Bradycardia in Athletes: Prevalence, Mechanisms, and Risks

Sinus bradycardia is a well-recognized physiological adaptation in endurance athletes, primarily attributed to sinus node remodeling or increased vagal modulation. Although genetic influences on resting heart rate (HR) have been observed, the genetic contribution to athletic bradycardia has not been elucidated.

We phenotyped current and former elite endurance athletes in the Pro@Heart cohort study using multimodal cardiac imaging, cardiopulmonary exercise testing, and Holter monitoring. Genetic susceptibility to bradycardia was assessed using a validated HR-associated polygenic risk score (HR-PRS), in which lower scores are associated with a lower HR, and compared with healthy nonathletic controls. Clinical and genetic features of bradycardic endurance athletes with minimum HR ≤40 bpm on a Holter monitor (bradycardic athletes [BAs]) were compared with non-BAs). A healthy cohort of nonathletes from the ASPREE study (Aspirin in Reducing Events in the Elderly) were used for genetic comparisons.

Among 465 endurance athletes (median age, 23 [18-49] years, 75% men), 175 (38%) had a minimum HR on a Holter monitor ≤40 bpm, of whom 7 (2% of total) had a HR ≤30bpm. Pauses ≥2 s were observed in 115 (25%) athletes, of whom 12 (3% of total) had pauses ≥3 s. Mobitz I second-degree atrioventricular block was observed in 15 (3% of total) athletes. BAs were younger and fitter and exhibited greater athletic cardiac remodeling than non-BAs. Mean HR-PRS was significantly lower in all athletes compared with ASPREE nonathletes (P<0.001) and in BAs compared with non-BAs (P=0.006). When the distribution of HR-PRS within our athletic cohort was considered, athletes with scores in the bottom quartile had a lower minimum HR (median HR, 41 [35-45] bpm versus 45 [40-49] bpm, P<0.001) and higher bradycardia burden (14 [2-37]% versus 2 [0%-25]%, P<0.001) than those with scores in the top quartile. After adjusting for age, sex, fitness, and indexed right atrial volume, HR-PRS was independently associated with lower minimum HR and increased the odds of resting bradycardia by 2-fold (odds ratio [OR], 2.2 [95% CI, 1.3-3.9]; P=0.004). Neither bradycardia nor pauses were associated with increased risk of adverse outcomes over 5.5 years.

Resting bradycardia (HR ≤40 bpm) and pauses of 2 to 3 s are present in a significant proportion of endurance athletes and are well tolerated. Our data suggest that both fitness and genetic variation contribute to sinus node function in endurance athletes. Intriguingly, HR-PRS differed between athletes and nonathletes, raising the possibility that genetics may be a determinant of athleticism.