Counterpoint: Exercise training-induced bradycardia: the case for enhanced parasympathetic regulation.

TRAINING BRADYCARDIA is a well-established consequence of endurance exercise training and is, in fact, often used to demonstrate that an exercise training program had been effective (3). Despite decades of research, the mechanisms responsible for this reduction in baseline heart rate (HR) remain controversial (7, 9, 10, 13). Exercise training-induced changes in HR could result from either shifts in the autonomic neural balance toward dominant parasympathetic regulation of cardiac pacemaker cells (increased parasympathetic and/or reduced sympathetic neural regulation, the autonomic neural hypothesis), changes in spontaneous sinoatrial nodal (SAN) cell depolarization rates (changes in the inherent cardiac pacemaker rate, the intrinsic rate hypothesis), or some combination of the two mechanisms. Because of space limitations, the present article will provide only a selective and limited summary of the evidence in support of the autonomic neural hypothesis. Three main lines of evidence support the autonomic neural hypothesis: 1) studies that indirectly evaluated cardiac autonomic regulation using changes in various indices of the beat-to-beat variation in HR, heart rate variability (HRV); 2) studies that used pharmacologic interventions to evaluate cardiac autonomic neural regulation; and 3) studies that directly evaluated the cardiac autonomic regulation using surgical approaches (selective cardiac denervation). Finally, the effects exercise training on atrial electrophysiology will also be described briefly.