The two-process model of sleep regulation: a reappraisal.
AI Summary
This study examines the two-process model of sleep regulation, which has served as a major conceptual framework in sleep research for three decades. The model describes how sleep is regulated by the interaction between a homeostatic process (Process S) that builds sleep pressure during wakefulness, and a circadian process (Process C) controlled by the body's internal clock. The research suggests this model successfully simulates sleep timing and intensity across diverse experimental conditions. The study reveals that these processes interact continuously through the suprachiasmatic nuclei (SCN), the brain's master clock. Additionally, the research indicates that peripheral oscillators linked to energy metabolism can operate independently of the central pacemaker, particularly during restricted feeding or certain drug administration. The model has practical applications, supporting the development of non-pharmacological psychiatric treatments that manipulate circadian phase, sleep timing, and light exposure. The findings suggest sleep serves both short-term restorative functions and helps optimize metabolic processes by enforcing rest and fasting at appropriate times in the 24-hour cycle.
Key Findings
- The two-process model successfully simulates sleep timing and intensity across diverse experimental protocols through interaction of homeostatic and circadian processes
- Peripheral oscillators linked to energy metabolism can operate independently of the central circadian pacemaker under certain conditions
- Sleep serves to enforce rest and fasting, thereby supporting optimization of metabolic processes at appropriate phases of the 24-hour cycle
- The model has supported development of non-pharmacological psychiatric treatments based on manipulating circadian phase, sleep, and light exposure
Abstract
In the last three decades the two-process model of sleep regulation has served as a major conceptual framework in sleep research. It has been applied widely in studies on fatigue and performance and to dissect individual differences in sleep regulation. The model posits that a homeostatic process (Process S) interacts with a process controlled by the circadian pacemaker (Process C), with time-courses derived from physiological and behavioural variables. The model simulates successfully the timing and intensity of sleep in diverse experimental protocols. Electrophysiological recordings from the suprachiasmatic nuclei (SCN) suggest that S and C interact continuously. Oscillators outside the SCN that are linked to energy metabolism are evident in SCN-lesioned arrhythmic animals subjected to restricted feeding or methamphetamine administration, as well as in human subjects during internal desynchronization. In intact animals these peripheral oscillators may dissociate from the central pacemaker rhythm. A sleep/fast and wake/feed phase segregate antagonistic anabolic and catabolic metabolic processes in peripheral tissues. A deficiency of Process S was proposed to account for both depressive sleep disturbances and the antidepressant effect of sleep deprivation. The model supported the development of novel non-pharmacological treatment paradigms in psychiatry, based on manipulating circadian phase, sleep and light exposure. In conclusion, the model remains conceptually useful for promoting the integration of sleep and circadian rhythm research. Sleep appears to have not only a short-term, use-dependent function; it also serves to enforce rest and fasting, thereby supporting the optimization of metabolic processes at the appropriate phase of the 24-h cycle.
Authors
Alexander A Borbély, Serge Daan, Anna Wirz-Justice, Tom Deboer