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Regular Aerobic Exercise Counteracts Endothelial Vasomotor Dysfunction Associated With Insufficient Sleep
American Journal of Physiology-Heart and Circulatory Physiology ( IF 4.1 ) Pub Date : 2021-01-08 , DOI: 10.1152/ajpheart.00615.2020
Kelly A Stockelman 1 , Anthony R Bain 2 , Caitlin A Dow 1 , Kyle J Diehl 1 , Jared J Greiner 1 , Brian L Stauffer 3, 4 , Christopher A DeSouza 1, 3
Affiliation  

Insufficient sleep is associated with endothelial vasomotor dysfunction and increased cardiovascular risk. Regular aerobic exercise is an effective lifestyle strategy for improving endothelial function and, in turn, reducing cardiovascular risk. We tested the hypotheses that regular aerobic exercise would: 1) improve endothelial vasodilation; and 2) decrease ET-1-mediated vasoconstrictor tone in middle-aged adults who chronically sleep <7 h/night. Thirty-six healthy, middle-aged adults were studied: 16 with normal sleep duration (age: 57±2 yr; sleep duration: 7.4±0.1 h/night) and 20 with short sleep duration (56±1 yr; 6.2±0.1 h/night). The 20 short sleepers completed a 3-month aerobic exercise training intervention. Forearm blood flow was determined (via plethysmography) in response to intra-arterial acetylcholine (ACh), BQ-123 (ETAreceptor antagonist), ACh+BQ-123 and sodium nitroprusside. Forearm blood flow responses to ACh were lower (20%; P<0.05) in the short (from 4.2±0.2 to 10.5±0.6 mL/100 mL tissue/min) vs normal (4.2±0.2 to 12.7±0.6 mL/100 mL tissue/min) sleepers. In response to BQ-123, the short sleep group had a significantly greater increase in resting forearm blood flow than the normal sleep group (~25% vs ~8%). ACh+BQ-123 resulted in a significant (~25%) increase in the ACh-vasodilation in the short sleep group only. After exercise training, although nightly sleep duration was unchanged (6.4±0.1 h/night), ACh-mediated vasodilation was significantly higher (~20%), ET-1-mediated vasoconstriction was significantly lower (~80%) and the vasodilator response to ACh was not increased with ETAreceptor blockade. Regular aerobic exercise, independent of changes in nightly sleep duration, can counteract insufficient sleep-related endothelial vasomotor dysfunction.

中文翻译:

定期有氧运动可抵消与睡眠不足相关的内皮血管舒缩功能障碍

睡眠不足与内皮血管舒缩功能障碍和心血管风险增加有关。有规律的有氧运动是一种有效的生活方式策略,可以改善内皮功能,进而降低心血管风险。我们测试了定期有氧运动会:1)改善内皮血管舒张的假设;2) 降低长期睡眠 <7 小时/晚的中年人的 ET-1 介导的血管收缩张力。研究了 36 名健康的中年成年人:16 名睡眠时间正常(年龄:57±2 岁;睡眠时间:7.4±0.1 小时/晚)和 20 名睡眠时间短(56±1 岁;6.2±0.1小时/晚)。20名短卧者完成了为期3个月的有氧运动训练干预。响应动脉内乙酰胆碱 (ACh)、BQ-123 (ET) 测定前臂血流(通过体积描记法)受体拮抗剂) 、 ACh+BQ-123 和硝普钠。短期(从 4.2±0.2 到 10.5±0.6 mL/100 mL 组织/分钟)与正常(4.2±0.2 到 12.7±0.6 mL/100 mL)相比,前臂血流对 ACh 的反应较低(20%;P<0.05)组织/分钟)枕木。针对 BQ-123,短睡眠组的静息前臂血流显着高于正常睡眠组(~25% vs ~8%)。ACh+BQ-123 仅在短睡眠组中导致 ACh 血管舒张显着增加 (~25%)。运动训练后,虽然夜间睡眠时间没有变化(6.4±0.1 小时/晚),但 ACh 介导的血管舒张显着更高(~20%),ET-1 介导的血管收缩显着降低(~80%)和血管舒张反应用 ET A不增加对 ACh 的影响受体阻滞剂。有规律的有氧运动,独立于夜间睡眠时间的变化,可以抵消睡眠不足的内皮血管舒缩功能障碍。
更新日期:2021-01-10
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