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

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Abstract
Autonomic nervous alterations are apparently responsible for the bradycardia of the endurance athlete. To determine whether there is also a non-autonomic component in the bradycardia of long-term training, intrinsic heart rate (HR) of highly trained bicyclists (heart volume: 995 .+-. 155 ml) was compared to that of untrained men (heart volume: 805 .+-. 195 ml) at rest and during bicycle ergometer exercise at 50, 75 and 100% of maximal O2 uptake (.ovrhdot.VO2 max). Intrinsic HR was achieved by combined vagal and .beta.-adrenergic blockade with atropine and propranolol or metoprolol (cardioselective) injected i.v. 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 2 groups. Nearly identical intrinsic HR were achieved with atropine and either .beta.-adrenergic antagonist. HR differences between T and UT were very similar in magnitude, .apprx. 13 beats/min, at rest and during exercise at a given percentage of .ovrhdot.VO2 max, with and without autonomic blockade. There is 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 .ovrhdot.VO2 max. The lower intrinsic HR in well-trained men might be explained by the cardiac enlargement.