Abstract
To seek possible mechanisms for the relative bradycardia induced by physical conditioning we studied the effects of an eight-week swimming programme upon cardiac beta-adrenergic and muscarinic-cholinergic receptors in rats. A training effect was documented by an increase in the ratio of heart wet weight to body weight in the conditioned animals compared with sedentary controls. Cardiac beta-adrenergic receptors as assessed in crude membrane fractions by the binding of (-) (3H) dihydroalprenolol did not differ significantly in either number or affinity in conditioned hearts (30 +/- 2 fmol.mg-1 protein; KD = 1.4 +/- 0.1 nmol.litre-1) compared with sedentary hearts (33 +/- 2 fmol.mg-1; KD = 1.5 +/- 2 nmol.litre-1). Likewise cardiac muscarinic-cholinergic receptors as assessed by the binding of (3H) quinuclidinyl benzilate to crude cardiac membranes did not differ significantly in either number or affinity in conditioned hearts (116 +/- 6 fmol.mg-1 protein; KD = 0.17 +/- 0.03 nmol.litre-1) compared with sedentary hearts (125 +/- 11 fmol.mg-1; KD = 0.19 +/- 0.03 nmol.litre-1). We conclude that the bradycardia of physical training is probably mediated by mechanisms other than alterations in cardiac beta-adrenergic or muscarinic-cholinergic receptors.
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