If you give an identical training program to 10 different runners, you’ll get 10 different results—even if they all start from the same baseline and follow the training program faithfully. This idea of genetic variation in the response to training has been discussed a lot over the past few years, thanks in part to books like David Epstein’s The Sports Gene.
There’s another aspect of genetic variation that gets less attention, though in some ways it’s just as important to runners. If you give 10 people the same training program, after a certain period of time some will be injured and others won’t. What determines who gets injured and who doesn’t?
When I write about running injuries, I like to cite one of biomechanist Benno Nigg’s claims, which is that training decisions—or more to the point, training errors—explain about 80 per cent of running injury risk. The precise number isn’t important, but running too far, too fast, too soon, and not allowing enough recovery are often more important than, say, what shoe you’re wearing.
But there’s an emerging body of research suggesting that even if you eliminate all the variation in training decisions, shoes, running routes, and so on, some people are more susceptible to injury than others. A new review in the British Journal of Sports Medicine, from Malcolm Collins and his colleagues at the University of Cape Town, sums up what’s known about the genetic factors that affect risk for tendon and ligament injuries.
The research at this point is fairly preliminary, but there have been some interesting studies identifying, for example, specific gene variants that affect risk of Achilles tendinopathy. In one cohort, those with a particular variant of the COL5A1 gene were 58 per cent less likely to develop Achilles tendinopathy. A different gene, COL1A1, is associated with Achilles tendon and ACL ruptures, and several other genes have been associated with injuries ranging from tennis elbow to carpal tunnel syndrome.
The common link among these genes is that they affect the structure of collagen fibrils, which are “the basic structural components of tendons, ligaments and other connective tissue structure.” In other words, some Achilles tendons are simply built better than others.
So what do we do with this information? The review notes disapprovingly that a number of direct-to-consumer genetic tests are now being marketed, promising to reveal potential injury susceptibilities. This is bad, they say, because the data are “not interpreted together with clinical indicators and lifestyle factors to identify an altered risk for injury by an appropriately qualified healthcare professional.”
I’m a little torn on this. I do tend to share their overall skepticism of these sorts of consumer tests, but not necessarily because of the lack of clinical context and professional advice. If there’s a gene variant that changes the risk of Achilles problems by even 10 or 20 per cent, that does seem potentially interesting to know if you have it. (As for 58 per cent, that’s huge—but I want to see more replications before I put too much faith in that number.)
To me, the question is: what does knowing that change? For a competitive athlete, my assumption is you train as hard as you can handle without getting injured. That’s such an inexact science that knowing that you’re 10 percent more or less likely to get a tendon injury seems unlikely to alter your day-to-day decisions. If you’ve been training for any length of time, you’ll know what injuries you’re susceptible to because you’ve already had them!
On this note, the review concludes by “reminding” clinicians that you don’t need genetic data to figure out if someone is vulnerable to certain types of injuries. Among the questions they suggest asking is whether you have a family history of tendon or ligament injuries. That’s standard practice for evaluating risk of things like heart disease, but I hadn’t really thought about it for running injuries. It’s low-tech, but maybe it’s enough.
