Department of Kinesiology and Health, College of Education, Health and Society, Miami University, 420 South Oak Street, Oxford, OH, 45056, USA.
Human Nutrition Program, College of Education and Human Ecology, The Ohio State University, Columbus, OH, 43210, USA.
Eur J Appl Physiol. 2017 Dec;117(12):2509-2518. doi: 10.1007/s00421-017-3738-2. Epub 2017 Oct 10.
Acute aerobic exercise prevents sitting-induced impairment of flow-mediated dilation (FMD). Further, evidence suggests that sitting-induced impairment of FMD occurs via an oxidative stress-dependent mechanism that disrupts endothelial function.
We hypothesized that acute aerobic exercise would prevent impairment of femoral artery FMD by limiting oxidative stress responses that increase endothelin-1 (ET-1) levels and disrupt nitric oxide (NO) status.
In a randomized, cross-over study, healthy men (n = 11; 21.2 ± 1.9 years) completed two 3 h sitting trials that were preceded by 45 min of either quiet rest (REST) or a single bout of continuous treadmill exercise (65% maximal oxygen consumption) (EX). Superficial femoral artery FMD, plasma glucose, malondialdehyde (MDA), ET-1, arginine (ARG) and its related metabolites [homoarginine (HA), asymmetric dimethylarginine (ADMA), symmetric dimethylarginine (SDMA)] were assessed at baseline, 1 h following EX (or REST) (0 h), and at 1 h intervals during 3 h of uninterrupted sitting. Data were analyzed using repeated measures ANOVA.
During REST, femoral artery FMD declined from baseline (2.6 ± 1.8%) at 1, 2, and 3 h of sitting and resting shear rate decreased at 3 h. In contrast, when sitting was preceded by EX, femoral artery FMD (2.7 ± 2.0%) and resting shear rate responses were unaffected. No between trial differences were detected for plasma glucose, MDA, ET-1, ARG, HA, ADMA, or SDMA.
Prior aerobic exercise prevented the decline in femoral artery FMD that is otherwise induced by prolonged sitting independent of changes in oxidative stress, ET-1, and NO status.
急性有氧运动可预防久坐导致的血流介导的扩张(FMD)受损。此外,有证据表明,久坐导致的 FMD 受损是通过一种依赖于氧化应激的机制发生的,该机制会破坏内皮功能。
我们假设急性有氧运动可以通过限制氧化应激反应来预防股动脉 FMD 受损,这些反应会增加内皮素-1(ET-1)水平并破坏一氧化氮(NO)状态。
在一项随机交叉研究中,健康男性(n=11;21.2±1.9 岁)完成了两次 3 小时的坐姿试验,此前分别进行了 45 分钟的安静休息(REST)或单次连续跑步机运动(65%最大摄氧量)(EX)。在基线、EX(或 REST)后 1 小时(0 小时)以及在 3 小时不间断坐姿期间每隔 1 小时评估股浅动脉 FMD、血浆葡萄糖、丙二醛(MDA)、ET-1、精氨酸(ARG)及其相关代谢物[同型精氨酸(HA)、不对称二甲基精氨酸(ADMA)、对称二甲基精氨酸(SDMA)]。使用重复测量方差分析对数据进行分析。
在 REST 期间,股动脉 FMD 从基线(2.6±1.8%)开始在 1、2 和 3 小时的坐姿和休息时剪切率下降,而当坐姿前进行 EX 时,股动脉 FMD(2.7±2.0%)和休息时剪切率反应不受影响。在两个试验之间,血浆葡萄糖、MDA、ET-1、ARG、HA、ADMA 或 SDMA 没有差异。
与长时间坐姿引起的股动脉 FMD 下降不同,有氧运动前可以预防这种下降,这与氧化应激、ET-1 和 NO 状态的变化无关。