Does running harden your arteries?

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An article in the Wall Street Journal reports on a recent conference presentation that found higher rates of atherosclerosis - hardening and narrowing of the arteries - in competitive masters athletes running more than 35 miles a week or cycling more than 93 miles a week compared to those running less or not at all.

The first thing to note is that this is a conference presentation that hasn’t yet been published or peer-reviewed. It was presented at the European Society of Cardiology conference in August 2015; I initially figured that I’d hold off on writing about it until the results are published, since not all the methodological details are available and these analyses sometimes change quite drastically by the time they’ve been peer-reviewed. However, now that it’s making the rounds, I’ll add my two cents.

The WSJ article gives the study details. In brief, researchers at hospitals in London studied a group of 169 serious masters runners and cyclists. Their average age was 54, and they trained for an average of 7.7 hours per week and had been training for an average of 31 years - a pretty hardcore group, in other words. These athletes were compared with mostly sedentary controls matched for age, sex, ethnicity and heart disease risk factors like blood pressure and cholesterol (more on that below), but got only 90 minutes of exercise a week on average.

The headline result is that the male athletes had more evidence of coronary artery disease. Moreover, there was a dose-response relationship between artery calcification and mileage: those running less than 35 miles a week had healthier arteries, while those running more than 35 miles a week seemed to have less healthy arteries than the controls.

So the first point to note is that... this is progress! A few years ago, the claim (also reported in the WSJ) was that running just 20 miles a week would put “one running shoe in the grave.”

In all seriousness, the new study appears to be a well-done study, and the authors have been careful to present the results in context. We should all be interested in finding out how various doses of exercise affect our cardiac health, so this is important research. But it’s also important not to leap too far ahead to conclusions based on proxy measures of health.

For example, the study’s main outcome measure is artery calcification, which indicates how much your arteries are hardening and narrowing, and is thus a risk factor for heart attacks and strokes. But calcification is only part of the picture: if you have plaques building up in your arteries, the actual risk depends on what type of plaque it is.

Here’s what Ahmed Merghani, the cardiologist who presented the findings, said at the conference: “For me, the plaque morphology and what a plaque looks like is more important than the presence or absence of atherosclerosis. Because different types of plaques relate (to) different prognoses. So if you’ve got a plaque which is rich in calcium, this is a stable plaque. But if you’ve got a plaque which is soft and full of lipids, then this can later fissure and cause problems.”

So the logical next question is: did runners and non-runners have the same type of plaques in their arteries? The answer is an emphatic no. The male runners were vastly more likely (more than 70 per cent) to have stable plaques, while the male non-runners were vastly more likely (around 70 per cent) to have unstable or mixed plaques. For females, both runners and non-runners had mostly stable plaques.

It’s clear, in other words, that long-term, high-level endurance training has effects on the structure of the cardiovascular system: marathoners are different. But we need to be cautious in assuming that the differences are good or bad in terms of overall health outcome.

Another minor point I wanted to mention is that, as noted above, the sedentary control group was matched to have roughly the same cardiovascular risk factors as the running group, meaning that they had similar blood pressure and cholesterol. There are, of course, logical reasons for doing this, to ensure you’re comparing apples to apples. Still, it makes me wonder whether this produces an unusually healthy control group: after all, these people somehow have the same cholesterol as the runners, even though regular exercise is known to lower cholesterol. This has been a serious issue in some of the previous “too much exercise” studies.

It’s also worth looking more broadly at the determinants of cardiovascular health. Plaques that partially block arteries are certainly a concern; but long-term exercisers actually have coronary arteries that can dilate significantly more than non-exercisers. In fact, as Michael Joyner pointed out in an email, the autopsy of Clarence DeMar (“Mr. Marathon”),published in the New England Journal of Medicine in 1961, found that though he had some mild atherosclerosis, his coronary arteries were actually two or three times wider than normal!

Similarly, research by Ben Levine and his colleagues has shown that committed masters athletes have more compliant and less stiff hearts than both sedentary controls and casual exercisers.

The point here isn’t that everyone can cherry-pick the study that supports their pre-existing view (though that’s certainly true); it’s that isolated measurements of imperfect risk factors don’t give the whole picture. If you take a more global measurement like aerobic fitness (i.e. VO2 max), the picture that emerges is pretty simple: the fitter you are, the lower your chance of dying in any given period of time. To me, that’s the outcome that matters most.