1Graduate School of Physical Education, Kyung Hee University, Seocheon-dong Giheung-gu Yongin-si Gyeonggi-do, KOREA; and 2Department of Internal Medicine, Division of Cardiovascular Medicine, University of California at Davis, Davis, CA.
Med Sci Sports Exerc. 2015 Aug;47(8):1605-12. doi: 10.1249/MSS.0000000000000573.
Previously, we found that the pressor response to muscle metaboreflex activation is enhanced in prehypertension and associated with peripheral vasoconstriction. However, mechanisms underlying this exaggerated response are not clear. Therefore, we tested the hypothesis that activation of this reflex is augmented owing to increased production of muscle metabolites (i.e., lactate, K, and H).
Twenty-two men (11 normotensive and 11 prehypertensive) were studied. Changes in cardiac output (Q˙), mean arterial pressure (MAP), and total peripheral resistance (TPR) were compared between the two groups during static exercise (SE) and postexercise muscular ischemia (PEMI). Subjects completed 2 min of SE at 50% of maximal voluntary contraction (MVC) followed by 2 min of PEMI. Venous blood samples for determination of metabolites and hormones (catecholamines, vasopressin, and plasma renin activity) were taken from the exercising and nonexercising arm, respectively.
Mean arterial pressure responses to SE (39 ± 3 vs 31 ± 2 mm Hg) and PEMI (24 ± 3 vs 19 ± 3 mm Hg) were significantly higher in the prehypertensive group. Increases in lactate and decreases in pH during PEMI were seen in both groups. However, changes in these variables were greater in the prehypertensive group (lactate, 50.1 ± 6.2 vs 32.8 ± 7.6 mg·dL; pH, -0.06 ± 0.02 vs -0.01 ± 0.01) (P < 0.05). Postexercise muscular ischemia did not evoke increases in hormones in either group.
Compared to the normotensive group, the augmented pressor response to the metaboreflex in the prehypertensive group was associated with greater production of muscle metabolites that activate its afferent arm. The augmented response was not associated with activation of the vasopressin and renin-angiotensin systems and greater activation of the sympathetic nervous system was not apparent. Consequently, additional factors specific to prehypertension, such as arterial stiffness, may have been involved.
此前，我们发现肌肉代谢反射激活引起的升压反应在高血压前期增强，并与外周血管收缩有关。然而，这种夸大反应的机制尚不清楚。因此，我们假设这种反射的激活是由于肌肉代谢产物（即乳酸、钾和氢离子）的产生增加所致。
22 名男性（11 名血压正常和 11 名高血压前期）参加了研究。在两组中比较了静息运动（SE）和运动后肌肉缺血（PEMI）期间心输出量（Q˙）、平均动脉压（MAP）和总外周阻力（TPR）的变化。受试者在最大自主收缩（MVC）的 50%下完成 2 分钟的 SE，然后进行 2 分钟的 PEMI。分别从运动和非运动手臂抽取静脉血样，以测定代谢物和激素（儿茶酚胺、血管加压素和血浆肾素活性）。
高血压前期组 SE（39 ± 3 对 31 ± 2 mmHg）和 PEMI（24 ± 3 对 19 ± 3 mmHg）的平均动脉压反应显著更高。两组 PEMI 期间均可见乳酸增加和 pH 值降低。然而，高血压前期组这些变量的变化更大（乳酸，50.1 ± 6.2 对 32.8 ± 7.6 mg·dL；pH 值，-0.06 ± 0.02 对-0.01 ± 0.01）（P < 0.05）。两组运动后肌肉缺血均未引起激素增加。
与血压正常组相比，高血压前期组代谢反射引起的升压反应增强与肌肉代谢产物产生增加有关，这些代谢产物激活了其传入臂。这种增强的反应与血管加压素和肾素-血管紧张素系统的激活无关，也没有明显的交感神经系统的更大激活。因此，可能涉及高血压前期特有的其他因素，如动脉僵硬。
