Lockwood Jennifer M, Pricher Mollie P, Wilkins Brad W, Holowatz Lacy A, Halliwill John R
Department of Human Physiology, University of Oregon, Eugene, Oregon 97403-1240, USA.
J Appl Physiol (1985). 2005 Feb;98(2):447-53. doi: 10.1152/japplphysiol.00787.2004. Epub 2004 Oct 1.
In normally active individuals, postexercise hypotension after a single bout of aerobic exercise occurs due to an unexplained peripheral vasodilation. Prostaglandin production has been suggested to contribute to the increases in blood flow during and after exercise; however, its potential contribution to postexercise hypotension has not been assessed. The purpose of this study was to determine the potential contribution of a prostaglandin-dependent vasodilation to changes in systemic vascular conductance underlying postexercise hypotension; this was done by inhibiting production of prostaglandins with the cyclooxygenase inhibitor ibuprofen. We studied 11 healthy normotensive men (aged 23.7 +/- 4.2 yr) before and during the 90 min after a 60-min bout of cycling at 60% peak O(2) uptake on a control and a cyclooxygenase inhibition day (randomized). Subjects received 10 mg/kg of oral ibuprofen on the cyclooxygenase inhibition day. On both study days, arterial blood pressure (automated auscultation) and cardiac output (acetylene uptake) were measured, and systemic vascular conductance was calculated. Inhibition of cyclooxygenase had no effect on baseline values of mean arterial pressure or systemic vascular conductance (P > 0.2). After exercise on both days, mean arterial pressure was reduced (-2.2 +/- 1.0 mmHg change with the control condition and -3.8 +/- 1.5 mmHg change with the ibuprofen condition, both P < 0.05 vs. preexercise) and systemic vascular conductance was increased (5.2 +/- 5.0% change with the control condition and 8.7 +/- 4.1% change with the ibuprofen condition, both P < 0.05 vs. preexercise). There were no differences between study days (P > 0.6). These data suggest that prostaglandin-dependent vasodilation does not contribute to the increased systemic vascular conductance underlying postexercise hypotension.
在正常活动的个体中，单次有氧运动后出现运动后低血压是由于不明原因的外周血管舒张。有人提出前列腺素的产生有助于运动期间和运动后的血流增加；然而，其对运动后低血压的潜在作用尚未得到评估。本研究的目的是确定依赖前列腺素的血管舒张对运动后低血压基础上全身血管传导变化的潜在作用；通过用环氧化酶抑制剂布洛芬抑制前列腺素的产生来实现。我们在对照日和环氧化酶抑制日（随机）对11名健康的血压正常男性（年龄23.7±4.2岁）进行了研究，研究在60分钟的骑车运动（峰值摄氧量的60%）前及运动后90分钟内进行。在环氧化酶抑制日，受试者口服10mg/kg的布洛芬。在两个研究日，均测量动脉血压（自动听诊）和心输出量（乙炔摄取），并计算全身血管传导率。环氧化酶的抑制对平均动脉压或全身血管传导率的基线值没有影响（P>0.2）。在两天的运动后，平均动脉压均降低（对照条件下变化-2.2±1.0mmHg，布洛芬条件下变化-3.8±1.5mmHg，两者与运动前相比P<0.05），全身血管传导率均增加（对照条件下变化5.2±5.0%，布洛芬条件下变化8.7±4.1%，两者与运动前相比P<0.05）。研究日之间无差异（P>0.6）。这些数据表明，依赖前列腺素的血管舒张对运动后低血压基础上全身血管传导率增加没有作用。
