Sleep loss results in an elevation of cortisol levels the next evening.
Sleep loss results in an elevation of cortisol levels the next evening.
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DOI：
10.1093/sleep/20.10.865
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发表时间：
1997-10
期刊：
影响因子：
5.6
通讯作者：
R. Leproult;G. Copinschi;O. Buxton;E. Cauter
中科院分区：
文献类型：
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作者：
R. Leproult;G. Copinschi;O. Buxton;E. Cauter
睡眠不足在工业化社会中越来越普遍，人们认为它影响的是情绪和表现，而不是生理功能。没有证据表明睡眠缺失对下丘脑-垂体-肾上腺（HPA）轴有长期或延迟的影响。我们评估了急性部分或全部睡眠剥夺对夜间和白天皮质醇水平的影响。在32小时内（从第一天的1800点到第三天的0200点），对接受三种不同睡眠方案的正常年轻男性的血浆皮质醇谱进行了测定：正常睡眠时间表（2300-0700小时），部分睡眠剥夺（0400-0800小时）和完全睡眠剥夺。皮质醇水平的变化只有在睡眠不足的晚上才会显现出来。在正常睡眠后，1800-2300小时的血浆皮质醇水平在第1天和第2天是相似的。在部分和全部睡眠剥夺后，血浆皮质醇水平在第2天高于第1天（分别增加37%和45%，p = 0.03和0.003），皮质醇分泌静息期的开始至少延迟了1小时。我们的结论是，即使是部分急性睡眠缺失也会延迟HPA从清晨昼夜节律刺激中恢复，因此可能涉及糖皮质激素负反馈调节的改变。因此，睡眠不足可能会影响应激反应的恢复能力，并可能加速糖皮质激素过量导致的代谢和认知后果的发展。
Sleep curtailment constitutes an increasingly common condition in industrialized societies and is thought to affect mood and performance rather than physiological functions. There is no evidence for prolonged or delayed effects of sleep loss on the hypothalamo-pituitary-adrenal (HPA) axis. We evaluated the effects of acute partial or total sleep deprivation on the nighttime and daytime profile of cortisol levels. Plasma cortisol profiles were determined during a 32-hour period (from 1800 hours on day 1 until 0200 hours on day 3) in normal young men submitted to three different protocols: normal sleep schedule (2300-0700 hours), partial sleep deprivation (0400-0800 hours), and total sleep deprivation. Alterations in cortisol levels could only be demonstrated in the evening following the night of sleep deprivation. After normal sleep, plasma cortisol levels over the 1800-2300-hour period were similar on days 1 and 2. After partial and total sleep deprivation, plasma cortisol levels over the 1800-2300-hour period were higher on day 2 than on day 1 (37 and 45% increases, p = 0.03 and 0.003, respectively), and the onset of the quiescent period of cortisol secretion was delayed by at least 1 hour. We conclude that even partial acute sleep loss delays the recovery of the HPA from early morning circadian stimulation and is thus likely to involve an alteration in negative glucocorticoid feedback regulation. Sleep loss could thus affect the resiliency of the stress response and may accelerate the development of metabolic and cognitive consequences of glucocorticoid excess.