Physical activity has many positive effects on the cardiovascular system, but intense endurance training can also be detrimental. Athletes, especially those with a long training history, are more likely to develop arrhythmias. Sinus bradycardia (a slow resting heart rate) is the most common training-associated arrhythmia. Although it is often a benign physiological adaptation to maintain normal cardiac output and blood pressure by compensating for training-induced increases in stroke volume, bradycardia can become pathological and lead to the need for electronic pacemaker implantation. High incidences of pacemaker implantation to control bradyarrhythmias have been reported among former professional cyclists and among elderly marathon runners.

Training-induced bradycardia has been attributed to changes in the autonomic nervous system, such as an increase in vagal tone. But bradycardia is observed in athletes even when the autonomic nervous system is blocked. Instead, some data suggest that long-term endurance training may induce pathological remodeling of the heart that manifests in arrhythmia. A study recently published by Mark Boyett (University of Manchester, UK) and colleagues supports this explanation. Boyett's work shows that training-induced bradycardia is caused by electrophysiological changes in the sinus node, the pacemaker of the heart, and, more specifically, by a remodeling of the ion channels that control pacemaking (Nat. Commun. 5, 3775; 2014).

In Boyett's study, rats and mice underwent exercise training (running or swimming), and their cardiovascular function was compared with that of sedentary controls. Trained animals developed sinus bradycardia that persisted after blockade of the autonomous nervous system. Exercise training also induced a widespread remodeling of pacemaker ion channels, decreasing expression of the HCN4 channel and activity of its corresponding ionic current. 'Detraining' the mice reversed these changes.

The results indicate that heart rate adaption to endurance training does not result from changes in autonomic tone but is primarily caused by remodeling of the sinus node. The higher incidence of sinus node disease and pacemaker implantation among veteran endurance athletes is likely a consequence of this remodeling. Sinus-node remodeling may also help explain syncope in young athletes, and analogous remodeling of other parts of the heart may explain other training-associated arrhythmias (e.g., atrial fibrillation, heart block and bundle branch block). Although sinus-node remodeling and its consequences were reversible after short-term endurance training, it is unclear whether they remain reversible after long-term training. The findings provide a molecular explanation for potentially pathological heart rate adaptations to endurance training and may help inform lifestyle choices in athletes.