Schaefer M E, Allert J A, Adams H R, Laughlin M H
Department of Veterinary Biomedical Sciences, University of Missouri, Columbia 65202.
Med Sci Sports Exerc. 1992 Aug;24(8):887-94.
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.
运动训练大鼠的心动过缓是由于窦房（SA）结内在自律性降低和/或心房起搏细胞β受体反应性改变所致。将雄性Sprague-Dawley大鼠分为运动训练（ET）组和久坐不动（SED）组。ET组大鼠接受为期12 - 16周的渐进式跑步机训练计划，在此期间，SED组大鼠被关在笼中。在体内，ET组大鼠（301±8次/分钟）的静息心率显著低于SED组（320±6次/分钟）（P<0.05）。对从ET组和SED组大鼠分离的心房进行体外实验，使用β肾上腺素能受体激动剂异丙肾上腺素来研究心脏肾上腺素能对自发搏动右心房变时机制以及电起搏（1Hz）左心房变力机制的控制。在变时或变力反应的异丙肾上腺素剂量 - 反应关系的效能（最大反应）或效价（EC50）方面，ET组和SED组心脏标本之间没有显著差异。在普萘洛尔阻断β肾上腺素能受体和阿托品阻断胆碱能毒蕈碱受体的情况下，测得的ET组大鼠右心房固有搏动频率较低。我们得出结论，训练诱导的大鼠心动过缓至少部分与SA结起搏组织的内在自律性改变有关，但似乎与SA起搏细胞或心房肌细胞中β1肾上腺素能受体及其相关信号转导机制的特性变化无关。
