{"title":"The impact of acute sleep fragmentation on muscle blood flow responses to handgrip exercise.","authors":"Gabriel Narvaez, Joaquin U Gonzales","doi":"10.1152/japplphysiol.00509.2026","DOIUrl":null,"url":null,"abstract":"<p><p>Sleep fragmentation is reported to impair resting vascular function. The aim of this study was to test the hypothesis that acute sleep fragmentation would impair muscle blood flow during exercise. Twenty adults (10 females and 10 males) participated in a randomized crossover study that included one night of habitual sleep and one night of fragmented sleep. Sleep was assessed at home using wrist actigraphy. Arousals from sleep were increased by an audio alarm sounding every 30 min. The morning following each sleep condition, participants performed single handgrip contractions and rhythmic handgrip exercise at 15%, 30%, and 45% MVC. Forearm blood flow (FBF) was measured using Doppler ultrasound. Nightly awakenings and wake after sleep onset significantly increased by 18% and 43%, respectively, after fragmented sleep, leading to lower sleep duration (<i>P</i> < 0.001). Peak FBF and total hyperemic responses following single contractions were similar between sleep conditions (all <i>P</i> > 0.05). During rhythmic handgrip exercise, brachial artery dilation was reduced after fragmented sleep (main effect: 5.5 ± 4.8 vs. 3.3 ± 3.7%; <i>P</i> = 0.01), leading to a lower FBF response to rhythmic exercise (main effect: 122 ± 58 vs. 110 ± 56 mL/min; <i>P</i> = 0.04). Endothelial sensitivity to shear rate was similar between sleep conditions (habitual vs. fragmented: 0.039 ± 0.024 vs. 0.042 ± 0.031%/s<sup>-1</sup>; <i>P</i> = 0.77). In summary, acute sleep fragmentation decreases skeletal muscle blood flow during exercise. This finding suggests that blunted oxygen delivery may be a contributing factor for exercise performance deficits after disturbed sleep.<b>NEW & NOTEWORTHY</b> We demonstrate that one night of fragmented sleep decreases steady-state blood flow and vascular conductance during low- to moderate-intensity handgrip exercise. This impairment was not due to an impaired rapid vasodilation to single contractions nor altered endothelial sensitivity to shear rate as these variables were unchanged after acute sleep fragmentation. These results reveal a negative impact of disrupted sleep on the steady-state muscle vasodilatory response to rhythmic contractions.</p>","PeriodicalId":15160,"journal":{"name":"Journal of applied physiology","volume":" ","pages":"802-812"},"PeriodicalIF":3.7000,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of applied physiology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1152/japplphysiol.00509.2026","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2026/8/7 0:00:00","PubModel":"Epub","JCR":"Q1","JCRName":"PHYSIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Sleep fragmentation is reported to impair resting vascular function. The aim of this study was to test the hypothesis that acute sleep fragmentation would impair muscle blood flow during exercise. Twenty adults (10 females and 10 males) participated in a randomized crossover study that included one night of habitual sleep and one night of fragmented sleep. Sleep was assessed at home using wrist actigraphy. Arousals from sleep were increased by an audio alarm sounding every 30 min. The morning following each sleep condition, participants performed single handgrip contractions and rhythmic handgrip exercise at 15%, 30%, and 45% MVC. Forearm blood flow (FBF) was measured using Doppler ultrasound. Nightly awakenings and wake after sleep onset significantly increased by 18% and 43%, respectively, after fragmented sleep, leading to lower sleep duration (P < 0.001). Peak FBF and total hyperemic responses following single contractions were similar between sleep conditions (all P > 0.05). During rhythmic handgrip exercise, brachial artery dilation was reduced after fragmented sleep (main effect: 5.5 ± 4.8 vs. 3.3 ± 3.7%; P = 0.01), leading to a lower FBF response to rhythmic exercise (main effect: 122 ± 58 vs. 110 ± 56 mL/min; P = 0.04). Endothelial sensitivity to shear rate was similar between sleep conditions (habitual vs. fragmented: 0.039 ± 0.024 vs. 0.042 ± 0.031%/s-1; P = 0.77). In summary, acute sleep fragmentation decreases skeletal muscle blood flow during exercise. This finding suggests that blunted oxygen delivery may be a contributing factor for exercise performance deficits after disturbed sleep.NEW & NOTEWORTHY We demonstrate that one night of fragmented sleep decreases steady-state blood flow and vascular conductance during low- to moderate-intensity handgrip exercise. This impairment was not due to an impaired rapid vasodilation to single contractions nor altered endothelial sensitivity to shear rate as these variables were unchanged after acute sleep fragmentation. These results reveal a negative impact of disrupted sleep on the steady-state muscle vasodilatory response to rhythmic contractions.
据报道,睡眠碎片会损害静息血管功能。这项研究的目的是验证一个假设,即急性睡眠断裂会损害运动期间的肌肉血液流动。20名成年人(10名女性,10名男性)参加了一项随机交叉研究,其中包括一晚习惯性睡眠和一晚断断续续的睡眠。在家中使用腕部活动记录仪评估睡眠。每隔30分钟响起一次声音警报声,就会增加睡眠中的觉醒程度。在每一种睡眠状态之后的早晨,参与者分别以15%、30%和45%的MVC进行单握收缩和有节奏的握握锻炼。采用多普勒超声测量前臂血流量(FBF)。碎片化睡眠导致睡眠时间缩短后,夜间醒觉率和睡眠后醒觉率分别显著增加18%和43% (p 0.05)。在有节奏的握力训练中,断片睡眠后肱动脉扩张减少(主效应:5.5±4.8 vs 3.3±3.7 %;p=0.01),导致节律性运动的FBF反应降低(主效应:122±58 vs 110±56 mL/min; p=0.04)。内皮细胞对剪切率的敏感性在不同睡眠状态下相似(习惯性睡眠和碎片化睡眠:0.039±0.024 vs 0.042±0.031 %/s-1; p=0.77)。总之,急性睡眠断裂会减少运动时骨骼肌的血流量。这一发现表明,缺氧输送可能是睡眠紊乱后运动表现不足的一个因素。
期刊介绍:
The Journal of Applied Physiology publishes the highest quality original research and reviews that examine novel adaptive and integrative physiological mechanisms in humans and animals that advance the field. The journal encourages the submission of manuscripts that examine the acute and adaptive responses of various organs, tissues, cells and/or molecular pathways to environmental, physiological and/or pathophysiological stressors. As an applied physiology journal, topics of interest are not limited to a particular organ system. The journal, therefore, considers a wide array of integrative and translational research topics examining the mechanisms involved in disease processes and mitigation strategies, as well as the promotion of health and well-being throughout the lifespan. Priority is given to manuscripts that provide mechanistic insight deemed to exert an impact on the field.