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There’s no doubt running changes your heart. Like all muscles, it adapts to the stress of any regular endurance exercise. Whether these adaptations are good or bad has been debated for over a century. Recently, the occasional tragic death at a major marathon and periodic sensationalist headlines have caused concern, but rest assured that in the current view of medical science the obvious changes are, at worst, harmless. Runner’s enlarged heart? That’s stronger muscle and bigger chambers to pump more blood, not a sign of heart failure. Low resting heart rate? It’s not a sign of an arrhythmia (irregular heart rhythm), as it is in non-runners; it’s just that each contraction pumps so much blood that the heart doesn’t need to beat as often.

In recent decades, the debate about running and cardiac risk has focused on sudden deaths at endurance races. In 1977, Dr Paul Thompson a cardiologist and 2:28 marathoner, was running San Francisco’s Bay to Breakers 12K when one such death occurred. The tragedy sent Thompson on a lifelong career path; he is now perhaps the world’s leading authority on the cardiac consequences of running. In 1979, Thompson published research on 18 men and women who died during or immediately after running, 13 of whom had heart disease. ‘Superior physical fitness does not guarantee protection against exercise deaths,’ he warned.

Related: Running: Heart Healthy or a Heart Risk?

Such deaths were incredibly rare in the 1970s, partly because running as a mass-participation sport was new. But as the global numbers of marathon finishers have grown exponentially, so, sadly, have the tragic deaths such as that of Captain David Seath at last year’s London Marathon. These incidents generate headlines and provide ammunition for those who argue that running is dangerous, but the truth is, when runners younger than 40 die during a race, it’s usually due to an undiagnosed genetic heart abnormality; when older participants die, they usually had pre-existing heart disease. Sometimes, there’s no explanation. Whatever the cause, the heart’s electrical system goes haywire, causing an arrhythmia called ventricular brillation, in which the heart stops pumping blood.

If that were the whole story, the case against running would be easily dismissed. Yes, vigorous activity temporarily raises your risk of cardiac arrest. But regular exercise has such a dramatic effect on other cardiac risk factors such as blood pressure, obesity and cholesterol, that its protective benefits during your non-exercising hours swamp any risks during exercise.

That’s not the whole story, though. Recently the discussion has focused less on sudden deaths, and more on the possibility that decades of running can cause wear and tear on your heart. According to this theory, each marathon pushes your heart a little beyond its limits, and over time all the vigorous beating leads to fibrosis, or scarring. That fibrosis, along with other damage, might lead to atrial fibrillation (rapid and irregular heartbeat). And the turbulent flow of blood through your coronary arteries during running might contribute to the formation of artery-clogging plaques, raising heart attack risk.

This means, in theory, that long-term runners should be less healthy and long-lived. It’s only now, four decades after the first running boom, that we have large numbers of people entering their retirement years having run for most of their adult lives. And their mortality statistics reveal that – well, interpreting those stats is what scientists have been arguing about, the media have been sensationalising, and non-running colleagues have been lecturing you about.


This debate erupted at the 2012 American College of Sports Medicine (ACSM) meeting in San Francisco. Epidemiologist Dr Duck-chul Lee presented an analysis of more than 50,000 patients who had visited the Cooper Clinic in Texas between 1971 and 2002, including 14,000 regular runners. The good news: 15 years after their initial visits, the runners were 19 per cent less likely to have died than the non-runners. The bad news: those benefits accrued primarily to those running less than 20 miles per week. Those who ran more were statistically no better off than non-runners.

Related: Here's why all runners should know how to do CPR

Shortly afterwards, cardiologist Dr James O’Keefe published a review in the Mayo Clinic Proceedings, summarising the potential negative cardiac effects of too much running: fibrosis, calcified arteries, arrhythmias. It was a potent combination-punch: O’Keefe’s paper explaining what could go wrong and Lee’s data seemingly providing evidence that it was happening. News outlets around the world picked up the story, amplified on social media by a mix of fear and schadenfreude: ‘You smug runners still think you’re so healthy, eh?’

Later in 2012, O’Keefe and cardiologist Dr Carl J Lavie argued in the journal Heart that vigorous exercise should be limited to 30-50 minutes a day. ‘In contrast,’ they wrote, ‘running too fast, too far and for too many years may speed one’s progress towards the finish line of life.’ Again, this was catnip to headline writers. That pattern recurred over the next few years: between 2012 and 2015, O’Keefe alone wrote more than a dozen academic publications about the dangers of excessive endurance training, mostly referring to the earlier research. With repetition, the headlines became increasingly familiar and the claims began to feel like fact.

But the evidence was still very much in dispute. The next study to garner headlines about the risks of running, from researchers in Copenhagen, drew conclusions from just two deaths among ‘strenuous’ runners – a statistically dubious claim that incited an avalanche of criticism. Lee’s data from 2012, though frequently cited as evidence of running’s deadly potential, still hadn’t gone through peer review to be published in an academic journal. In a 2013 response to O’Keefe and Lavie’s Heart editorial, cardiovascular researcher Dr Thomas Weber pointed out a flaw in Lee’s statistical analysis: The researchers had ‘adjusted’ the data to eliminate differences in body mass index, blood pressure and cholesterol levels – the risk factors that running would be expected to lower. ‘This represents a selective interpretation of the data, at the best,’ wrote Weber.

"The fruits of the debate are 'intellectually interesting, clinically worth knowing, but not worth worrying about"

Weber highlighted a major challenge of this type of research: how do you compare groups of people with widely differing behaviours and physical characteristics? ‘Statistical adjustment’ was used to correct for these differences in the Cooper Clinic subjects, in effect allowing them to compare groups as if everyone had the same age, smoking history, etc. But this breaks down when the differences between the groups are a direct consequence of the behaviour you’re studying. Comparing death rates of smokers and non-smokers, you might find smokers have higher rates of lung cancer. But it would be wrong to ‘statistically adjust’ the results to make the group’s rates of lung cancer equal, because smoking causes lung cancer, which, in turn, raises death rates. The difference in lung cancer rates isn’t a fluke to be brushed aside; it’s the whole point! Similarly, running is known to lower BMI, blood pressure and cholesterol levels, which lowers heart disease risk. By equalising these parameters, the researchers were in effect saying: if you ignore the known health benefits of running, running has no health benefits.

Lee and his colleagues finally published their peer-reviewed Cooper Clinic data in 2014, with no statistical adjustment and a very different message. Instead of warning about the dangers of running more than 20 miles a week, they emphasised the dramatic reduction in risk of dying from heart disease from running just five to 10 minutes a day. Running further they said, didn’t offer further benefits, but neither did it make things worse. Media reaction was muted. ‘The press loves the “exercise is bad” story,’ says Lavie. ‘We wanted to emphasise that even a little running is good.’ Still, the debate was far from over.


On the first day of 2016’s ACSM conference, the world’s leading experts gathered for a symposium called ‘Optimal Dose of Running for Health: Is More Better or Worse?’. Lee, Lavie and Thompson were joined by Dr Paul Williams, a biostatistician whose research on runners has been following 156,000 men and women since the early 1990s. Lee emphasised the benefits of just a little vigorous exercise (five to 10 minutes a day). He also said that even in the very top mileage subgroup of his subjects, there was no statistically significant increase in cardiac risk. ‘It doesn’t support that more is worse,’ Lee said. ‘But more may not be better.’

Williams argued that more really is better. His 156,000 subjects, many initially recruited from Runner’s World subscribers in the US, walk or run 156 million miles per year, giving him masses of data. He has published 65 studies on how running affects conditions ranging from diabetes to cataracts, Alzheimer’s and breast cancer. In nearly every case, not only does running help, but more is better. For example, men running at least 40 miles a week were 26 per cent less likely to develop coronary heart disease than those running 13. Why the apparent contradiction with Lee’s results? Williams permitted himself a smile when the question was posed during the Q&A session. ‘At 156,000 subjects, we’re bigger than they are,’ he said. ‘So I’ll stand behind our data.’

While that data is reassuring for most runners, it doesn’t tell us much about those at the extremes of the distance curve. For them, we need to look at what changes and what potential warning signs appear in their hearts after decades of training. Later at the conference Lavie and Thompson offered the cardiologist’s perspective on these changes.

The most well documented risk is atrial fibrillation, the most common of the irregular or abnormal heart rhythms known as arrhythmias. Studies have linked atrial fibrillation to cumulative years of exercise. While the condition can raise stroke risk when combined with other risk factors such as high blood pressure, it’s generally more inconvenience than imminent threat. Not everyone agrees running is a risk factor – in Williams’ data, those running 39+ miles per week were least likely to report cardiac arrhythmias – but Thompson and many others are convinced it is.

Related: 5 facts about a runner's heart

More concerning is the possibility that high doses of exercise cause atherosclerosis, as calcium-rich plaques accumulate in the arteries leading to your heart. This was diagnosed in 1968 Boston Marathon winner Amby Burfoot. The resulting narrowed, stiffened arteries can reduce blood supply to the heart, or a plaque can rupture, triggering a heart-attack-inducing blockage. It’s possible that the rush of blood through these arteries during exercise accelerates plaque formation, or that exercise alters hormone levels associated with plaques. It’s also possible people who run most are different in other ways, Lavie noted: ‘They may have extreme personalities, so they’re always mentally stressed, sleep-deprived and so on.’

Even less clear is whether plaques in marathoners’ arteries pose the same risks as plaques in non-runners. Denser plaques actually lower heart disease risk, Thompson said, and there’s mounting evidence that marathoners tend to have dense, stable plaques that are much less likely to rupture and cause a blockage. Data presented by researchers from various London hospitals to the European Society of Cardiology in 2015 showed long-term runners had more highly calcified arteries if they clocked 35+ miles a week. But more than 70 per cent of plaques in male athletes were dense, stable plaques, compared with just 30 per cent in non-athletes. ‘For me,’ says cardiologist Ahmed Merghani, who led the study, ‘what a plaque looks like is more important than the presence or absence of atherosclerosis.’

Perhaps the most controversial topic is fibrosis, patches of scar tissue that may accumulate in the heart and could contribute to other conditions, such as atrial fibrillation. In 2011, UK researchers examined the hearts of 12 veteran athletes who had been training hard for an average of 43 years and had completed an average of 178 marathons, 65 ultra marathons and four Ironman triathlons each. Half of them showed signs of fibrosis – ‘an unexpectedly high prevalence’. In contrast, last year, German scientists assembled 33 equally remarkable masters endurance athletes, with an average age of 45 and including former Olympians, a marathon champion and Ironman winners, and found no evidence of exercise-induced fibrosis. Thompson’s take: The phenomenon is probably real, but very rare.


All this is pretty confusing. The hearts of longtime runners are different, it seems, but the consequences are unclear. More clarity would come from a clinical trial in which people were assigned to run various weekly distances for decades. ‘But that’s impossible,’ says Lavie. And so we are stuck making our decisions with imperfect information.

l be left to roll the dice, as we do in countless decisions every day. What if it turned out that running 40+ miles a week would extend life by two years for 99 per cent of people, but shorten it by 10 years for the other one per cent? Would you carry on? Such decisions are deeply uncomfortable, which is why we avoid thinking about them when we, say, take an antibiotic or step outside on a sunny day. That’s why, for Thompson, the fruits of the debate are ‘intellectually interesting, clinically worth knowing, but not worth worrying about’.

That would change if we could work out, in advance, who is among the 0.1 per cent with a vulnerable heart. We know that rare heart conditions are associated with certain genetic defects, and those with the defect are more likely to develop the disease if they exercise a lot. The same may turn out to be true for fibrosis and atrial fibrillation: exercise raises your risk, but only if you already have a genetic predisposition. ‘This is a potential game-changer,’ says Thompson of the future prospects of genetic testing. That doesn’t mean people with the wrong genes can’t run, but they’ll understand the risks and perhaps run 10Ks rather than 100-milers.

By the end of the conference, I’m feeling good about my running. With two young kids, I’m lucky to log 30 miles in a week and my racing is limited to 5Ks and 10Ks. But I dream of mountain ultras. This debate reminds me not to assume I’m invincible – to be aware that my arteries could get clogged or my heart could go haywire. Whether or not running raises or lowers the risk, being aware will help me watch for warning signs.

For now, even Lavie is loathe to discourage anyone from running. ‘I don’t think the data is nearly enough to say, “Stop at 30 miles per week,”’ he told me after his talk. He wants people to understand that running’s health benefits can come from as little as five or 10 minutes a day, that you don’t need to be a marathoner to be healthy, and that pushing to extremes may even whittle away some of those benefits. If you’re older and have other risk factors for heart disease, he might suggest an exercise stress test and coronary artery calcium testing, or statins to lower cholesterol. ‘If someone is running 40 miles per week, I ask what their purpose is,’ he says. ‘If they love it, I’m not going to try to scare them.’

I’m surprised. Having read the scary headlines, I’d expected to meet an anti-running crusader. But that’s not Lavie. He runs for 45 minutes on most days, logging over 30 miles a week. And once he’s out on the roads, he’s no longer thinking about his heart. ‘I feel better. I’m able to eat more,’ he says. ‘But mostly, I enjoy it.’


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