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A commonly held view is that extended wakefulness is causal for a broad spectrum of deleterious effects at molecular, cellular, network, physiological, psychological, and behavioral levels. Consequently, it is often presumed that sleep plays an active role in providing renormalization of the changes incurred during preceding waking. Not surprisingly, unequivocal empirical evidence supporting such a simple bi-directional interaction between waking and sleep is often limited or controversial. One difficulty is that, invariably, a constellation of many intricately interrelated factors, including the time of day, specific activities or behaviors during preceding waking, metabolic status and stress are present at the time of measurement, shaping the overall effect observed. In addition to this, although insufficient or disrupted sleep is thought to prevent efficient recovery of specific physiological variables, it is also often difficult to attribute specific changes to the lack of sleep proper. Furthermore, sleep is a complex phenomenon characterized by a multitude of processes, whose unique and distinct contributions to the purported functions of sleep are difficult to determine, because they are interrelated. Intensive research effort over the last decades has greatly progressed current understanding of the cellular and physiological processes underlying the regulation of vigilance states. Notably, it also highlighted the infinite complexity within both waking and sleep, and revealed a number of fundamental conceptual and technical obstacles that need to be overcome in order to fully understand these processes. A promising approach could be to view sleep not as an entity, which has specific function(s) and is subject to direct regulation, but as a manifestation of the process of metaregulation, which enables efficient moment-to-moment integration between internal and external factors, preceding history and current homeostatic needs.

Sleep, recovery, and metaregulation: explaining the benefits of sleep