Human Sleep: Its Duration and Organization Depend on Its Circadian Phase

Czeisler, Charles A.; Weitzman, Elliot D.; Moore‐Ede, Martin C.; Zimmerman, Janet C.; Knauer, Richard S.

doi:10.1126/science.7434029

Cited by 816 publications

(329 citation statements)

References 11 publications

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“…Under these circumstances, PS propensity increases shortly after the circadian minimum of CBT (12), a feature that is present also in spontaneously desynchronized human subjects (17,19). The robust Ͼ24 h oscillation of CBT in the present study hinted to the possibility that this tight correlation between CBT circadian rhythmicity and PS may also be present in the forced desynchronized rat.…”

Section: Resultssupporting

confidence: 48%

“…Although humans do not exhibit two rhythms of rest-activity as our rats do, this may be a consequence of the experimenter-imposed forced rest-activity cycle. Notably, human subjects under spontaneous internal desynchronization do show evidence of two rest-activity periodicities, one that freeruns with a much longer than 24-h period and another that is in phase with the circa 24-h rhythm in CBT (17,18).…”

Section: Resultsmentioning

confidence: 99%

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Circadian desynchronization of core body temperature and sleep stages in the rat

Cambras

Weller

Anglès-Pujoràs

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

101

102

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Proper functioning of the human circadian timing system is crucial to physical and mental health. Much of what we know about this system is based on experimental protocols that induce the desynchronization of behavioral and physiological rhythms within individual subjects, but the neural (or extraneural) substrates for such desynchronization are unknown. We have developed an animal model of human internal desynchrony in which rats are exposed to artificially short (22-h) light-dark cycles. Under these conditions, locomotor activity, sleep-wake, and slow-wave sleep (SWS) exhibit two rhythms within individual animals, one entrained to the 22-h light-dark cycle and the other free-running with a period >24 h ( >24 h). Whereas core body temperature showed two rhythms as well, further analysis indicates this variable oscillates more according to the >24 h rhythm than to the 22-h rhythm, and that this oscillation is due to an activity-independent circadian regulation. Paradoxical sleep (PS), on the other hand, shows only one freerunning rhythm. Our results show that, similarly to humans, (i) circadian rhythms can be internally dissociated in a controlled and predictable manner in the rat and (ii) the circadian rhythms of sleep-wake and SWS can be desynchronized from the rhythms of PS and core body temperature within individual animals. This model now allows for a deeper understanding of the human timekeeping mechanism, for testing potential therapies for circadian dysrhythmias, and for studying the biology of PS and SWS states in a neurologically intact model.

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Section: Resultssupporting

confidence: 48%

Section: Resultsmentioning

confidence: 99%

Circadian desynchronization of core body temperature and sleep stages in the rat

Cambras

Weller

Anglès-Pujoràs

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

101

102

View full text Add to dashboard Cite

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“…2 makes it clear that, as with older individuals, the sleep of these younger subjects was differentially affected in the second half of night. The dramatic rise in wakefulness during the last two hours of sleep reflects the difficulties associated with maintaining sleep on the rising portion of the temperature curve (Czeisler et al 1980;Akerstedt and Gillberg 1981;Gillberg and Akerstedt 1982;Akerstedt 1988;Dawson and Campbell 1991). In an earlier study using morning bright light exposure, Dijk and co-workers (Dijk et al 1987) reported similar results, though in a different context.…”

Section: Discussionmentioning

confidence: 99%

Aging young sleep: a test of the phase advance hypothesis of sleep disturbance in the elderly

Campbell

Dawson

1992

Journal of Sleep Research

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S U M M A R YWith aging, the phase relationship between sleep a n d body core temperature is altered such that the temperature minimum occurs substantially earlier in the major nocturnal sleep period. T h e sleep maintenance difficulties that often accompany normal aging a r e generally assumed t o b e associated with this age-related change in the phase angle between sleep and temperature. To test this notion, we used timed exposure t o bright light t o reproduce in healthy young adults a similar phase relationship between temperature and sleep, t o determine If. such a manipulation would induce the same fragmented nocturnal sleep commonly observed in individuals over 65 years of age. Seven young adults were exposed to morning bright light for 3 consecutive days following a baseline night. Bright light exposure caused a 97 min phase advance of the fitted temperature minimum when compared with baseline. Significant declines in several measures of sleep quality were associated with the phase advance, including wakefulness after initial sleep onset (WASO), sleep efficiency and number of stage changes. Yet, the severity of sleep disturbance exhibited by these subjects did not approach that exhibited by most elderly subjects. T h e findings suggest that while chronophysiological changes appear to be strongly associated with the tendency to awaken in the early morning, they cannot account entirely for the severity of sleep disturbance frequently observed in older subjects.

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“…The direct soporific effects of melatonin on nighttime sleep in normal subjects have been described as modest (e.g., . The advantage of using the phase-shifting properties of melatonin to treat non-24-h sleep-wake disorder is based on the fact that sleep quality and quantity are maximal if sleep occurs at the optimal circadian phase (Czeisler et al, 1980;Dijk and Czeisler, 1994), and it appears that even a small degree of desynchrony may result in insomnia symptoms (Morris et al, 1990). Recent evidence in the blind suggests that if the circadian system continues to free run during melatonin treatment, the sleep-wake cycle also continues to free run, despite the acute sleep-improving effects of melatonin (Lockley et al, unpublished results), and thus the underlying cause of the sleep disorder remains untreated.…”

Section: Discussionmentioning

confidence: 99%

The Effects of Low-Dose 0.5-mg Melatonin on the Free-Running Circadian Rhythms of Blind Subjects

et al. 2003

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Exogenous melatonin (0.5-10 mg) has been shown to entrain the freerunning circadian rhythms of some blind subjects. The aim of this study was to assess further the entraining effects of a daily dose of 0.5 mg melatonin on the cortisol rhythm and its acute effects on subjective sleep in blind subjects with free-running 6-sulphatoxymelatonin (aMT6s) rhythms (circadian period [τ] 24.23-24.95 h). Ten subjects (9 males) were studied, aged 32 to 65 years, with no conscious light perception (NPL). In a placebo-controlled, single-blind design, subjects received 0.5 mg melatonin or placebo p.o. daily at 2100 h (treatment duration 26-81 days depending on individuals' circadian period). Subjective sleep was assessed from daily sleep and nap diaries. Urinary cortisol and aMT6s were assessed for 24 to 48 h weekly and measured by radioimmunoassay. Seven subjects exhibited an entrained or shortened cortisol period during melatonin treatment. Of these, 4 subjects entrained with a period indistinguishable from 24 h, 2 subjects continued to free run for up to 25 days during melatonin treatment before their cortisol rhythm became entrained, and 1 subject appeared to exhibit a shortened cortisol period throughout melatonin treatment. The subjects who entrained within 7 days did so when melatonin treatment commenced in the phase advance portion of the melatonin PRC (CT6-18). When melatonin treatment ceased, cortisol and aMT6s rhythms free ran at a similar period to before treatment. Three subjects failed to entrain with initial melatonin treatment commencing in the phase delay portion of the PRC. During melatonin treatment, there was a significant increase in nighttime sleep duration and a reduction in the number and duration of daytime naps. The positive effect of melatonin on sleep may be partly due to its acute soporific properties. The findings demonstrate that a daily dose of 0.5 mg melatonin is effective at entraining the free-running circadian systems in most of the blind subjects studied, and that circadian time (CT) of administration of melatonin may be important in determining whether a subject entrains to melatonin treatment. Optimal treatment with melatonin for this non-24-h sleep disorder should correct the underlying circadian disorder (to entrain the sleep-wake cycle) in addition to improving sleep acutely.

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Human Sleep: Its Duration and Organization Depend on Its Circadian Phase

Cited by 816 publications

References 11 publications

Circadian desynchronization of core body temperature and sleep stages in the rat

Circadian desynchronization of core body temperature and sleep stages in the rat

Aging young sleep: a test of the phase advance hypothesis of sleep disturbance in the elderly

The Effects of Low-Dose 0.5-mg Melatonin on the Free-Running Circadian Rhythms of Blind Subjects

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