practice of taking suggestive evidence and insisting that it’s incontrovertible. Lustig certainly doesn’t dabble in shades of gray.

Indeed, that’s precisely what’s at issue with Lustig’s lecture: not whether sugar is a problem, but whether it’s the problem. And to make that case, Taubes stacks the deck with statements like this:

The conventional wisdom has long been that the worst that can be said about sugars of any kind is that they cause tooth decay and represent “empty calories” that we eat in excess because they taste so good.

Who the heck claims this? (In journalistic jargon, phrases like “The conventional wisdom has long been…” are known as “weasel words,” because they allow you to make statements that help your argument without finding anyone stupid enough to actually say them.) It’s a convenient distortion, because it lends some misplaced novelty to the “Men Land on the Moon!” discussion that follows, about the links between sugar and metabolic syndrome. Come on, we’ve been talking about “glycemic index,” in which glucose is assigned the nominal maximum value, since the early 1980s. This is an important topic, and perhaps one that not everyone fully appreciates, but it’s tangential to Lustig’s central claim that sugar (and fructose in particular) is a “toxin.”

The central question here is really about dose. Is sugar “unsafe at any dose,” as Ralph Nader might put it? Or is it only unsafe when consumed to excess? And if the latter, what constitutes “excess”? To his credit, Taubes makes this point, though he weakens it by putting it in the mouth of someone he identifies as a lobbyist for the corn refining industry:

[S]ugar and high-fructose corn syrup might be toxic, as Lustig argues, but so might any substance if it’s consumed in ways or in quantities that are unnatural for humans. The question is always at what dose does a substance go from being harmless to harmful? How much do we have to consume before this happens?

Much of the rest of Taubes’s article explores how much sugar we’re now eating, how much it has increased, and how diseases like diabetes and cancer have increased in parallel. It makes a strong case for eating less added sugar — pretty much exactly the same case that Taubes made in his 2007 book Good Calories, Bad Calories, as far as I can tell. Heck, I was convinced in 2007, and I’ve been very conscious of my sugar intake — along with other highly refined carbohydrates — ever since then. What I don’t see here is any reason to be more scared of sugar than I was before on the basis of Lustig’s “sugar is a toxin” argument.

Taubes describes the mechanism of fructose’s action as follows:

In animals, or at least in laboratory rats and mice, it’s clear that if the fructose hits the liver in sufficient quantity and with sufficient speed, the liver will convert much of it to fat. This apparently induces a condition known as insulin resistance…

Again, scary stuff. But how is this different from, say, glucose, or even refined carbs from white bread, which are thought to stimulate insulin resistance if they enter the body “in sufficient quantity and with sufficient speed”? If we’re concluding that fructose is “toxic,” shouldn’t we also conclude that glucose and white bread and all other refined carbs are too? Oh wait, that’s what Gary Taubes proposed in 2007. So what has Lustig added? Fructose causes the same problems as other foods, but through a different biochemical pathway.

What would get my attention is evidence that cumulative exposure to fructose — independent of the rate of intake — accumulates over time to produce problems. In other words, does eating 50 pounds of sugar spread out over 30 years ultimately produce essentially the same bad effects as eating 50 pounds of sugar in a single year? Or is it only a problem when the dose comes “in sufficient quantity and with sufficient speed”?

To be clear, I have no doubt whatsoever that Lustig is right that we eat too much sugar and it’s causing health problems. I just wonder if there’s actually anyone in the country who didn’t already think that.

The beet goes on: nitrates improve cycling time trial performance

April 13th, 2011

Wow. This study is really impressive. Drinking 500 mL of beet juice 2.5 hours before a cycling time trial improves 4 km TT time by 2.8% and 10 mile TT time by 2.7%. On the one hand, this shouldn’t be surprising, because there have been a bunch of recent studies showing beet juice boosting time-to-exhaustion and reducing oxygen cost… But still, those types of studies often don’t end up translating into real differences in the parameter that matters: actual performance. So, as I said: Wow.

The study, published online last week in Medicine & Science in Sports & Exercise, is legit. It’s from Andrew Jones’s group in Exeter. It’s a properly designed placebo-controlled crossover study. The placebo was beet juice with the nitrates (the active ingredient) filtered out with an ion resin, thus indistinguishable from the active beet juice. The subjects (nine competitive cyclists) visited the lab at least five times before the actual experiment even started, to practice taking the time trials until they achieved repeatability of less than 1%.

To reiterate what’s most striking:

  • Performance benefits of 2.8% (6.26 vs 6.45 min) over 4 km and 2.7% (26.9 vs 27.7 min) over 10 miles.
  • This improvement was achieved with just one dose of 500 mL of beet juice, taken 2.5 hours before the event. (Note that this dose is equivalent to 1.6 kg of spinach or 3.1 kg of lettuce!)

They also took other measurements: the amount of oxygen used was the same with and without nitrates, but the power generated was higher with nitrates. Also, plasma level of nitrites was higher after the beet juice, consistent with previous studies suggesting that the beet juice works because nitrates are converted to nitrites then to nitric oxide, which lowers the oxygen cost of muscle contractions.

On another note (further to this previous post):

The subjects also abstained from using antibacterial mouthwash and chewing gum during the supplementation periods since these are known to eradicate the oral bacteria which are necessary for the conversion of nitrate to nitrite.

So what more is there to say, other than “Buy stocks in beet juice companies pronto”? Well, one caveat is that it hasn’t yet been shown that these results can be duplicated in elite athletes. It’s notoriously easier to produce big improvements in less-trained athletes, and these subjects were recreationally competitive. So further studies will be required in elites. But it’s time to acknowledge once again that my initial predictions when I first heard about this research in August 2009 were wrong, wrong, wrong!