Atkinson Ceri L, Carter Howard H, Naylor Louise H, Dawson Ellen A, Marusic Petra, Hering Dagmara, Schlaich Markus P, Thijssen Dick H J, Green Daniel J
School of Sports Science, Exercise and Health, The University of Western Australia, Crawley, Western Australia;
Research Institute for Sport and Exercise Science, Liverpool John Moores University, Liverpool, United Kingdom;
J Appl Physiol (1985). 2015 Oct 15;119(8):858-64. doi: 10.1152/japplphysiol.01086.2014. Epub 2015 Aug 20.
While the impact of changes in blood flow and shear stress on artery function are well documented, the acute effects of increases in arterial pressure are less well described in humans. The aim of this study was to assess the effect of 30 min of elevated blood pressure, in the absence of changes in shear stress or sympathetic nervous system (SNS) activation, on conduit artery diameter. Ten healthy male subjects undertook three sessions of 30 min unilateral handgrip exercise at 5, 10, and 15% of maximal voluntary contractile (MVC) strength. Brachial artery shear rate and blood flow profiles were measured simultaneously during exercise in the active and contralateral resting arms. Bilateral brachial artery diameter was simultaneously assessed before and immediately postexercise. In a second experiment, six subjects repeated the 15% MVC condition while continuous vascular measurements were collected during muscle sympathetic nerve activity (MSNA) assessment using peroneal microneurography. We found that unilateral handgrip exercise at 5, 10, and 15% MVC strength induced stepwise elevations in blood pressure (P < 0.01, Δmean arterial pressure: 7.06 ± 2.44, 8.50 ± 2.80, and 18.35 ± 3.52 mmHg, P < 0.01). Whereas stepwise increases were evident in shear rate in the exercising arm (P < 0.001), no changes were apparent in the nonexercising limb (P = 0.42). Brachial artery diameter increased in the exercising arm (P = 0.02), but significantly decreased in the nonexercising arm (P = 0.03). At 15% MVC, changes in diameter were significantly different between arms (interaction effect: P = 0.01), whereas this level of exertion produced no significant changes in MSNA. We conclude that acute increases in transmural pressure, independent of shear rate and changes in SNS activation, reduce arterial caliber in normotensive humans in vivo. These changes in diameter were mitigated by exercise-induced elevations in shear rate in the active limb.
虽然血流和剪切应力变化对动脉功能的影响已有充分记载，但动脉压升高的急性效应在人体中的描述较少。本研究的目的是评估在剪切应力或交感神经系统（SNS）激活无变化的情况下，30分钟血压升高对传导动脉直径的影响。10名健康男性受试者进行了三次30分钟的单侧握力运动，强度分别为最大自主收缩（MVC）强度的5%、10%和15%。在运动过程中，同时测量活动侧和对侧静息手臂的肱动脉剪切速率和血流情况。在运动前和运动后立即同时评估双侧肱动脉直径。在第二个实验中，6名受试者重复15%MVC强度的运动，同时在使用腓骨微神经ography评估肌肉交感神经活动（MSNA）期间收集连续的血管测量数据。我们发现，5%、10%和15%MVC强度的单侧握力运动导致血压逐步升高（P<0.01，平均动脉压变化：7.06±2.44、8.50±2.80和18.35±3.52mmHg，P<0.01）。虽然运动侧手臂的剪切速率明显逐步增加（P<0.001），但非运动侧肢体无明显变化（P=0.42）。运动侧手臂的肱动脉直径增加（P=0.02），而非运动侧手臂的肱动脉直径显著减小（P=0.03）。在15%MVC强度时，两侧手臂的直径变化有显著差异（交互作用效应：P=0.01），而这种运动强度对MSNA无显著影响。我们得出结论，在体内正常血压的人体中，跨壁压力的急性增加，与剪切速率和SNS激活变化无关，会减小动脉管径。活动肢体中运动诱导的剪切速率升高减轻了这些直径变化。
