Pulmonary Function and Clinical Exercise Physiology Unit, Division of Respiratory Medicine, Department of Medicine, Federal University of São Paulo , Brazil.
Postgraduate Program in Pulmonary Medicine, Department of Medicine, Federal University of São Paulo , Brazil.
J Appl Physiol (1985). 2018 Jul 1;125(1):215-225. doi: 10.1152/japplphysiol.00009.2018. Epub 2018 Mar 22.
Physical exercise potentiates the carotid chemoreflex control of ventilation (VE). Hyperadditive neural interactions may partially mediate the potentiation. However, some neural interactions remain incompletely explored. As the potentiation occurs even during low-intensity exercise, we tested the hypothesis that the carotid chemoreflex and the muscle mechanoreflex could interact in a hyperadditive fashion. Fourteen young healthy subjects inhaled randomly, in separate visits, 12% O to stimulate the carotid chemoreflex and 21% O as control. A rebreathing circuit maintained isocapnia. During gases administration, subjects either remained at rest (i.e., normoxic and hypoxic rest) or the muscle mechanoreflex was stimulated via passive knee movement (i.e., normoxic and hypoxic movement). Surface muscle electrical activity did not increase during the passive movement, confirming the absence of active contractions. Hypoxic rest and normoxic movement similarly increased VE [change (mean ± SE) = 1.24 ± 0.72 vs. 0.73 ± 0.43 l/min, respectively; P = 0.46], but hypoxic rest only increased tidal volume (Vt), and normoxic movement only increased breathing frequency (BF). Hypoxic movement induced greater VE and mean inspiratory flow (Vt/Ti) increase than the sum of hypoxic rest and normoxic movement isolated responses (VE change: hypoxic movement = 3.72 ± 0.81 l/min vs. sum = 1.96 ± 0.83 l/min, P = 0.01; Vt/Ti change: hypoxic movement = 0.13 ± 0.03 l/s vs. sum = 0.06 ± 0.03 l/s, P = 0.02). Moreover, hypoxic movement increased both Vt and BF. Collectively, the results indicate that the carotid chemoreflex and the muscle mechanoreflex interacted, mediating a hyperadditive ventilatory response in healthy humans. NEW & NOTEWORTHY The main finding of this study was that concomitant carotid chemoreflex and muscle mechanoreflex stimulation provoked greater ventilation increase than the sum of ventilation increase induced by stimulation of each reflex in isolation, which, consequently, supports that the carotid chemoreflex and the muscle mechanoreflex interacted, mediating a hyperadditive ventilatory response in healthy humans.
体育锻炼可增强颈动脉化学感受器对通气的控制（VE）。超相加的神经相互作用可能部分介导这种增强作用。然而，一些神经相互作用仍未得到充分探索。由于这种增强作用甚至在低强度运动时也会发生，我们测试了颈动脉化学感受器和肌肉机械感受器以超相加方式相互作用的假设。14 名年轻健康受试者在单独的访问中随机吸入 12% O 以刺激颈动脉化学感受器，作为对照吸入 21% O。再呼吸回路维持等碳酸血症。在给予气体期间，受试者要么保持休息（即，低氧和常氧休息），要么通过被动膝关节运动刺激肌肉机械感受器（即，低氧和常氧运动）。表面肌肉电活动在被动运动期间没有增加，这证实了没有主动收缩。低氧休息和常氧运动同样增加了 VE [变化（平均值±SE）= 1.24±0.72 与 0.73±0.43 l/min，分别；P=0.46]，但低氧休息仅增加潮气量（Vt），而常氧运动仅增加呼吸频率（BF）。低氧运动引起的 VE 和平均吸气流量（Vt/Ti）增加大于低氧休息和常氧运动孤立反应之和（VE 变化：低氧运动=3.72±0.81 l/min 与总和=1.96±0.83 l/min，P=0.01；Vt/Ti 变化：低氧运动=0.13±0.03 l/s 与总和=0.06±0.03 l/s，P=0.02）。此外，低氧运动增加了 Vt 和 BF。总的来说，这些结果表明颈动脉化学感受器和肌肉机械感受器相互作用，介导了健康人类的超相加通气反应。
此研究的主要发现是，同时刺激颈动脉化学感受器和肌肉机械感受器引起的通气增加大于单独刺激每个反射引起的通气增加之和，这表明颈动脉化学感受器和肌肉机械感受器相互作用，介导了健康人类的超相加通气反应。
