Human Technology Research Institute, National Institute of Advanced Industrial Science and Technology Ibaraki, Japan.
Human Technology Research Institute, National Institute of Advanced Industrial Science and Technology Ibaraki, Japan ; Department of Biomedical Engineering, Toyo University Kawagoe, Japan.
Front Physiol. 2014 Jun 24;5:229. doi: 10.3389/fphys.2014.00229. eCollection 2014.
To prevent orthostatic hypotension, arterial blood pressure (BP) is neurally and hormonally regulated via increases in heart rate (HR) and peripheral vascular tone. After dynamic exercise, however, the latter arm is blunted because of the increased vasodilators in exercised muscles. Orthostatic tachycardia is likely a more important compensatory mechanism for post-exercise orthostatic intolerance in individuals who have higher leg vasodilator capacity, such as endurance-trained athletes. To test the hypothesis that regular endurance training was associated with the greater augmentation of tachycardia response to post-exercise orthostasis, we compared hemodynamic responses to 5-min 60° head-up tilt (HUT) before and after 60 min of cycling at 70% of HR reserve in the endurance-trained (n = 8) and sedentary men (n = 9). Calf peak vascular conductance was 62% greater in the endurance-trained than the sedentary (P < 0.001). After the exercise, the HUT-induced reduction of SV was significantly augmented in the endurance-trained (from -27.7 ± 6.9 to -33.7 ± 7.7 ml, P = 0.03) but not in their sedentary peers. Nevertheless, MAP was well maintained during post-exercise HUT even in the endurance-trained (from 81 ± 10 to 80 ± 8 mmHg). Tachycardia responses during sustained orthostasis were significantly increased in the sedentary (1.3-fold vs. pre-exercise) and more in the endurance-trained (2.0-fold). The augmented response of HUT-induced tachycardia was greater in the endurance-trained than the sedentary (P = 0.04). Additionally, cardiovagal baroreflex sensitivity (BRS), evaluated by the HR response to the hypotensive perturbation, was improved after the exercise in the endurance-trained (from -0.56 ± 0.32 to -1.03 ± 0.26 bpm/mmHg, P = 0.007) but not in the sedentary. These results suggest that in the endurance-trained men the increased orthostatic tachycardia and augmented cardiovagal BRS may favorably mitigate accumulated risks for orthostatic intolerance in the early phase of post-exercise.
为了预防体位性低血压,动脉血压(BP)通过心率(HR)和外周血管张力的增加在神经和激素水平上得到调节。然而,在动态运动后,后者的手臂会变得迟钝,因为运动肌肉中的血管舒张剂增加。在腿部血管舒张能力较高的个体中,如耐力训练的运动员,体位性心动过速可能是运动后体位不耐受的更重要代偿机制。为了检验常规耐力训练与运动后体位性不耐受时心率反应增强的相关性假设,我们比较了 8 名耐力训练者和 9 名久坐者在 70%的心率储备下进行 60 分钟自行车运动前后 5 分钟 60°头高位倾斜(HUT)时的血流动力学反应。耐力训练者的小腿峰值血管传导率比久坐者高 62%(P<0.001)。运动后,HUT 引起的 SV 减少在耐力训练者中显著增加(从-27.7±6.9 到-33.7±7.7 ml,P=0.03),但在久坐者中没有增加。然而,即使在耐力训练者中,MAP 在运动后 HUT 期间也能得到很好的维持(从 81±10 到 80±8 mmHg)。在久坐者中,持续的体位性心动过速反应增加了 1.3 倍(与运动前相比),在耐力训练者中增加了 2.0 倍。HUT 引起的心动过速反应的增强在耐力训练者中比久坐者更大(P=0.04)。此外,通过 HR 对低血压刺激的反应评估,心脏迷走神经反射敏感性(BRS)在运动后在耐力训练者中得到改善(从-0.56±0.32 到-1.03±0.26 bpm/mmHg,P=0.007),但在久坐者中没有改善。这些结果表明,在耐力训练的男性中,增加的体位性心动过速和增强的心脏迷走神经反射敏感性可能在运动后早期有利地减轻体位不耐受的累积风险。