Non-autonomic component in bradycardia of endurance trained men at rest and during exercise.

TLDR: Evidence is provided for a non-autonomic component in the bradycardia of well-trained men which may be responsible for a parallel downward shift in the relationship between HR and percentage of VO2 max, which might be explained by the cardiac enlargement.

Abstract: Autonomic nervous alterations have generally been held responsible for the bradycardia of the endurance athlete. In order to determine whether there is also a non-autonomic component in the bradycardia of long-term training, we compared the intrinsic heart rate (HR) of highly trained bicyclists (heart volume: 995 +/- 155 ml) with that of untrained men (heart volume: 805 +/- 195 ml) at rest and during bicycle ergometer exercise at 50, 75 and 100% of maximal oxygen uptake (VO2 max.) Intrinsic HR was achieved by combined vagal and beta-adrenergic blockade with atropine and propranolol or metoprolol (cardioselective) injected intravenously. Intrinsic HR was significantly lower in trained (T) than in untrained (UT) at rest and at all levels of exercise. The chronotropic reserve from resting HR to maximal HR was identical in the two groups. Nearly identical intrinsic HRs were achieved with atropine and either beta-adrenergic antagonist. HR differences between T and UT were very similar in magnitude--approximately 13 beats/min--at rest and during exercise at a given percentage of VO2 max, with and without autonomic blockade. Evidence is thus provided for a non-autonomic component in the bradycardia of well-trained men which may be responsible for a parallel downward shift in the relationship between HR and percentage of VO2 max. The lower intrinsic HR in well-trained men might be explained by, i.a. the cardiac enlargement.