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Adult male rats were progressively trained 5 days/weeks on a motor-driven treadmill. The training period lasted 12 weeks and consisted of 60 min/day of wind-sprints and endurance work. No significant difference in resting heart rates was observed between the control and exercise groups during week 1 (394 +/- 7 vs. 388 +/- 5). However, at week 12 the exercise group had a lower resting heart rate (359 +/- 6 vs. 331 +/- 4). Heart rates observed following saline, propranolol, atropine, and propranolol plus atropine injections were lower in the exercise group in all cases. The difference in heart rates between the control and exercise groups was 19 beats/min following propranolol plus atropine which was less than the 28 beats/min difference observed under control conditions. With atropine and then with propranolol the differences were 33 and 27 beats/min. These heart rate differences were observed without the presence of cardiac hypertrophy as assesssed from ventricle weights. Our data indicate that the bradycardia resulting from exercise training is due primarily to changes other than neural influences on the heart.

Maximum exercise heart rate decreases with maturation in the rat as well as in man. The present study was undertaken to investigate the mechanism(s) which might be responsible for this reduction in max exercise heart rate in the rat. Maximum exercise heart rates were 618 +/- 7 vs. 580 +/- 9 beats/min for the young (5 wk) and mature (19 wk) rats, respectively. Atropine had no effect on max exercise heart rate. Propranolol reduced max heart rate in both groups with the older rats having the lowest value. Resting heart rates were recorded following injections of atropine propranolol, and propranolol plus atropine. Under all conditions, including control, heart rates were lower in the mature rats. Electrical stimulation in situ showed a significant difference in the threshold voltage for stimulation at 600 beats/min: 1.1 +/- 0.2 vs. 1.6 +/- 0.1 V for the young and mature rats, respectively. These data suggest that intrinsic changes occur in the myocardium with maturation and the reduction in max exercise heart rate is due to these intrinsic changes as opposed to changes in neural influences.

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