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肌肉传入激活会导致人类在同时发生高碳酸血症时出现通气和心血管反应。

Muscle afferent activation causes ventilatory and cardiovascular responses during concurrent hypercapnia in humans.

机构信息

School of Sport and Exercise Sciences, University of Birmingham, Edgbaston, Birmingham B15 2TT, UK.

出版信息

Exp Physiol. 2012 Feb;97(2):208-18. doi: 10.1113/expphysiol.2011.061606. Epub 2011 Nov 4.

Abstract

Respiratory and cardiovascular responses to muscle mechanoreflex (passive calf stretch) and metaboreflex activation (local circulatory occlusion) were examined during inhalation of a hypercapnic gas mixture in four trials. These controlled for the effects of central command, metabolite sensitization of muscle afferents and hypercapnia-induced elevation of central respiratory drive. In an isokinetic dynamometer, with circulation through the right leg occluded by inflation of a thigh cuff, 13 participants either rested (control trial; CON) or plantarflexed their ankle at 50% maximal force for 1.5 min (voluntary exercise trial; EX). Thereafter, circulatory occlusion was maintained and the calf passively stretched before return to the resting position. Both trials were performed while breathing air, as well as while breathing a normoxic, hypercapnic (5% CO(2)) gas mixture (CO(2) trial and CO(2)+EX trial). Hypercapnic gas inhalation increased baseline minute ventilation (V), heart rate and mean arterial pressure (+27.67 ± 1.74 l min(-1), +7 ± 0.85 beats min(-1) and +13 ± 3.41 mmHg, respectively; means ± SEM) above control values (9.78 ± 0.86 l min(-1), 62 ± 2.3 beats min(-1) and 88 ± 2.6 mmHg, respectively). Voluntary exercise further increased these variables from baseline during both trials (P < 0.05). During the continued circulatory occlusion after voluntary exercise, mean arterial pressure remained significantly elevated (P < 0.05). Minute ventilation returned to baseline during circulatory occlusion following exercise in the EX trial, but in the CO(2)+EX trial the V remained elevated at end-exercise levels during this period (+7.12 ± 1.13 l min(-1)). Passive stretch caused further increases in V during CO(2)+EX and CO(2) trials but not in CON and EX. These results indicate that in the absence of central command, either muscle metaboreflex and/or mechanoreflex activation stimulates ventilation during concurrent hypercapnia.

摘要

在四项试验中,当吸入高碳酸血症混合气体时,研究了肌肉机械反射(被动小腿伸展)和代谢反射激活(局部循环闭塞)对呼吸和心血管的反应。这些试验控制了中枢命令、肌肉传入纤维代谢敏感性以及高碳酸血症引起的中枢呼吸驱动升高的影响。在等速测力计中,通过充气大腿袖带闭塞右腿循环,13 名参与者要么休息(对照试验;CON),要么以 50%最大力量背屈脚踝 1.5 分钟(自愿运动试验;EX)。此后,在返回休息位置之前,保持循环闭塞并被动伸展小腿。在呼吸空气以及呼吸正常氧合、高碳酸血症(5%CO2)混合气体(CO2 试验和 CO2+EX 试验)时,进行了这两个试验。高碳酸血症气体吸入使基础分钟通气量(V)、心率和平均动脉压升高(分别增加 27.67 ± 1.74 l min(-1)、+7 ± 0.85 次 min(-1)和 +13 ± 3.41 mmHg;平均值 ± SEM),高于对照值(分别为 9.78 ± 0.86 l min(-1)、62 ± 2.3 次 min(-1)和 88 ± 2.6 mmHg)。自愿运动在两个试验中进一步增加了这些变量(P < 0.05)。在自愿运动后的持续循环闭塞期间,平均动脉压仍然显著升高(P < 0.05)。在 EX 试验中,运动后循环闭塞期间分钟通气量恢复到基础水平,但在 CO2+EX 试验中,在此期间,V 仍保持在运动结束时的水平升高(+7.12 ± 1.13 l min(-1))。被动伸展在 CO2+EX 和 CO2 试验中进一步增加了 V,但在 CON 和 EX 试验中没有增加。这些结果表明,在没有中枢命令的情况下,肌肉代谢反射和/或机械反射激活在并发高碳酸血症期间刺激通气。

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