McDonald Matthew J, Marsh Megan L, Fears Sharon D, Shariffi Brian, Kanaley Jill A, Limberg Jacqueline K
Department of Nutrition and Exercise Physiology, University of Missouri, Columbia, Missouri, United States.
Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri, United States.
J Appl Physiol (1985). 2025 Jan 1;138(1):282-288. doi: 10.1152/japplphysiol.00648.2024. Epub 2024 Dec 11.
Chronic exposure to shortened sleep is associated with an increased risk of Alzheimer's disease and dementia. Previous studies show insufficient (e.g., poor or fragmented) sleep impairs cerebrovascular reactivity to metabolic stress and may have a detrimental effect on the link between cerebral blood flow (CBF) and neural activity (i.e., neurovascular coupling, NVC). The purpose of this study was to examine the effect of acute sleep restriction on CBF in response to a metabolic (carbon dioxide, CO) and a cognitive stressor. We hypothesized sleep restriction (4-h time in bed) would attenuate CBF and NVC. Sixteen young adults (8 M/8 F, 28 ± 8 yr, 25 ± 3 kg/m) completed two morning visits following a night of normal (7.38 ± 0.82 h) or restricted (4.27 ± 0.93 h, < 0.001) sleep duration. Middle cerebral artery velocity (MCAv, transcranial Doppler ultrasound) was measured at rest and during ) 5 min of carbogen air-breathing and ) five trials consisting of a period of eyes closed (30 s), followed by eyes open (40 s) while being challenged with a validated visual paradigm (Where's Waldo). Baseline MCAv was unaffected by acute sleep restriction (control: 64 ± 14 cm/s; restricted 61 ± 13 cm/s; = 0.412). MCAv increased with CO; however, there was no effect of restricted sleep ( = 0.488). MCAv increased in response to visual stimulation; the peak NVC response was reduced from control following restricted sleep (control: 16 ± 12%; restricted: 9 ± 7%; = 0.008). Despite no effect of acute sleep restriction on resting CBF or the response to CO in young men and women, NVC was attenuated following a night of shortened sleep. These data support an important role for sleep in NVC and may have implications for the development of neurodegenerative disease states, such as Alzheimer's and dementia. Chronic exposure to shortened sleep is associated with an increased risk of Alzheimer's disease and dementia. We examined the effect of acute sleep restriction (4-h time in bed) on cerebral blood flow in response to a metabolic (carbon dioxide) and a cognitive stimulus. Despite no effect of acute sleep restriction on resting cerebral blood flow or the response to carbon dioxide in young men and women, neurovascular coupling was attenuated following a night of shortened sleep.
长期暴露于缩短的睡眠时间与患阿尔茨海默病和痴呆症的风险增加有关。先前的研究表明，睡眠不足（如质量差或碎片化）会损害脑血管对代谢应激的反应性，并可能对脑血流量（CBF）与神经活动之间的联系（即神经血管耦合，NVC）产生不利影响。本研究的目的是检验急性睡眠限制对CBF的影响，该影响是针对代谢（二氧化碳，CO）和认知应激源而言的。我们假设睡眠限制（卧床4小时）会减弱CBF和NVC。16名年轻成年人（8名男性/8名女性，28±8岁，体重指数25±3kg/m²）在经历了一晚正常（7.38±0.82小时）或受限（4.27±0.93小时，P<0.001）睡眠时间后，于两个上午前来就诊。在静息状态下以及在吸入卡波金空气5分钟期间和进行五次试验（每次试验包括闭眼30秒，然后睁眼40秒，同时接受经过验证的视觉范式“威利在哪里”的刺激）期间，测量大脑中动脉血流速度（MCAv，经颅多普勒超声）。急性睡眠限制对基线MCAv无影响（对照组：64±14cm/s；受限组：61±13cm/s；P = 0.412）。MCAv随CO增加；然而，睡眠受限对此无影响（P = 0.488）。MCAv对视觉刺激有增加反应；睡眠受限后，NVC的峰值反应相对于对照组降低（对照组：16±12%；受限组：9±7%；P = 0.008）。尽管急性睡眠限制对年轻男性和女性的静息CBF或对CO的反应没有影响，但缩短睡眠时间一晚后，NVC会减弱。这些数据支持了睡眠在NVC中的重要作用，并且可能对神经退行性疾病状态（如阿尔茨海默病和痴呆症）的发展有影响。长期暴露于缩短的睡眠时间与患阿尔茨海默病和痴呆症的风险增加有关。我们检验了急性睡眠限制（卧床4小时）对大脑血流的影响，该影响是针对代谢（二氧化碳）和认知刺激而言的。尽管急性睡眠限制对年轻男性和女性的静息脑血流量或对二氧化碳的反应没有影响，但缩短睡眠时间一晚后，神经血管耦合会减弱。
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