Author + information
- Salman K. Bhatti, MD,
- James H. O'Keefe, MD∗ ( and )
- Carl J. Lavie, MD
- ↵∗Saint Luke's Cardiovascular Consultants, 4330 Wornall Road, Suite 2000, Kansas City, Missouri 64111
We commend the efforts of Guasch et al. (1) in using an animal model to understand the association between atrial fibrillation (AF) and chronic high-level endurance exercise (EE). It is clear from their study that a complex interplay culminates in the increased prevalence of AF in individuals performing chronic excessive EE. Caution should be applied in extrapolating the results from an animal study to humans, but their compelling findings add to the growing body of literature that suggests that chronic EE may induce autonomic disturbances and atrial dilation/fibrosis, which might play a major role in the initiation of AF. Prior investigations have consistently found that autonomic perturbations involving fluctuations in sympathetic and/or parasympathetic tone immediately precede the onset of AF. The overall autonomic imbalance appears to be more important than vagal or sympathetic drive alone. In some extreme EE athletes, heightened baseline vagal tone increases the heterogeneity of atrial refractoriness, and high sympathetic tone generated during daily protracted exercise sessions work in synergy to markedly increase the risk for AF.
The left atrial (LA) dilation and fibrosis that developed after 16 weeks of intense aerobic training created a substrate for arrhythmias in the mice (1). Similarly, LA dilation and fibrosis have been described in veteran athletes who have been performing sustained vigorous aerobic activity for year to decades, and these EE athletes have been noted to have up to a 5-fold increase in the prevalence of AF (2). Hypothetically, the sustained volume overload caused by protracted EE efforts stretches the pliable cardiac chambers (especially the atria and right ventricle) and provokes excess oxidative stress and sustained elevations of catecholamines, all of which can lead to micro-tears in the myocardium that over time evolve into scattered fibrosis and remodeling of the LA—the substrate for AF. This cardiac strain immediately after such extreme EE events is manifested by an increase in cardiac troponin, which generally returns to normal after a few hours, but may result in persistent atrial enlargement with increased fibrosis when such activities are performed chronically (2–4). Although the myocardial fibrosis in the animals did not regress with the cessation of EE, the AF inducibility did resolve, theoretically due to the normalization of autonomic tone—a finding with potential clinical relevance to humans.
In summary, the paper by Guasch et al. (1) provides additional insight into the emerging understanding of possible cardiovascular damage induced by chronic excessive EE.
- American College of Cardiology Foundation
- Guasch E.,
- Benito B.,
- Qi X.,
- et al.
- O'Keefe J.H.,
- Lavie C.J.
- O'Keefe J.H.,
- Schnohr P.,
- Lavie C.J.