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. 2009 Jun;4(2):111-125.
doi: 10.1016/j.jsmc.2009.02.001. Epub 2009 Jun 9.

Circadian and Homeostatic Regulation of Human Sleep and Cognitive Performance and Its Modulation by PERIOD3

Derk-Jan Dijk  1 , Simon N Archer  1
Affiliations

Circadian and Homeostatic Regulation of Human Sleep and Cognitive Performance and Its Modulation by PERIOD3

Derk-Jan Dijk et al. Sleep Med Clin. 2009 Jun.
No abstract available

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Figures

Fig 1.
Fig 1.
Circadian and homeostatic regulation of sleep and wakefulness in humans. Panel A: Increase of homeostatic sleep pressure during wakefulness and its dissipation during sleep as reflected in EEG SWA during daytime naps and nocturnal sleep . Circadian variation in wake/sleep propensity as reflected in the latency to sleep onset (Panel B) after 18h:40 min of wakefulness and wakefulness (Panel C) in sleep opportunities, measured during forced desynchrony of the sleep-wake cycle and endogenous circadian rhythms of melatonin (Panel D) and core body temperature (Panel E)
Fig 2.
Fig 2.
Increase in the apparent circadian amplitude of calculation performance with increasing homeostatic sleep pressure. The circadian variation in performance was assessed while subjects were schedule to 28-h sleep-wake cycles in a forced desynchrony protocol, and data were segmented per quarter of the 18h:40 min scheduled wake episode. Whereas during the first quarter (0–3.1 hours awake), the circadian amplitude is very low, it increases progressively such that during the last quarter performance is very much impaired, in particular at and shortly after the nadir of the core body temperature rhythm (o degrees). Modified from ;.
Fig 3.
Fig 3.
Individual and average oscillations in endocrine and mRNA markers of circadian rhythms assessed during constant routine conditions. Left Panel: z-scored normalized rhythms for PER2, BMAL1, PER3, melatonin and cortisol plotted relative to clock time. Right Panel: Average z-score curves (±SD). Mean sleep onset and wake times (±SD) are indicated by the black bar above the melatonin profile. With permission from .
Fig 4.
Fig 4.
Faster increase of homeostatic sleep pressure and more rapid deterioration of waking performance in PER35/5 (open symbols) than PER34/4 (filled symbols) during approximately 40 h of wakefulness. Homeostatic sleep pressure is assessed by increase of theta EEG activity and slow eye movements during wakefulness. Error bars represent SEMs. Data are plotted relative to the melatonin midpoint. With permission from .
Fig 5.
Fig 5.
Conceptual model for the regulation of sleep-wake and performance in PER35/5 and PER34/4. Top panel: A circadian signal promoting wakefulness (black) and sleep (red) does not differ in either phase or amplitude, between the genotypes. Second Panel: The homeostatic process S, increases during wakefulness and declines during S. The time constants of this process are shorter in PER35/5 than in PER34/4 and there the amplitude of the S oscillation during a normal sleep-wake cycle (left side of panel) is greater in PER35/5. During sleep deprivation (right side of panel) there is a prolonged increase in Process S followed by its return to baseline during recovery sleep. Third Panel. The circadian process modulated by S. Please note that at the end of the waking day, the attenuation of the wake promoting signal by homeostatic sleep pressure is greater in PER35/5 than in PER34/4, during sleep deprivation, the sleep-promoting signal, which is maximal in the morning hours, is amplified by homeostatic sleep pressure and more so in PER35/5 than in PER34/4. Performance, which is a simple function of (C modulated by S) and S, is near stable during a normal waking day, although a small decline is observed in PER35/5 (typical for morning types) and in PER34/4 (typical for evening types) performance increases. During sleep deprivation performance is poorest in the early morning hours and in particular so in PER35/5. Please note the correspondence between this time course and the time course of performance in Fig 4.
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