On 1 July 2023, as Tour de France riders pedaled out of Bilbao, Spain, toward the French Pyrenees mountains, sports cardiologist Andre La Gerche tuned in from Melbourne, Australia. “It’s exciting watching the screen and knowing the engines”—the hearts powering the cyclists forward, says La Gerche, who works at the St. Vincent’s Institute of Medical Research and the Victor Chang Cardiac Research Institute. Five of the cyclists who won daily stages early in the race are also participants in an ambitious study, led by La Gerche, of the effects of endurance exercise on the heart. These include powerful protection against heart disease—but also the potential, in some endurance athletes, to bring on a troublesome arrhythmia called atrial fibrillation (AF).
Most AF patients are older than 65 and have known risk factors, particularly high blood pressure, obesity, and sleep apnea. Why cyclists, runners, and other athletes in otherwise impeccable health are sometimes at risk is poorly understood, and could involve both genetic factors and exercise-related remodeling of the heart and its electrical rhythms. La Gerche and others are now studying this paradox. Not only could such work help affected athletes, but it also offers the chance to study AF without the confounding effects of other health concerns, says exercise physiologist Jack Goodman of the University of Toronto.
The efforts are important because AF represents a “burgeoning epidemic,” driven largely by obesity and an aging population, says Mina Chung, a cardiac electrophysiologist at the Cleveland Clinic. It affects more than 5 million people in the United States alone, and the global prevalence is expected to double from 2010 to 2030, she says.
In AF, the upper chambers of the heart, called the atria, beat erratically and at runaway speeds, out of sync with the lower chambers. The condition can cause fatigue, fainting, chest pain, and other symptoms, and it comes with more serious hazards when it persists long term. Last month, a study from Denmark reported that about 40% of people in that country with AF eventually developed heart failure and 20% suffered a stroke, caused by blood clots that form when the atria don’t pump properly. Treatment, which includes blood thinners and other drugs as well as a procedure that destroys heart tissue fueling abnormal activity, is often not a cure.
For years, doctors have urged both their sedentary AF patients and those at risk to get moving. Activity is a potent force for good, reducing the heart’s stiffness, improving blood flow, and promoting electrical stability—all of which likely help prevent and manage AF, says Adrian Elliott, a cardiac physiologist at the University of Adelaide. But studies over the past 2 decades suggest it may be possible to get too much of a good thing: Engaging in intense exercise over many years may itself tip the heart into an unhappy electrical state, giving some athletes a risk of AF as much as five times higher than nonathletes the same age. Most studies show endurance athletes develop AF later in life, though in some cases it can turn up during their sporting careers, Elliott says.
Until recently, women athletes were rarely studied and considered potentially exempt from AF risk. But a handful of recent papers are overturning that assumption. A study published in July 2023 in the British Journal of Sports Medicine put the risk for women athletes at three to five times that of nonathletes, which is “similar to men,” says Nikola Drca, the lead author and a cardiac electrophysiologist at Karolinska University Hospital. Still, he cautions, the study was small, with only 10 AF cases diagnosed among the 228 Swedish women endurance athletes.
La Gerche’s study, called Pro@Heart, is among the largest efforts to learn more. It launched in 2016 with collaborators in Australia and Belgium and so far includes nearly 500 elite athletes who were between 16 and 23 years old when they enrolled. The study aims to follow them for at least 25 years and track changes to the heart, including in its size and electrical conduction patterns. A separate arm is exploring AF prevalence and susceptibility in 128 former elite competitive rowers between the ages of 45 and 80, along with a matched comparator group of people who are not competitive athletes.
It’s already known that the heart gets larger in endurance athletes. MRI scans during exercise in the younger Pro@Heart cohort have also shown some athletes’ hearts “are so large that [they get] pushed up against the chest wall and the spine,” says La Gerche, who wonders whether that friction could cause cardiac inflammation. Such inflammation has long been eyed as a potential AF driver, and it can also arise from conditions such as diabetes and obesity. La Gerche’s team, which also includes Elliott, will track whether there’s rubbing of the atria against the spine that leads to inflammation and later AF.
Pro@Heart’s older cohort, the retired rowers, has a startling rate of AF: 20%, compared with 3% in the control group. Elite rowers may have a higher AF risk than some other endurance athletes—perhaps because the sport attracts taller people. Height is a documented AF risk factor, though the reasons are still being explored. Another factor may be that rowers routinely train as much as 20 or 30 hours a week. “How much exercise is too much?” Goodman wonders.
The answer isn’t clear, and it likely depends on other factors, including genetics. With a $14 million, 5-year grant from the National Institutes of Health, Chung and her colleagues are exploring which genes might set the stage for the disease in the general population and are looking for potential drug targets. Another study, launched last year by pediatric cardiologist Greg Webster at the Ann & Robert H. Lurie Children’s Hospital of Chicago and his colleagues, will hunt for genetic variants linked to AF in people who develop it while still extraordinarily young, before age 35, and probe how those variants contribute. “It can lend an understanding of the broad spectrum of disease, if you know what happens at the extremes,” Elliott says.
What to advise endurance athletes with AF is unclear. Many aren’t comfortable with standard medicines. Blood thinners reduce stroke risk but also heighten bleeding if athletes fall off their bike or while running or skiing; beta blockers, prescribed to slow a racing heart, can reduce performance.
One common prescription for athletes with AF is to pare back physical activity. Marius Myrstad, an internal medicine doctor who studies and treats AF at Baerum Hospital, recently launched the first trial to see whether that’s good advice—especially given that exercise has many benefits, too. The researchers will randomize 120 athletes with AF who run at least 5 hours or cycle at least 8 hours a week to either continue their regimen or reduce its intensity and shorten it by about 20%. Heart monitors implanted under participants’ skin and training watches will track the number and duration of AF episodes in the two groups.
These athletes “really don’t want to stop competing or stop training” if they don’t have to, Myrstad says. “It’s the most natural thing to ask the patient in front of you, ‘Do you have to run this marathon? Can’t you just reduce the training?’” he says, “but I’m not sure it’s right.”
More: https://www.science.org/content/article/why-are-elite-athletes-prone-abnormal-heart-rhythms
