Exercise linked to 22% lower odds of atrial fibrillation, with higher odds only at very high training loads

Exercise goes with better heart health on most of the measures that have been studied, with one exception that has puzzled cardiologists for years: endurance athletes seem to get more atrial fibrillation, a common rhythm disorder, than people who do no sport at all. A new analysis has tried to find where on the scale of exercise the benefit gives way to that extra risk.

Pooling 37 studies of nearly 1.3 million people, it found that ordinary physical activity went with 22% lower odds of atrial fibrillation, and that the lowest odds came at a moderate dose. Higher odds appeared only beyond a level the authors equate to 6 to 7 hours of endurance training a week. That threshold comes from studies that watched people rather than from experiments, and those studies differed widely from one another.

Why exercise and atrial fibrillation is debated

Atrial fibrillation is an irregular and often fast heartbeat that starts in the upper chambers of the heart. A research group that pooled earlier studies calls it the most common arrhythmia worldwide, meaning the most common disturbance of heart rhythm, and ties it to more illness, more deaths and a poorer quality of life.

For most heart conditions, more exercise goes with less disease, but for this one the record has been mixed. A 2021 analysis in Heart Rhythm opened by saying that the part physical activity plays in atrial fibrillation risk is less well established than its part in preventing other heart disease.

The authors of the new paper lay out the same puzzle: regular activity may lower the risk in the general population, while the people who exercise the most may exhibit a paradoxical rise in it. In a conference version of the work, published earlier, the team noted that this pattern is usually termed the extreme exercise hypothesis.

What nobody had pinned down was where the line turns. Researchers call a plot of the odds against the weekly amount of exercise a dose-response curve, and the paper says the point at which the curve reverses remains unclear.

Part of the problem was how earlier work had been organized. Pooled analyses, which combine the results of many earlier studies, had typically looked at the general population and athletes separately, the conference abstract noted. With recreational exercisers in one pile and athletes in another, there was no single scale on which to find a crossing point.

How the atrial fibrillation analysis worked

A team with C. L. Davies as first author and G. P. McCann as last author published the analysis on October 9 in the European Journal of Preventive Cardiology. They searched four databases for studies from January 1990 to June 2025 and kept those that compared physical activity against a sedentary control group, meaning inactive people, and that measured either incidence, the new cases arising over time, or prevalence, everyone who has the condition at one moment.

In the end 37 studies were included, covering 1,298,291 people: 22 looked at physical activity in the general population and 15 compared athletes with non-athletes.

To put a weekend walker and a marathon runner on one scale, the team converted every study’s measure of activity into a single unit built on the metabolic equivalent of task (MET), the energy a person uses sitting quietly. An activity rated at 8 METs burns eight times that, and an hour of it counts as 8 MET-hours, so a week of exercise becomes a number of MET-hours per week. The conference abstract says the conversion relied on the 2024 Compendium of Physical Activities, a standard reference table.

The analysis produced two kinds of result. One was a straight comparison of active with inactive people, and of athletes with non-athletes, expressed as odds (the chance of something happening set against the chance of it not happening). The other was the dose-response curve itself, fitted across the 26 studies, of 1,022,790 people, that gave enough detail on dose.

What the analysis found about activity and atrial fibrillation

In the general population, physical activity went with 22% lower odds of atrial fibrillation than being sedentary, with a range around that estimate from 11% lower to 32% lower. Among athletes the direction flipped: being an athlete was associated with an increase in the odds, to 2.74 times those of non-athletes, with a range from 1.72 to 4.39. That range is wide, a sign that the athlete studies disagreed with one another or were small.

The dose-response curve joined the two results into one shape. The greatest reduction in odds of atrial fibrillation came at a weekly total of 26 MET-hours, and past that point the benefit shrank. Beyond 78 MET-hours a week the odds were higher than in sedentary people, a level the authors equate to 6 to 7 hours per week of endurance training.

So the dose with the lowest odds is one third of the dose beyond which odds exceeded those of sedentary people. The authors describe the pattern as U-shaped, with odds high at both ends and lowest in the middle, and they hedge their conclusion: beyond the threshold, they write, the protective effect of exercise may reverse.

How firm is the number 78? The conference version of the analysis, published in June, had put the threshold at 73 MET-hours and the best range at 20 to 37, and described that threshold as 6 to 7 hours per week of high-intensity sport. The figures moved a little between the two versions. A curve fitted to several dozen studies gives a region where the line turns, and small changes in method shift it.

How earlier research on activity and atrial fibrillation compares

The lower-odds half of the curve matches earlier pooled work. The 2021 Heart Rhythm analysis combined 15 studies of 1,464,539 people and found that those who met the guideline level of activity, which it defined as 450 MET-minutes a week (7.5 MET-hours), had a 6% lower risk, with a range from 3% to 10%. On these figures, the level beyond which odds were raised in the new analysis is about ten times the guideline level.

That earlier curve stopped short of the new one. In the Heart Rhythm analysis, activity up to 1900 MET-minutes per week went with a lower risk, with less certainty beyond that level. That is about 32 MET-hours a week, close to where the new analysis puts the greatest benefit, and above it those authors could say only that the benefit is less clear at 2000 MET-minutes per week and beyond. The new analysis added studies of athletes to carry the curve further.

Single long-running studies have traced the same bend. The Tromsø Study in Norway followed 20,484 adults for 20 years and found that moderately active people had a 19% lower risk of any atrial fibrillation than the least active, a benefit the most vigorous exercisers did not share. Its authors described leisure-time activity as linked to atrial fibrillation in a J-shaped pattern, with higher activity levels weakening the benefits of moderate activity.

Sex may matter too. A pooled analysis of 23 cohorts, with 1,930,725 participants and 45,839 cases, found no overall difference between the most and least active people, but split by sex it showed a higher risk in men and a decreased risk in women. The lower risk in active people was also more marked in women in UK Biobank, a study of 402,406 people aged 40 to 69, followed for over 2.8 million person-years, which is the years of follow-up added up across all participants.

The athlete result has precedent as well. A 2021 analysis in the British Journal of Sports Medicine found that athletes compared with non-athlete controls had 2.46 times the odds of atrial fibrillation, with a range from 1.73 to 3.51. Its authors asked for future studies to measure risk by exercise dose, including training and competition history, which is what the new analysis attempts.

A Swedish study shows what the extra cases might mean in practice. It followed 208,654 people who had completed the Vasaloppet, a long cross-country ski race, and 527,448 matched non-skiers. Female skiers had a lower incidence of atrial fibrillation than female non-skiers, while the incidence in male skiers was similar to that of nonskiers. Among the skiers, incidence was highest in those with the most races or fastest finishing times.

The same study tracked strokes, the main danger of atrial fibrillation. Skiers of either sex had about a third lower incidence of stroke than nonskiers, although skiers who developed atrial fibrillation had more strokes than skiers who did not.

What may explain the link between heavy training and atrial fibrillation

The new paper is about dose rather than cause, but others have proposed explanations, cautiously. A 2018 review conceded that the mechanisms are not well understood. It pointed to exercise-induced changes in autonomic tone, the balance of the nerves that speed and slow the heart without conscious control, and to the development of an arrhythmogenic atrial substrate, meaning upper-chamber tissue that has changed in a way that makes rhythm problems easier to start.

The 23-cohort analysis suggested more candidates: increased vagal tone (a stronger brake from the vagus nerve, which slows the heart), bradycardia or a slow heart rate, increased volume load and stretch, and atrial fibrosis, which is scarring, along with inflammation. The idea is that years of heavy training load and stretch the upper chambers and slow the resting heart rate. These are proposals, and none was tested in the new analysis.

What the atrial fibrillation analysis cannot show

Association, not cause. Every study in the analysis observed people as they were. Active people differ from sedentary people in weight, blood pressure, smoking and much else, and the analysis cannot separate the effect of exercise from those differences.

Uneven studies. The conference version reported that results varied between studies far more than chance would explain, and that the athlete studies were of poorer quality than general population studies of physical activity. The authors wrote then that better studies, particularly in athletes, are required to confirm the result.

Self-reported exercise. Most large studies in this field ask people how much they exercise. In the 23-cohort analysis, all studies assessed physical activity through questionnaires that people filled in themselves, and converting such answers into MET-hours adds a further layer of approximation.

A threshold from a fitted curve. The figure of 78 MET-hours is where a statistical curve crosses a line, and it moved between the conference version and the published paper.

Prevalence as well as incidence. The analysis accepted studies that counted existing cases at one moment as well as studies of new cases. The first kind cannot show whether the exercise came before the rhythm problem.

No absolute risks. The pooled results are odds relative to sedentary people, so they do not say how many athletes in every thousand develop atrial fibrillation, or how that compares with the number who avoid other heart disease through training.

Whether a given training load is a concern for a particular person’s heart rhythm is assessed by their doctor.

Across 26 studies of about 1 million people, the odds of atrial fibrillation were lowest in the moderately active and higher only at very high training loads.