Sleep is considered essential for the brain and body. A predominant concept is that sleep is regulated by circadian rhythmicity and sleep homeostasis, processes that were posited to be functionally and mechanistically separate. Here we review and re-evaluate this concept and its assumptions using findings from recent human and rodent studies. Alterations in genes that are central to circadian rhythmicity affect not only sleep timing but also putative markers of sleep homeostasis such as electroencephalogram slow-wave activity (SWA). Perturbations of sleep change the rhythmicity in the expression of core clock genes in tissues outside the central clock. The dynamics of recovery from sleep loss vary across sleep variables: SWA and immediate early genes show an early response, but the recovery of non-rapid eye movement and rapid eye movement sleep follows slower time courses. Changes in the expression of many genes in response to sleep perturbations outlast the effects on SWA and time spent asleep. These findings are difficult to reconcile with the notion that circadian- and sleep–wake-driven processes are mutually independent and that the dynamics of sleep homeostasis are reflected in a single variable. Further understanding of how both sleep and circadian rhythmicity contribute to the homeostasis of essential physiological variables may benefit from the assessment of multiple sleep and molecular variables over longer time scales.

睡眠被认为对大脑和身体至关重要。一个主要的概念是，睡眠受到昼夜节律和睡眠稳态的调节，这些过程被认为在功能上和机械上是分开的。在这里，我们利用最近的人类和啮齿动物研究的结果来回顾和重新评估这个概念及其假设。对昼夜节律至关重要的基因的改变不仅影响睡眠时间，还影响睡眠稳态的假定标志，例如脑电图慢波活动（SWA）。睡眠扰动会改变中央生物钟以外组织中核心生物钟基因的表达节律。睡眠不足恢复的动态因睡眠变量而异：SWA 和立即早期基因显示出早期反应，但非快速眼动睡眠和快速眼动睡眠的恢复遵循较慢的时间进程。许多基因因睡眠干扰而发生的表达变化比对 SWA 和睡眠时间的影响更持久。这些发现很难与以下观点相一致：昼夜节律和睡眠觉醒驱动的过程是相互独立的，并且睡眠稳态的动态反映在单个变量中。对睡眠和昼夜节律如何促进基本生理变量的稳态的进一步了解可能会受益于在较长时间尺度上对多个睡眠和分子变量的评估。