Sleep Length and Circadian Regulation in Humans

摘要 数以百万计的美国人患有昼夜节律睡眠障碍，包括轮班工作睡眠障碍、喷气式飞机 迟缓，睡眠相延迟综合症，可能还有冬季抑郁症。这些情况通常是 以持续性失眠和/或白天过度嗜睡、表现不佳和 胃肠道不适。这些阴性症状是由于 外部社交世界和内部生物钟的计时。昼夜节律睡眠障碍是 有效地用明亮的光处理，这会使生物钟相移，从而使它与 外部社会世界。 人们普遍认为，社会影响导致了现代社会中越来越普遍的睡眠限制 社会。我们最近首次证明，与长时间睡眠相比，短时间的睡眠 插曲，明显减少了向明亮光线的相位推进。因此，当人们缩短睡眠时间时，他们 不经意间降低了它们对强光的昼夜反应。这些减少背后的机制(S) 光的相移是未知的。然而，短时睡眠至少有两个方面可能 对这一影响负有责任。首先，短时睡眠与部分睡眠不足有关。 其次，由于人类睡觉时闭着眼睛，醒着时通常暴露在光线下，所以睡眠时间很短 发作也与较短的黑暗长度有关。我们的总体目标是确定生物行为 短时睡眠损害了向明亮光线相移的机制。具体目标1是确定 部分睡眠剥夺对阶段的影响推进到了光明，同时控制了黑暗的长度。特定目标 二是确定在最大限度减少睡眠剥夺的同时，较短的黑暗长度对向光明阶段推进的影响。 我们将通过测量唾液褪黑激素(一种神经内分泌)来估计人类生物钟的时间。 松果体释放的荷尔蒙，通过活动记录收集睡眠指标，以及嗜睡， 情绪、胃肠不适和认知表现通过计算机评估。 睡眠剥夺和黑暗长度对昼夜向光的相移的单独影响的特征 对于理解人类在日常生活活动中对光的反应是至关重要的。 此外，这项研究的发现将提出重要和实用的建议，以避免 减少到相移到光，从而优化昼夜节律睡眠的强光治疗 从而改善公共健康和安全、福祉、情绪、认知功能和生活质量。叙事 这项研究将研究为什么睡眠限制会降低生物钟对强光的反应。结果是 将使强光治疗能够优化患有昼夜节律睡眠的人 睡眠障碍，包括轮班工作睡眠障碍、时差、睡眠相延迟综合症和冬季 抑郁，从而改善公共健康和安全、幸福感、情绪、心理功能和生活质量。

SUMMARY Millions of Americans suffer from circadian rhythm sleep disorders, which include shift work sleep disorder, jet lag, delayed sleep phase syndrome and possibly winter depression. These conditions are typically characterized by persistent insomnia and/or excessive daytime sleepiness, impaired performance, and gastrointestinal distress. These negative symptoms result from a misalignment between the timing of the external social world and the timing of the internal circadian (body) clock. Circadian rhythm sleep disorders are effectively treated with bright light, which phase shifts the circadian clock, thereby realigning it with the timing of the external social world. It is widely recognized that social influences have led to an increasing prevalence of sleep restriction in modern society. We recently demonstrated for the first time that short sleep episodes, when compared to long sleep episodes, markedly reduce phase advances to bright light. Thus when people cut their sleep short, they inadvertently reduce their circadian responsiveness to bright light. The mechanism(s) behind these reduced phase shifts to light are unknown. However, there are at least two aspects of short sleep episodes that could be responsible for this effect. First, short sleep episodes are associated with partial sleep deprivation. Second, as humans sleep with their eyes closed and are usually exposed to light when awake, short sleep episodes are also associated with short dark lengths. Our overall goal is to determine the biobehavioral mechanisms by which short sleep episodes impair phase shifts to bright light. Specific Aim 1 is to determine the effect of partial sleep deprivation on phase advances to light, while controlling for dark length. Specific Aim 2 is to determine the effect of short dark lengths on phase advances to light while minimizing sleep deprivation. We will estimate the timing of the human circadian clock by measuring salivary melatonin, a neuroendocrine hormone released from the pineal gland, and collecting measures of sleep via actigraphy, and sleepiness, mood, gastrointestinal distress and cognitive performance via computerized assessment. Characterization of the separate effects of sleep deprivation and dark length on circadian phase shifts to light in humans is critical to understanding how humans respond to light during their daily life activities. Furthermore, the findings of this research will produce important and practical recommendations for avoiding decrements to phase shifts to light, thereby optimizing the bright light treatment of circadian rhythm sleep disorders, and thus improving public health and safety, well-being, mood, cognitive function, and quality of life. NARRATIVE This research will examine why sleep restriction reduces the body clock's response to bright light. The results will enable the optimization of the bright light treatment of people who suffer from circadian rhythm sleep disorders, which include shift work sleep disorder, jet lag, delayed sleep phase syndrome and winter depression, thereby improving public health and safety, well-being, mood, mental function, and quality of life.