Raven P B, Welch-O'Connor R M, Shi X
Department of Integrative Physiology, University of North Texas Health Science Center at Fort Worth 76107, USA.
Med Sci Sports Exerc. 1998 Jul;30(7):1041-52. doi: 10.1097/00005768-199807000-00004.
The aim of this study was to test the hypothesis that a sustained reduction of physical activity (deconditioning) would alter the cardiovascular regulatory function.
Nineteen young, healthy volunteers participated in physical deconditioning for a period of 8 wk. Before (pre) and following (post) physical deconditioning, the responses of heart rate (HR), mean arterial pressure (MAP, measured by Finapres), central venous pressure (CVP), stroke volume (SV, Doppler), and forearm blood flow (FBF, plethysmography) were determined during lower body negative pressure (LBNP). The carotid baroreflex (CBR) function was assessed using a train of pulsatile neck pressure (NP) and suction, and the aortic baroreflex control of HR was assessed during steady-state phenylephrine (PE) infusion superimposed by LBNP and NP to counteract the PE increased CVP and carotid sinus pressure, respectively.
Active physical deconditioning significantly decreased maximal oxygen uptake (-7%) and LBNP tolerance (-13%) without a change in baseline hemodynamics. Plasma volume (-3% at P = 0.135), determined by Evans Blue dilution, and blood volume (-4% at P = 0.107) were not significantly altered. During LBNP -20 to -50 torr, there was a significantly greater drop of SV per unit decrease in CVP in the post- (14.7 +/- 1.6%/mm Hg) than predeconditioning (11.2 +/- 0.7%/mm Hg) test accompanied by a greater tachycardia. Deconditioning increased the aortic baroreflex sensitivity (pre vs post: -0.61 +/- 0.12 vs -0.84 +/- 0.14 bpm.mm-1 Hg, P = 0.009) and the slope of forearm vascular resistance (calculated from [MAP-CVP]/FBF) to CVP (-2.75 +/- 0.26 vs -4.94 +/- 0.97 PRU/mm Hg, P = 0.086). However, neither the CBR-HR (-0.28 +/- 0.03 VS -0.39 +/- 0.10 bpm.mm-1 Hg) nor the CBR-MAP (-0.37 +/- 0.16 vs -0.25 +/- 0.07 mm Hg/mm Hg) gains were statistically different between pre- and postdeconditioning.
We concluded that the functional modification of the cardiac pressure-volume relationship resulted in the reduced LBNP tolerance, despite the accentuated aortic and cardiopulmonary baroreflex function following deconditioning.
本研究旨在验证以下假设，即身体活动的持续减少（去适应）会改变心血管调节功能。
19名年轻健康志愿者参与了为期8周的身体去适应过程。在身体去适应之前（预）和之后（后），在下半身负压（LBNP）期间测定心率（HR）、平均动脉压（MAP，通过Finapres测量）、中心静脉压（CVP）、每搏输出量（SV，多普勒法）和前臂血流量（FBF，体积描记法）的反应。使用一系列搏动性颈部压力（NP）和吸力评估颈动脉压力反射（CBR）功能，在稳态去氧肾上腺素（PE）输注期间叠加LBNP和NP分别抵消PE引起的CVP和颈动脉窦压力增加，评估主动脉压力反射对HR的控制。
积极的身体去适应显著降低了最大摄氧量（-7%）和LBNP耐受性（-13%），而基线血流动力学无变化。通过伊文思蓝稀释法测定的血浆量（P = 0.135时为-3%）和血容量（P = 0.107时为-4%）无显著改变。在LBNP -20至-50托期间，与去适应前（11.2±0.7%/mmHg）测试相比，去适应后（14.7±1.6%/mmHg）每单位CVP降低时SV的下降幅度显著更大，同时伴有更大的心动过速。去适应增加了主动脉压力反射敏感性（去适应前与去适应后：-0.61±0.12对-0.84±0.14次/分·mmHg，P = 0.009）以及前臂血管阻力（根据[MAP - CVP]/FBF计算）对CVP的斜率（-2.75±0.26对-4.94±0.97 PRU/mmHg，P = 0.086）。然而，去适应前后CBR - HR（-0.28±0.03对-0.39±0.10次/分·mmHg）和CBR - MAP（-0.37±0.16对-0.25±0.07 mmHg/mmHg）增益在统计学上无差异。
我们得出结论，尽管去适应后主动脉和心肺压力反射功能增强，但心脏压力 - 容量关系的功能改变导致LBNP耐受性降低。
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