* School of Sport, Exercise & Rehabilitation Sciences, College of Life and Environmental Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK.
Exp Physiol. 2014 Feb;99(2):300-5. doi: 10.1113/expphysiol.2013.074377. Epub 2013 Aug 30.
What is the topic of this review? The autonomic nervous system plays a key role in bringing about the cardiovascular responses to exercise necessitated by the increased metabolic requirements of the active skeletal muscle. The complex interaction of central and peripheral neural control mechanisms evokes a decrease in parasympathetic activity and an increase sympathetic activity to the heart during exercise. What advances does it highlight? This review presents some of the recent insights provided by human studies into the role of mechanically and metabolically sensitive skeletal muscle afferents in the regulation of cardiac autonomic control during exercise. The autonomic responses to exercise are orchestrated by the interactions of several central and peripheral neural mechanisms. This report focuses on the role of peripheral feedback from skeletal muscle afferents in the autonomic control of the heart during exercise in humans. Heart rate responses to passive calf stretch are abolished with cardiac parasympathetic blockade, indicating that the activation of mechanically sensitive skeletal muscle afferents (muscle mechanoreceptors) can inhibit cardiac parasympathetic activity and is likely to contribute to the increase in heart rate at the onset of exercise. Recent experiments show that the partial restriction of blood flow to the exercising skeletal muscles, to augment the activation of metabolically sensitive skeletal muscle afferents (muscle metaboreceptors) in humans, evokes an increase in heart rate that is attenuated with β1-adrenergic blockade, thus suggesting that this response is principally mediated via an increase in cardiac sympathetic activity. Heart rate remains at resting levels during isolated activation of muscle metaboreceptors with postexercise ischaemia following hand grip, unless cardiac parasympathetic activity is inhibited, whereupon a sympathetically mediated increase in heart rate is unmasked. During postexercise ischaemia following leg cycling exercise, heart rate appears to remain elevated due to withdrawal of parasympathetic tone and/or the activation of sympathetic activity to the heart. Although the importance of skeletal muscle afferent feedback to the autonomic control of the heart during exercise is incontrovertible, the complexity of cardiac sympathetic-parasympathetic interactions and the absence of direct intraneural recordings in humans mean that it remains incompletely understood.
这篇综述探讨了什么主题？自主神经系统在产生运动时骨骼肌代谢需求增加所必需的心血管反应中起着关键作用。中枢和外周神经控制机制的复杂相互作用在运动过程中引起副交感神经活动的减少和交感神经对心脏的活动增加。它强调了哪些进展？这篇综述介绍了一些最近的人类研究提供的关于机械和代谢敏感的骨骼肌传入在运动期间心脏自主控制中的作用的新见解。运动时的自主反应是由几个中枢和外周神经机制的相互作用协调的。本报告重点介绍了运动期间骨骼肌传入在外周反馈对心脏自主控制的作用，在人类中。被动小腿伸展引起的心率反应被心脏副交感神经阻断所消除，这表明机械敏感的骨骼肌传入（肌肉机械感受器）的激活可以抑制心脏副交感神经活动，并且可能有助于运动开始时心率的增加。最近的实验表明，部分限制运动骨骼肌的血流以增强代谢敏感的骨骼肌传入（肌肉代谢感受器）的激活，可引起心率增加，这种增加可被β1-肾上腺素能阻断所减弱，因此表明这种反应主要是通过增加心脏交感神经活动介导的。在进行握力后运动后缺血时单独激活肌肉代谢感受器期间，心率保持在静息水平，除非心脏副交感神经活动被抑制，此时会出现由交感神经介导的心率增加。在腿部自行车运动后的运动后缺血期间，心率似乎仍然升高，这是由于副交感神经张力的撤回和/或心脏的交感神经活动的激活。虽然运动时骨骼肌传入对心脏自主控制的反馈作用是不可否认的，但心脏交感神经-副交感神经相互作用的复杂性以及人类缺乏直接的神经内记录意味着，这仍然没有得到完全理解。
