Repeating patterns of sleep restriction and recovery - do we get used to it?

描述（由申请人提供）：工作日限制睡眠，周末补觉是工作和学校人群中非常常见的模式，并且可以持续数十年。许多人认为，他们习惯于这种反复出现的睡眠限制模式，周末睡懒觉（即，获得“恢复睡眠”）完全恢复一周中失去的任何睡眠。然而，目前还没有证据支持这一假设，并且仍然不清楚参与应激反应的系统（例如，下丘脑-垂体-肾上腺[HPA]轴、交感-肾上腺系统和炎症系统）对这些反复的睡眠丧失和恢复模式作出反应。睡眠不足是一种重要而独特的生理应激源，因为睡眠本身是调节和维持各种生理系统所必需的生物资源。由于压力反应系统的失调与广泛的疾病状态有关，因此了解这些系统如何受到这些常见睡眠模式的影响非常重要。具体来说，压力反应是否变得习惯化，并对重复的睡眠限制和恢复睡眠表现出反应减弱，或者它是否变得敏感并表现出反应增强？还有一个问题是，通常分配给恢复睡眠的时间（即，周末晚上）足以从一周中积累的睡眠债务中恢复过来。关于从任何类型的睡眠丧失中恢复的情况知之甚少;然而，初步数据表明，即使是单次睡眠丧失，也可能存在生物和主观恢复的分离。我们建议使用23天的住院方案研究重复暴露于睡眠不足的影响，其中三个周期的五天睡眠限制在每晚4小时，然后是两天的恢复睡眠，因此非常类似于普通人群中许多人所经历的现实生活中的睡眠限制-恢复模式。我们将研究HPA，交感肾上腺和炎症系统的反应模式，以及主观情绪和疼痛评级，无论是在睡眠限制之间和之内。我们还将测试一种潜在的致敏机制：单核细胞对皮质醇抗炎作用的敏感性受损。这项研究的结果将为以下问题提供重要见解：反复睡眠限制和恢复的常见模式是否会损害压力反应系统的完整性，从而增加对各种疾病的易感性，包括心血管，情绪和疼痛相关疾病。

DESCRIPTION (provided by applicant): Restricting sleep on week days and catching up on sleep over the weekend is an extremely common pattern among both working and school populations, and is one that can persist for decades. Many people believe that they habituate to this recurrent pattern of sleep restriction, and that sleeping in on the weekends (i.e., obtaining 'recovery sleep') fully restores any sleep lost during the week. However, there is currently no evidence to support this hypothesis, and it remains unknown how systems involved in the stress response (e.g., the hypothalamic-pituitary-adrenal [HPA} axis, the sympatho-adrenal system, and the inflammatory system) react to these recurrent sleep loss and recovery patterns. Sleep loss is a significant and unique physiological stressor, as sleep itself is a biological resource necessary to regulate and maintain various physiological systems. As dysregulation of stress response systems is associated with a broad range of disease states, it is important to understand how these systems are affected by these commonly observed sleep patterns. Specifically, does the stress response become habituated and show a decreased response to repeated episodes of sleep restriction and recovery sleep, or does it become sensitized and exhibit an increased response? There also remains a question of whether the time generally allotted for recovery sleep (i.e., weekend nights) is sufficient to recover from the sleep debt accumulated during the week. Little is known about recovery from any type of sleep loss; however, preliminary data suggests that there may be a dissociation of biological and subjective recovery even from single episodes of sleep loss. We propose to investigate the effects of repeated exposure to sleep loss using a 23-day in-hospital protocol with three cycles of five days sleep restricted to 4 hours per night followed by two days of recovery sleep, thus closely resembling a real-life sleep restriction-recovery pattern experienced by many in the general population. We will study response patterns of HPA, sympatho-adrenal, and inflammatory systems, as well as subjective mood and pain ratings, both between and within episodes of sleep restriction. We will also test a potential mechanism of sensitization: impaired sensitivity of monocytes to the anti-inflammatory effects of cortisol. Results from this research will provide critical insights into the question of whether common patterns of recurrent sleep restriction and recovery compromise the integrity of stress response systems, thereby increasing susceptibility to a variety of diseases including cardiovascular, mood- and pain-related disorders.