Sinoway L, Shenberger J, Leaman G, Zelis R, Gray K, Baily R, Leuenberger U
Division of Cardiology, Milton S. Hershey Medical Center, Pennsylvania State University, Hershey 17033, USA.
J Appl Physiol (1985). 1996 Oct;81(4):1778-84. doi: 10.1152/jappl.1996.81.4.1778.
We previously demonstrated that nonfatiguing rhythmic forearm exercise at 25% maximal voluntary contraction (12 2-s contractions/min) evokes sympathoexcitation without significant engagement of metabolite-sensitive muscle afferents (B.A. Batman, J.C. Hardy, U.A. Leuenberger, M.B. Smith, Q.X. Yang and L.I. Sinoway. J. Appl. Physiol. 76: 1077-1081, 1994). This is in contrast to the sympathetic nervous system responses observed during fatiguing static forearm exercise where metabolite-sensitive afferents are the key determinants of sympathetic activation. In this report we examined whether forearm exercise training would attenuate sympathetic nervous system responses to rhythmic forearm exercise. We measured heart rate, mean arterial blood pressure (MAP), muscle sympathetic nerve activity (microneurography), plasma norepinephrine (NE), and NE spillover and clearance (tritiated NE kinetics) during nonfatiguing rhythmic forearm exercise before and after a 4-wk unilateral forearm training paradigm. Training had no effect on forearm mass, maximal voluntary contraction, or heart rate but did attenuate the increase in MAP (increase in MAP: from 15.2 +/- 1.8 before training to 11.4 +/- 1.4 mmHg after training; P < 0.017), muscle sympathetic nerve activity (increase in bursts: from 10.8 +/- 1.4 before training to 6.2 +/- 1.1 bursts/min after training; P < 0.030), and the NE spillover (increases in arterial spillover: from 1.3 +/- 0.2 before training to 0.6 +/- 0.2 nmol.min-1.m-2 after training, P < 0.014; increase in venous spillover: from 2.0 +/- 0.6 before training to 1.0 +/- 0.5 nmol.min-1.m-2 after training, P < 0.037) seen in response to exercise performed by the trained forearm. Thus forearm training reduces sympathetic responses during a nonfatiguing rhythmic handgrip paradigm that does not engage muscle metaboreceptors. We speculate that this effect is due to a conditioning-induced reduction in mechanically sensitive muscle afferent discharge.
我们之前曾证明，在25%最大自主收缩强度下（12次2秒收缩/分钟）进行非疲劳性有节奏的前臂运动，会引发交感神经兴奋，而代谢产物敏感的肌肉传入神经未显著参与其中（B.A. 蝙蝠侠、J.C. 哈迪、U.A. 洛伊恩贝格、M.B. 史密斯、Q.X. 杨和L.I. 西诺韦。《应用生理学杂志》76: 1077 - 1081, 1994）。这与疲劳性静态前臂运动期间观察到的交感神经系统反应形成对比，在疲劳性静态前臂运动中，代谢产物敏感的传入神经是交感神经激活的关键决定因素。在本报告中，我们研究了前臂运动训练是否会减弱交感神经系统对有节奏的前臂运动的反应。我们在为期4周的单侧前臂训练模式前后，测量了非疲劳性有节奏的前臂运动期间的心率、平均动脉血压（MAP）、肌肉交感神经活动（微神经ography）、血浆去甲肾上腺素（NE）以及NE溢出和清除（氚标记NE动力学）。训练对前臂质量、最大自主收缩或心率没有影响，但确实减弱了MAP的升高（MAP升高：训练前为15.2±1.8，训练后为11.4±1.4 mmHg；P < 0.017）、肌肉交感神经活动（爆发增加：训练前为10.8±1.4，训练后为6.2±1.1次/分钟；P < 0.030）以及训练前臂进行运动时出现的NE溢出（动脉溢出增加：训练前为1.3±0.2，训练后为0.6±0.2 nmol·min⁻¹·m⁻²，P < 0.014；静脉溢出增加：训练前为2.0±0.6，训练后为1.0±0.5 nmol·min⁻¹·m⁻²，P < 0.037）。因此，前臂训练可降低在不涉及肌肉代谢感受器的非疲劳性有节奏握力模式期间的交感神经反应。我们推测这种效应是由于条件反射引起的机械敏感肌肉传入神经放电减少所致。
