Katayama Keisho, Ishida Koji, Saito Mitsuru, Koike Teruhiko, Ogoh Shigehiko
Research Center of Health, Physical Fitness and Sports, Nagoya University, Nagoya, Japan.
Graduate School of Medicine, Nagoya University, Nagoya, Japan.
Exp Physiol. 2016 Mar;101(3):377-86. doi: 10.1113/EP085632. Epub 2016 Jan 28.
What is the central question of this study? The cardiopulmonary baroreflex inhibits adjustment of sympathetic vasomotor outflow during mild-intensity dynamic exercise. However, it is unclear how suppression of sympathetic vasomotor outflow by the cardiopulmonary baroreflex is modulated by a powerful sympatho-excitatory drive from the exercise pressor reflex, central command and/or the arterial chemoreflex. What is the main finding and its importance? Hypoxia-induced heightened sympathetic nerve activity during dynamic exercise attenuated cardiopulmonary baroreflex control of sympathetic vasomotor outflow. This could facilitate the redistribution of blood flow to the active muscles by sympathetically mediated vasoconstriction of inactive muscles. Muscle sympathetic nerve activity (MSNA) does not increase during mild-intensity dynamic leg exercise in normoxic conditions, despite activation of central command and the exercise pressor reflex. Suppression of MSNA could be caused by muscle pump-induced loading of cardiopulmonary baroreceptors. In contrast, MSNA increases during mild dynamic leg exercise in hypoxic conditions. We hypothesized that hypoxic exercise, which induces a powerful sympatho-excitatory drive from the exercise pressor reflex, central command and/or arterial chemoreflex, attenuates cardiopulmonary reflex control of sympathetic vasomotor outflow. To test this hypothesis, MSNA was recorded during leg cycling in hypoxic conditions and with increased central blood volume by increasing the pedalling frequency to change the cardiopulmonary baroreflex. Subjects performed two leg cycle exercises at different pedal cadences of 60 and 80 r.p.m. (60EX and 80EX trials, respectively) in two (haemodynamic and MSNA) measurement conditions while breathing a hypoxic gas mixture (inspired oxygen fraction = 0.12). Thoracic impedance, stroke volume and cardiac output were measured non-invasively using impedance cardiography. During the MSNA test, MSNA was recorded via microneurography at the right median nerve at the elbow. Changes in thoracic impedance, stroke volume and cardiac output during the 80EX trial were greater than those during the 60EX trial. The MSNA burst frequency during hypoxic exercise in the 80EX trial (39 ± 4 bursts min(-1)) did not differ from that during the 60EX trial (39 ± 3 bursts min(-1)). These results suggest that the cardiopulmonary baroreflex of sympathetic vasomotor outflow during dynamic exercise is modulated by heightened hypoxia-induced sympathetic nerve activity.
本研究的核心问题是什么？心肺压力反射在轻度动态运动期间会抑制交感缩血管神经传出活动的调节。然而，尚不清楚心肺压力反射对交感缩血管神经传出活动的抑制是如何被运动压力反射、中枢指令和/或动脉化学反射产生的强大交感兴奋驱动所调节的。主要发现及其重要性是什么？动态运动期间缺氧诱导的交感神经活动增强减弱了心肺压力反射对交感缩血管神经传出活动的控制。这可通过交感介导的非活动肌肉血管收缩促进血液重新分配至活动肌肉。在常氧条件下进行轻度动态腿部运动时，尽管中枢指令和运动压力反射被激活，但肌肉交感神经活动（MSNA）并未增加。MSNA受到抑制可能是由于肌肉泵引起的心肺压力感受器负荷增加所致。相比之下，在缺氧条件下进行轻度动态腿部运动时，MSNA会增加。我们假设，缺氧运动通过运动压力反射、中枢指令和/或动脉化学反射产生强大的交感兴奋驱动，减弱了心肺反射对交感缩血管神经传出活动的控制。为验证这一假设，在缺氧条件下进行腿部蹬车运动期间记录MSNA，并通过增加蹬车频率以改变心肺压力反射，从而增加中心血容量。受试者在两种（血流动力学和MSNA）测量条件下，以60和80转/分钟的不同蹬踏频率（分别为60EX和80EX试验）进行两次腿部蹬车运动，同时呼吸低氧混合气体（吸入氧分数=0.12）。使用阻抗心动图无创测量胸段阻抗、每搏输出量和心输出量。在MSNA测试期间，通过微神经ography在肘部右侧正中神经记录MSNA。80EX试验期间胸段阻抗、每搏输出量和心输出量的变化大于60EX试验期间。80EX试验中缺氧运动期间的MSNA爆发频率（39±4次/分钟）与60EX试验期间（39±3次/分钟）无差异。这些结果表明，动态运动期间交感缩血管神经传出活动的心肺压力反射受缺氧诱导的交感神经活动增强的调节。
