Journal of Applied Physiology, Vol 51, Issue 5 1232-1237, Copyright © 1981 by American Physiological Society
Autonomic mechanisms of training bradycardia: beta-adrenergic receptors in humans
R. S. Williams, R. S. Eden, M. E. Moll, R. M. Lester and A. G. Wallace
To address the autonomic mechanisms underlying the bradycardia of physical
training in human subjects, we performed a cross-sectional study comparing
the heart-rate responses to graded doses of isoproterenol in 7 elite
marathon runners and 7 age-matched controls, and a longitudinal study in 12
normal volunteers of the effects of 6 wk of intense physical training on
lymphocyte beta-adrenergic receptors identified by l-[3H]dihydroalprenolol.
We observed no significant differences between marathoners and controls in
the dose of isoproterenol that produced a 25-beat/min increment in heart
rate, either in the absence (1.9 +/- 0.6 vs. 2.5 +/- 0.6 microgram; P,
0.509) or in the presence of cholinergic blockade (4.4 +/- 1.3 vs. 3.1 +/-
0.4 microgram: P, 0.320). Likewise, we observed no effects of physical
training on lymphocyte beta-adrenergic receptors in terms of receptors
number (53 +/- 11 vs. 56 +/- 10 fmol/mg protein) or receptor affinity (Kd
4.0 +/- 0.7 vs. 3.6 +/- 0.7 nM) (P, 0.9178). Although our data cannot
exclude reduced chronotropic sensitivity to catecholamines as contributing
to lowered heart rate in some highly conditioned individuals, these results
are consistent with the hypothesis that altered neuronal input to the sinus
node is usually a more important mechanism of training bradycardia.
