This transcript has been edited for clarity.
Rachel Lampert, MD: We all know that exercise is good for whatever ails you, but can there be too much of a good thing? Many prior epidemiologic studies have suggested that those performing endurance exercise at the highest level may actually have an increased incidence of atrial fibrillation (AF). This has been termed the reverse J-shaped curve.
Hi. I’m Rachel Lampert. I’m a professor of medicine at Yale University, an electrophysiologist and the director of Sports cardiology. Today we’re going to be talking about the topic of AF in elite athletes, and I’m really pleased to be talking to you today about a landmark study on this subject that came out in the European Heart Journal.
Exercise and the Reverse J-Shaped Curve
A sedentary lifestyle increases your likelihood of hypertension, coronary artery disease mortality, and for today, AF. Increasing your exercise level decreases the likelihood of developing these outcomes.
And for the most part, the effect of exercise is graded. As exercise levels increase, cardiac events decrease.
But can there be too much of a good thing? Many prior epidemiologic studies, such as in cross-country skiers in Scandinavia, have suggested that those performing endurance exercise at the highest level may actually have an increased incidence of AF — what has been termed the “reverse J-shaped curve” in this and other papers. Experimental studies such as the one shown here in goats have suggested that endurance exercise may facilitate AF in those who are vulnerable.
The ProAFHeart Study
The recently published ProAFHeart Study by Andre La Gerche’s group in Australia provides the strongest, most detailed, and most rigorous data to date that extreme levels of endurance exercise increase the likelihood of AF and starts to elucidate the reasons why.
The investigative team recruited 121 elite rowers aged 45-80 who had competed in national or world competitions, including 23 former Olympians. With the assistance of the Australian national rowing organization, the rowers underwent extensive evaluation including exercise history, review of medical records, ECG monitoring, cardiac MRI, and genetic testing.
They were compared to a control group that was drawn from UK Biobank participants who had previously undergone similar testing at a 1-to-100 ratio of athletes to controls. Atrial fibrillation prevalence was significantly higher among the former elite athletes, at 21.5%, than among the controls, at 3.2%.
To me, this seemed almost too big a difference to be true until I remembered a patient I saw a couple years ago. A mid-70-year-old former collegiate crew athlete from Yale, where I work, upon presenting with AF, told me he was not surprised since every other member of his collegiate eight already had it. I think he thought it was contagious.
Importantly, to exclude the possibility of enrollment bias — that is, were former rowers with AF more likely to choose to participate in the study? — the investigators also did a sensitivity analysis among 201 former rowers from the national organization who could have participated, assuming that they all did not have AF. They still found an increase in AF in the rowers. Among those who did not have a history of AF at baseline, incidence over 4 years was twice as high in the rowers compared with the nonrowers.
So how much of this difference is environmental due to long-term exercise and how much is genetic? Surprising to me, the rowers and the nonrowers had similar rates of diabetes and hypertension, both common risks for AF. On imaging, the left ventricular volume was larger in the rowers reflecting adaptation to long-term endurance exercise.
They were also more likely to have prolongations in their conduction with prolonged PR, QRS, and QT intervals, all normal adaptations to endurance exercise. While all of these features were associated with AF in the nonrowers, they did not differentiate the rowers with AF from the rowers without AF.
Genetic Vulnerability to AF
Why did some of the rowers get AF while others did not, despite similar degrees of structural and electrical adaptation to exercise?
To address this question, the investigators looked into their athletes’ genes. Specific monogenic variants, which have been shown to be associated with AF, were seen very rarely in both the rowers and the nonrowers.
This was not surprising because in the general AF population, these monogenic variants are much more often seen in those under 30 years old, in whom AF is rare rather than in the middle aged, such as the group in this study, in whom AF is more common in general. Unlike the authors of the study, I don’t think these data really address genetic testing in the young athlete with AF one way or the other.
However, in this group of middle-aged athletes, the investigators found that a high polygenic risk score was highly predictive of the development of AF: quadrupling the risk in the rowers and doubling it in the nonrowers.
To sum up, this landmark study, in addition to increasing our understanding of how and why elite endurance athletes are more likely to have AF, is an elegant example of the interplay between nature and nurture. It’s a combination of genetic vulnerability with the superimposed environment of endurance exercise that increases the likelihood of AF.
Treating AF in the Athlete
What should an elite athlete do to avoid or treat AF? One answer could be to retire. In this study among those without a history of AF at baseline, the rowers who had retired were much less likely to get AF moving forward than those who continued to row.
However, the incidence is still not that high, and another option is to continue and if AF develops treat it. Last year, the Heart Rhythm Society published a consensus statement on the treatment of arrhythmias in the athlete.
There’s always the choice to detrain. In a recent survey we did of a thousand middle-aged athletes with AF, detraining was completely or partially successful in some, although not all, athletes.
There’s an ongoing randomized clinical trial, NEXAF, looking into this question that has many of the same investigators who did this landmark European Heart Journal study.
Medications can sometimes work, but only in about half of AF patients in general, and in our survey, adverse effects were often reported by the athletes.
Finally, an ablation procedure can be an excellent choice. While there’s not 100% success with ablation, many studies have shown that ablation works just as well in athletes as in nonathletes.
Since none of the treatment choices impact mortality, it’s a shared decision about quality of life and more data are needed on best treatments for AF in athletes.
We look forward to hearing more from this group as well as others. Signing off for now, Rachel Lampert.