The purpose of this study was to test the hypothesis that bradycardia in exercise-trained rats results from decreased intrinsic automaticity of the sinoatrial (SA) node and/or alterations in the responsiveness of the beta-receptors of atrial pacemaker cells. Male Sprague-Dawley rats were divided into exercise trained (ET) and sedentary (SED) groups. ET rats underwent a 12-16 wk program of progressive treadmill training, during which time the SED rats were cage confined. In vivo, resting heart rates were significantly less (P less than 0.05) in ET rats (301 +/- 8 bpm) compared with the SED group (320 +/- 6 bpm). In vitro experiments were conducted on atria isolated from ET and SED rats, and the beta-adrenoceptor agonist isoproterenol was used to investigate cardiac adrenergic control of chronotropic mechanisms in spontaneously beating right atria and inotropic mechanisms in electrically paced (1 Hz) left atria. There were no significant differences between ET and SED cardiac preparations in either the efficacy (maximal response) or potency (EC50) of isoproterenol dose-response relationships for chronotropic or inotropic responses. Intrinsic right atrial beating frequency, measured in the presence of beta-adrenoceptor block by propranolol and cholinergic muscarinic block by atropine, was lower in ET rats. We conclude that training-induced bradycardia in rats is related, at least in part, to alterations in intrinsic automaticity of SA nodal pacemaker tissue, but does not appear to be associated with changes in the properties of the beta 1-adrenoceptors or their affiliated signal transduction mechanisms in either SA pacemaker cells or atrial myocytes.