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健康人运动期间颈动脉化学感受器对交感缩血管神经传出活动的调节

Carotid chemoreceptor modulation of sympathetic vasoconstrictor outflow during exercise in healthy humans.

作者信息

Stickland Michael K, Morgan Barbara J, Dempsey Jerome A

机构信息

Division of Pulmonary Medicine, Department of Medicine, 2E4.42 Walter C Mackenzie, Health Sciences Centre, University of Alberta, Edmonton, Alberta, Canada.

出版信息

J Physiol. 2008 Mar 15;586(6):1743-54. doi: 10.1113/jphysiol.2007.147421. Epub 2008 Jan 17.

DOI:10.1113/jphysiol.2007.147421
PMID:18202096
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2375684/
Abstract

Recently, we have shown that specific, transient carotid chemoreceptor (CC) inhibition in exercising dogs causes vasodilatation in limb muscle. The purpose of the present investigation was to determine if CC suppression reduces muscle sympathetic nerve activity (MSNA) in exercising humans. Healthy subjects (N = 7) breathed hyperoxic gas (F(IO(2)) approximately 1.0) for 60 s at rest and during rhythmic handgrip exercise (50% maximal voluntary contraction, 20 r.p.m.). Microneurography was used to record MSNA in the peroneal nerve. End-tidal P(CO(2)) was maintained at resting eupnoeic levels throughout and breathing rate was voluntarily fixed. Exercise increased heart rate (67 versus 77 beats min(-1)), mean blood pressure (81 versus 97 mmHg), MSNA burst frequency (28 versus 37 bursts min(-1)) and MSNA total minute activity (5.7 versus 9.3 units), but did not change blood lactate (0.7 versus 0.7 mm). Transient hyperoxia had no significant effect on MSNA at rest. In contrast, during exercise both MSNA burst frequency and total minute activity were significantly reduced with hyperoxia. MSNA burst frequency was reduced within 9-23 s of end-tidal P(O(2)) exceeding 250 mmHg. The average nadir in MSNA burst frequency and total minute activity was -28 +/- 2% and -39 +/- 7%, respectively, below steady state normoxic values. Blood pressure was unchanged with hyperoxia at rest or during exercise. CC stimulation with transient hypoxia increased MSNA with a similar time delay to that obtained with CC inhibition via hyperoxia. Consistent with previous animal work, these data indicate that the CC contributes to exercise-induced increases in sympathetic vasoconstrictor outflow.

摘要

最近,我们已经表明,在运动的犬类中特异性、短暂性地抑制颈动脉化学感受器(CC)会导致肢体肌肉血管舒张。本研究的目的是确定CC抑制是否会降低运动的人类的肌肉交感神经活动(MSNA)。健康受试者(N = 7)在静息时和有节奏的握力运动(50%最大自主收缩,20转/分钟)期间呼吸高氧气体(F(IO₂)约为1.0)60秒。使用微神经ography记录腓总神经中的MSNA。呼气末P(CO₂)在整个过程中维持在静息正常呼吸水平,呼吸频率由受试者自主固定。运动使心率(67对77次/分钟)、平均血压(81对97 mmHg)、MSNA爆发频率(28对37次/分钟)和MSNA总分钟活动(5.7对9.3单位)增加,但血乳酸没有变化(0.7对0.7 mmol)。短暂性高氧在静息时对MSNA没有显著影响。相比之下,在运动期间,高氧使MSNA爆发频率和总分钟活动均显著降低。在呼气末P(O₂)超过250 mmHg的9 - 23秒内,MSNA爆发频率降低。MSNA爆发频率和总分钟活动的平均最低点分别比稳态常氧值低-28±2%和-39±7%。在静息或运动时,高氧对血压没有影响。短暂性低氧刺激CC增加MSNA的时间延迟与通过高氧抑制CC时相似。与之前的动物研究一致,这些数据表明CC有助于运动诱导的交感缩血管流出增加。

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