Archive for July, 2010

Platelet-rich plasma for muscle injuries

July 15th, 2010
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The current issue of the British Journal of Sports Medicine has a couple of articles on platelet-rich plasma therapy, the experimental treatment that made headlines thanks to the Anthony Galea scandal and its links to Tiger Woods and other famous athletes. It’s most commonly used (in sports circles) for tendon injuries, but Kimberley Harmon of the University of Washington takes a look at the evidence for its use in muscle injuries (the full article is available for free at the BJSM site). Her conclusions are pretty much what you’d expect:

There is theory and preliminary evidence regarding the effectiveness of PRP, but its use is still investigational. It is incumbent upon physicians using this treatment to disclose its experimental status and to follow outcomes in a structured way. Further studies are needed to establish the effectiveness, indications and protocols for using PRP in the treatment of acute muscle injuries.

In other words, nobody really knows yet — but if you’re a pro athlete whose livelihood depends on getting that muscle or tendon fixed, it’s probably worth a try.

What I actually found most useful in the article was that it starts with a clear, detailed description of our current understanding of how muscles heal on a cellular level — the carefully choreographed sequence of platelets, growth factors, cytokines, neutrophils, and so on. This is a topic I was looking into recently during the research for another article, and I would have loved to find such a clear explanation.

(As an aside, she discusses the role of prostaglandin E2, which is affected by non-steroidal anti-inflammatory drugs like ibuprofen: “Recent studies have shown that NSAIDs likely tip the delicate balance of regeneration versus fibrosis toward fibrosis (scar).”)

More bad news for cyclists on bone density

July 13th, 2010
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A new study in the Journal of Strength and Conditioning Research follows up with a group of competitive masters cyclists seven years after the original study showing that they had abnormally low bone density. The cyclists now have an average age of 57, and 89.5% of them meet the criteria for osteopenia or osteoporosis. In comparison, only 61.1% of a group of matched controls meet the same criteria.

It’s still not entirely clear why cyclists seem to have poor bone density. Obviously cycling is a non-weight-bearing, non-impact activity, so they’re not getting any bone benefits from their time in the saddle. But it appears that their cycle training makes them less likely to do any weight-bearing activity even compared to non-athletic controls who don’t do any training at all. Another possibility is that they’re sweating out too much calcium, hindering bone formation and repair. This study doesn’t do much to clear up the mystery, but it does show that this is a real effect, not just an artifact of the general skinniness of cyclists — otherwise the equally skinny control group would show the same effects.

One important note: four of the 19 cyclists in the group started weight training during the seven-year interval, and they were able to slow their rate of bone loss. It’s another reminder to everyone whose main sports is something like cycling or swimming: you need to do something that stresses your bones, either through sharp impacts or the torque applied by strength training.


Shorter strides are easier on your knees and hips

July 12th, 2010

Yet another study advocating shorter, quicker strides when you run has just been posted on the Medicine & Science in Sports & Exercise site. In this one, researchers at the University of Wisconsin had 45 recreational runners run on a treadmill at their preferred stride rate, then increased or decreased the stride rate by 5% and 10% (keeping speed constant, so a faster stride rate resulted in shorter strides and vice versa).

The results aren’t that surprising: Increasing stride rate by 5% or 10% reduced the mechanical energy absorbed by the knee joint by 20% or 34% for each stride. The ankle joint didn’t change much, while the hip absorbed significantly less energy only when the stride rate was increased by 10%.

Of note, the researchers point out:

[M]any of the biomechanical changes we found when step rate increased are similar to those observed when running barefoot or with minimalist footwear.

So you could read this as an argument for minimalism — or, alternately, you could conclude that you can get the benefits of going barefoot simply by shortening your stride.

Three caveats. First, if you shorten your stride, you’ll take more steps to cover the same distance. Last year, researchers from Iowa State used a computer model to predict that, for a 10% increase in stride rate, the benefits of gentler foot-strike outweigh the downside of taking more strides in reducing your stress fracture risk. Still, it’s hard to know whether this conclusion is generalizable to other injuries. Second, studies have found that deviating from your preferred stride rate makes running feel harder, though there’s conflicting evidence about whether it actually makes you burn more energy. So this tactic might be most appropriate, the researchers suggest, when you’re returning from an injury and reduced load is more important than efficiency. And third, the study — as with virtually all the studies in the ongoing Shoe Debate — is a kinematic one that makes big assumptions about the connections between joint forces measured in the lab and ultimate injury rates. No one really knows whether “a more flexed knee at initial contact with less peak knee flexion during stance” will translate into a lower injury rate.


10K time predicts risk of heart disease, independent of training

July 11th, 2010
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The latest study from Paul Williams’s National Runners’ Health Study appears in the new issue of the American Journal of Cardiology. I like Amby Burfoot’s pithy summary of the results: “The faster you are, the longer you’ll live.

On the surface, the study is very simple. Williams looked at the 10K PBs of 29,721 men in his survey-based study, and then followed up 7.7 years later to see who had suffered heart attacks, angina, or died of factors related to heart disease. Not surprisingly, the faster subjects were less likely to suffer any of the negative outcomes:

Each meter/second increment in running performance was associated with a 44% lower risk for CHD death and nonfatal myocardial infarction, a 54% lower risk for nonfatal myocardial infarction, a 53% lower risk for angina pectoris, and 32% lower risk for revascularization procedures (percutaneous transluminal coronary angioplasty or coronary artery bypass grafting).

(An increase of one meter/second represents the difference between, for example, a 44-minute 10K and a 35-minute 10K.)

Pretty obvious, right? But there’s a twist: the results stay roughly the same even when you control for physical activity. In other words, if you’re trying to predict how likely you are to have a heart attack, it doesn’t matter how much you run, just how fast you are. In a sense, this is sort of bad news. We’ve generally assumed that being fit and being active are essentially the same thing. But Williams notes that “up to 70% of the variation in aerobic capacity is inherited in humans,” so some people need to be far more active than others to reach the same level of fitness (or running speed). This ties into an ongoing debate about “fatness versus fitness”: researchers like Stephen Blair argue that being active is more important than being skinny. But the new data goes further and argues that being active isn’t enough — you actually have to be aerobically fit, as measured by something like a 10K race or a VO2max test.

This doesn’t mean we’re captive to our genetic fates; it just means we may need to rethink how we approach exercise, according to Williams:

The present findings are relevant to the formulation of public health guidelines. Current guidelines primarily target the volume of physical activity rather than cardiorespiratory fitness, whereas fitness-targeted guidelines would place greater emphasis on vigorous exercise and interval training.

So this sounds like another argument for “high-intensity interval training,” which is already getting lots of press. But Williams makes a further distinction. These days, most experts are touting the time-saving benefits of interval training — i.e. get all the benefits of a 45-minute run by doing four 30-second spurts on an exercise bike. Instead of using intervals (and other forms of vigorous training) to reach the same fitness level in less time, he argues, we should spend the same amount of time and reach higher fitness levels. Want motivation? Here are the graphs of relative risk,for speeds ranging from slower than 51 minutes for 10K on the left to faster than 35 minutes on the right:


Cramps: training, pacing, genetic factors and pickle juice

July 8th, 2010

I’m back from a really incredible hiking trip in Papua New Guinea, during which I sweated out buckets of fluid but didn’t develop any muscles cramps… which brings me to the Jockology column in today’s Globe and Mail.

Back in April, I blogged about an interesting study reporting that pickle juice made muscle cramps disappear more quickly than water — an inexplicable finding if you subscribe to the theory that dehydration and/or electrolyte losses cause muscle cramps. Since then, another interesting study from the same group has appeared, and I also had the opportunity to visit the lab of Martin Schwellnus at the University of Cape Town, who proposed a different explanation for cramps a little over a decade ago. Today’s column takes a look at the evidence for Schwellnus’s “altered neuromuscular control” theory of muscle cramps.

If you’re already familiar with the theory, the most interesting new bit of data in the article comes from a new study that Schwellnus hasn’t published yet:

Interestingly, Dr. Schwellnus’s study of triathletes found that those who developed cramps had set higher pre-race goals and started at faster paces relative to their previous best times compared with non-crampers. And in a further study that has not yet been published, he found that crampers tend to have trained more in the final week before the race and have elevated blood levels of enzymes related to muscle damage before they start. [read the whole article…]

In other words, you may have set the stage for your muscle cramp by not resting enough before a race, and by starting too fast relative to your training. It’s likely a result of several different factors coming together, including genetic predisposition — but for those who are cramp-prone, the overtraining link offers something concrete that you can try changing before your next competition.