Presented at the Symposium on Experimental Preparations to Study the Effects of Training on the Cardiovascular System at the 24th Annual Meeting of the American College of Sports Medicine, May 25-28, 1977, Chicago, Illinois.
A modified Langendorff isolated heart preparation was utilized in a series of investigations concerned with the resting bradycardia of training. The primary advantage of the preparations is that it allows for the isolation of the extrinsic and intrinsic factors that influence heart rate. The chief disadvantage is the difficulty in measuring and controlling the many parameters that influence cardiac function and myocardial metabolism. Studies concerned with resting heart rate changes in unanesthetized male rats indicated that 10-12 weeks of endurance training was associated with lower rates, less acceleration after injections of atropine (an inhibitor of acetylcholine binding), lower rates after injections of neostigmine (an inhibitor of acetylcholinesterase), less of a decline after injections of propranolol (an inhibitor of beta receptor activity) and higher rates after injections of isoproterenol (a beta receptor stimulator). Investigations with the Langendorff preparation indicated that the intrinsic rate of the heart represented approximately 70% of the unanesthetized resting rate; but, was not significantly altered by the fact that the animals had participated in a training program. Chronic exercise did significantly alter the responsiveness of the intrinsic heart rate to pharmacological agents that modified the actions of the autonomic nervous system. Furthermore, the changes with perfusion were similar to the pattern observed in intact unanesthetized animals; namely, there was less acceleration with atropine, lower rates after neostigmine, less of a change with propranolol, and increased rates following isoproterenol. When acetylcholine was perfused, the findings did not support the concept that a change in cholinergic sensitivity had occured. When the trained animals were detrained and their hearts perfused with either atropine or isoproterenol, there were no intrinsic rate changes that were significantly different from the nontrained controls. Additional studies were performed on myocardial acetylcholine and catecholamine concentrations, and the trained had higher atrial acetylcholine concentrations than the nontrained rats. From these collective findings, we concluded that the bradycardia of training was primarily the result of an increased amount of acetylcholine and a decreased concentration of norepinephrine being present at cardiac receptor sites. To advance these concepts further, we believe that future investigations should be more neurophysiological and less pharmacological in nature.
BRADYCARDIA AND TRAINING, BRADYCARDIA AND DETRAINING, ISOLATED HEARTS AND TRAINING, LANGENDORFF PREPARATION, CHOLINERGIC RESPONSES TO TRAINING, ADRENERGIC RESPONSES TO TRAINING, CARDIAC ENLARGEMENT AND HEART RATE, CARDIAC RECEPTORS AND TRAINING, MYOCARDIAL ACETYLCHOLINE LEVELS
©1977The American College of Sports Medicine