Department of Internal Medicine, Division of Geriatrics University of Utah, Salt Lake City, UT, United States of America; Department of Neuroscience, Biomedicine, and Movement Sciences, University of Verona, Italy.
Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UT, United States of America.
Auton Neurosci. 2022 May;239:102969. doi: 10.1016/j.autneu.2022.102969. Epub 2022 Mar 4.
The role of nitric oxide (NO) as a modulator of functional sympatholysis has been debated in the literature, but the preponderance of evidence suggests that the magnitude of NO-mediated dilation is restrained by sympathetic vasoconstriction. Therefore, we hypothesized that passive leg movement (PLM)-induced vasodilation, which is predominantly NO-mediated, would be attenuated by an exercise-induced increase in muscle sympathetic nerve activity (MSNA). To test this hypothesis, MSNA, leg blood flow (LBF), and mean arterial blood pressure (MAP) were measured and leg vascular conductance (LVC) calculated in 9 healthy subjects (30 ± 3 yr), during PLM with and without sympathoexcitation evoked by arm-cranking exercise (ACE), at 25, 50, and 75% of maximal capacity. During this incremental intensity ACE, MSNA increased significantly (26 ± 2, 34 ± 3, and 41 ± 5 bursts/100 HB, respectively). LVC during PLM fell markedly (~1.2 ml/min/mmHg) with each increase in ACE intensity, and there was a strong relationship (r = 0.92; p < 0.05) between ∆MSNA and ∆Peak LVC induced by the three intensities of ACE. Thus, as anticipated, this study reveals that the, NO-mediated, PLM-induced vasodilation, is significantly and proportionally attenuated by exercise-induced MSNA. This finding highlights the dominant role of MSNA in regulating skeletal muscle vascular conductance.
一氧化氮（NO）作为功能交感神经弛缓的调节剂的作用在文献中存在争议，但大多数证据表明，NO 介导的扩张程度受到交感神经血管收缩的限制。因此，我们假设被动腿部运动（PLM）引起的血管舒张，主要是由 NO 介导的，会被运动引起的肌肉交感神经活动（MSNA）增加所减弱。为了验证这一假设，我们在 9 名健康受试者（30 ± 3 岁）中测量了 MSNA、腿部血流量（LBF）和平均动脉血压（MAP），并计算了腿部血管传导性（LVC），在进行 PLM 时和进行手臂旋转运动（ACE）引起的交感神经兴奋时，ACE 的强度分别为最大能力的 25%、50%和 75%。在这种递增强度的 ACE 中，MSNA 显著增加（分别为 26 ± 2、34 ± 3 和 41 ± 5 次/100 心跳）。随着 ACE 强度的增加，PLM 期间的 LVC 明显下降（约 1.2ml/min/mmHg），并且三个 ACE 强度引起的 ∆MSNA 和 ∆Peak LVC 之间存在很强的关系（r = 0.92；p < 0.05）。因此，正如预期的那样，这项研究表明，NO 介导的 PLM 诱导的血管舒张被运动引起的 MSNA 显著且成比例地减弱。这一发现强调了 MSNA 在调节骨骼肌血管传导性方面的主导作用。
