Chen C Y, DiCarlo S E, Scislo T J
Department of Physiology, Northeastern Ohio Universities, College of Medicine, Rootstown 44272.
Am J Physiol. 1995 Feb;268(2 Pt 2):H662-9. doi: 10.1152/ajpheart.1995.268.2.H662.
Exercise training attenuates arterial baroreflex function. Mechanisms responsible may include an attenuated aortic baroreceptor reactivity (afferent mechanisms) and/or an attenuated central baroreflex gain. We tested the hypothesis that the aortic baroreceptor reactivity and/or central gain is attenuated by daily spontaneous running (DSR). Eighteen anesthetized Sprague-Dawley rats (11 control and 7 DSR) were tracheotomized and instrumented with femoral venous and right carotid arterial catheters. Electrodes were placed around the left aortic depressor nerve and the lumbar sympathetic trunk. Eight to thirteen weeks of DSR were associated with a 20% increase in heart weight-to-body weight ratio (2.83 +/- 0.04 vs. 3.39 +/- 0.10 g/kg; P < 0.001) and resting bradycardia (413 +/- 6 vs. 384 +/- 10 beats/min; P = 0.01). DSR reduced the central gain of the baroreflex regulation of heart rate (0.210 +/- 0.046 vs. 0.005 +/- 0.021 beats.min-1.%-1; P = 0.004) during decreases in arterial pressure. However, the reactivity of aortic baroreceptor afferents and the central gain of the baroreflex control of lumbar sympathetic nerve activity were not different in control and DSR rats. Thus DSR reduced the central gain of the arterial baroreflex regulation of heart rate without changing the reactivity of aortic baroreceptor afferents. We conclude that afferent mechanisms are not responsible for the training-induced reduction in arterial baroreflex function.
运动训练会减弱动脉压力感受器反射功能。其相关机制可能包括主动脉压力感受器反应性减弱(传入机制)和/或中枢压力感受器反射增益减弱。我们检验了以下假设:每日自发跑步(DSR)会使主动脉压力感受器反应性和/或中枢增益减弱。将18只麻醉的Sprague-Dawley大鼠(11只作为对照,7只进行DSR)进行气管切开,并植入股静脉和右颈动脉导管。在左主动脉减压神经和腰交感干周围放置电极。8至13周的DSR与心脏重量与体重比增加20%(2.83±0.04 vs. 3.39±0.10 g/kg;P<0.001)以及静息性心动过缓(413±6 vs. 384±10次/分钟;P = 0.01)相关。在动脉压下降期间,DSR降低了压力感受器对心率调节的中枢增益(0.210±0.046 vs. 0.005±0.021次·分钟-1·%-1;P = 0.004)。然而,对照大鼠和DSR大鼠的主动脉压力感受器传入神经反应性以及压力感受器对腰交感神经活动控制的中枢增益并无差异。因此,DSR降低了动脉压力感受器对心率调节的中枢增益,而未改变主动脉压力感受器传入神经的反应性。我们得出结论,传入机制并非训练导致动脉压力感受器反射功能降低的原因。