Timing of human sleep: recovery process gated by a circadian pacemaker

Abstract

A model for the timing of human sleep is presented. It is based on a sleep-regulating variable (S)--possibly, but not necessarily, associated with a neurochemical substance--which increases during wakefulness and decreases during sleep. Sleep onset is triggered when S approaches an upper threshold (H); awakening occurs when S reaches a lower threshold (L). The thresholds show a circadian rhythm controlled by a single circadian pacemaker. Time constants of the S process were derived from rates of change of electroencephalographic (EEG) power density during regular sleep and during recovery from sleep deprivation. The waveform of the circadian threshold fluctuations was derived from spontaneous wake-up times after partial sleep deprivation. The model allows computer simulations of the main phenomena of human sleep timing, such as 1) internal desynchronization in the absence of time cues, 2) sleep fragmentation during continuous bed rest, and 3) circadian phase dependence of sleep duration during isolation from time cues, recovery from sleep deprivation, and shift work. The model shows that the experimental data are consistent with the concept of a single circadian pacemaker in humans. It has implications for the understanding of sleep as a restorative process and its timing with respect to day and night.

Effects of seganserin, a 5-HT2 antagonist, and temazepam on human sleepsstages and EEG power spectra

“…These data are in accordance with the hypothesis that EEG slow wave activity is under homeostatic control, and that the duration of sleep is to a large extent determined by the circadian phase during which sleep takes place (Borbrly, 1982;Daan et al, 1984). Spectral analysis of the recovery sleep EEG demonstrated the differential response of EEG frequencies to sleep deprivation.…”

All night spectral analysis of EEG sleep in young adult and middle-aged male subjects

“…In a recently developed model for the timing of sleep and wakefulness (4,6) these changes are thought to reflect a sleep regulatory process. In this model the timing of sleep and wakefulness results from an interaction between a homeostatic process S and a circadian process C. Process S reflects sleep debt which increases during waking in a saturating exponential way and decreases exponentially during sleep.…”

Different Effects of Phenelzine Treatment on EEG Topography in Waking and Sleep in Depressed Patients

“…The timing of sleep and wakefulness and the structure of sleep are regulated by the interaction of a homeostatic, sleep-wake-dependent process S and the circadian pacemaker located in the hypothalamus et al 1981;Daan et al 1984;Dijk et al 1987;Achermann et al 1993). Recent studies have indicated that an EEG correlate of sleep propensity can also be measured during wakefulness.…”

“…Different theories have been proposed to account for the antidepressant effects of sleep manipulations. They include prolonged major suppression of REM sleep (Vogel 1975;Vogel et al 1990), elevation of sleep propensity (Borbély and Wirz-Justice 1982), and reduction of non-REM sleep intensity (Beersma and Van den Hoofdakker 1992).The timing of sleep and wakefulness and the structure of sleep are regulated by the interaction of a homeostatic, sleep-wake-dependent process S and the circadian pacemaker located in the hypothalamus et al 1981;Daan et al 1984;Dijk et al 1987;Achermann et al 1993). Recent studies have indicated that an EEG correlate of sleep propensity can also be measured during wakefulness.…”

“…process S) accumulates during wakefulness and dissipates during sleep. The time course of this process has been estimated from low-frequency activity (power below ‫ف‬ 8 Hz) in central electroencephalogram (EEG) recordings during sleep (Borbély et al 1981;Daan et al 1984;Dijk et al 1987;Achermann et al 1993). Recent studies have indicated that an EEG correlate of sleep propensity can also be measured during wakefulness.…”