Int J Sports Med 1980; 01(1): 42-49
DOI: 10.1055/s-2008-1034629
© Georg Thieme Verlag Stuttgart · New York

Endurance Training and Heart Rate Control Studied by Combined Parasympathetic and β-Adrenergic Blockade

S. Lewis1 , P. Thompson2 , N.-H. Areskog3 , M. Marconyak, P. Vodak, R. DeBusk, W. Haskell
  • Cardiology Division, Stanford University, School of Medicine, Stanford, CA 94305, USA
  • 1Division of Cardiology, University of Texas Health Science Center at Dallas, Southwestern Medical School, Dallas, Tx
  • 2Division of Cardiology, Brown University School of Medicine, Memorial Hospital, Pawtucket, RI
  • 3Department of Clinical Physiology, Linköping University, Regionsjukhuset, Linköping, Sweden
Supported in part by Grant HL 18907 from the National Heart, Lung and Blood Institute.
Further Information

Publication History

Publication Date:
14 March 2008 (online)

Summary

Although a slower heart rate (HR) at rest and during sub-maximal exercise has been observed repeatedly after endurance training (“training bradycardia”) in man, the mechanisms involved are still controversial. To examine the mechanisms of the training bradycardia, ten initially sedentary healthy men were studied at rest and during submaximal arm exercise and leg exercise without drugs and after combined parasympathetic and (β-adrenergic blockade before and after 11 weeks of endurance training. Autonomic blockade was accomplished by injecting 0.04 mg/kg atropine and 0.2 mg/kg propranolol intravenously at rest and an additional dose of 0.05 mg/kg propranolol during submaximal exercise. Five subjects trained with arms only (AT) and five with legs only (LT). HR during supine rest fell 4 to 6 beats/min (P < 0.05) after AT and LT, but there were no changes in resting HR after autonomic blockade or in HR during a night's sleep. Without autonomic blockade submaximal exercise, HR was 26 and 17 beats/min and 17 and 22 beats/min lower (all P < 0.05) during arm and leg exercise after AT and LT, respectively. After autonomic blockade submaximal exercise HR was 8 and 5 beats/min and 5 and 10 beats/min lower (all P < 0.05) during arm and leg exercise after AT and LT, respectively. The present data suggest that several mechanisms, including nonautonomic changes other than a reduction in intrinsic HR, are involved in the training bradycardia after short-term endurance training.