Physical conditioning and membrane receptors for cardioregulatory hormones

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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 β-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 β-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·mg1 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 β-adrenergic or muscarinic-cholinergic receptors.