Resting bradycardia of exercise training: a concept based on currently available data.
The classic view that the resting bradycardia of exercise training is due to an increase in the tonic discharge of the vagi is no longer tenable; If it were true, full doses of atropine would accelerate the heart to a greater extent in the athletic animal. All investigators agree that the reverse is the case. Some workers report a decrease in cardiac sympathetic influence after training. This would cause a preponderance of vagal influence which may decrease to a lesser extent than the sympathetics or may not change at all. Several studies have demonstrated that training causes a distinct slowing of the intrinsic rate of the pacemaker. It is concluded that two factors operate to lower the resting heart rate after athletic training: 1) slowing of the intrinsic rate of the pacemaker, 2) Increase in cholinergic predominance on the pacemaker frequency as a result of a decrease in adrenergic influence. Vagal influence per se seems either to remain the same or to decrease slightly in the athlete compared to the nonathelete. It appears that slowing of the intrinsic rate plays a more important role, a factor that has been hitherto overlooked. The mechanisms underlying these changes remain obscure.
D000109:Acetylcholine / Q000378:metabolism; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D006325:Heart Atria / Q000378:metabolism; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D008297:Male; D009121:Muscle Denervation; D010806:Physical Education and Training; D005082:Physical Exertion; D011433:Propranolol / Q000494:pharmacology; D014630:Vagus Nerve / Q000502:physiology
D001285:Atropine; D011433:Propranolol; D000109:Acetylcholine