Ultrashort sleep-wake schedule ; III Gates and "forbidden zones" for sleep
01 Jan 1986-Vol. 63, pp 414-425
TL;DR: The results showed that in spite of the significant between-group differences in total sleep, the temporal structure of sleepiness was very similar in the 3 experiments, which demonstrate structured variations in sleepiness across the nycthemeron.
About: The article was published on 1986-01-01 and is currently open access. It has received 417 citations till now. The article focuses on the topics: Sleep (system call).
Citations
More filters
TL;DR: Analyses of the (nonadditive) interaction of the circadian and sleep-dependent components of sleep propensity and sleep structure revealed that the phase relation between the sleep-wake cycle and the circadian pacemaker during entrainment promotes the consolidation of sleep and wakefulness and facilitates the transitions between these vigilance states.
Abstract: The role of the endogenous circadian pacemaker in the timing of the sleep-wake cycle and the regulation of the internal structure of sleep, including REM sleep, EEG slow-wave (0.75-4.5 Hz) and sleep spindle activity (12.75-15.0 Hz) was investigated. Eight men lived in an environment free of time cues for 33-36 d and were scheduled to a 28 hr rest-activity cycle so that sleep episodes (9.33 hr each) occurred at all phases of the endogenous circadian cycle and variations in wakefulness preceding sleep were minimized. The crest of the robust circadian rhythm of REM sleep, which was observed throughout the sleep episode, was positioned shortly after the minimum of the core body temperature rhythm. Furthermore, a sleep-dependent increase of REM sleep was present, which, interacting with the circadian modulation, resulted in highest values of REM sleep when the end of scheduled sleep episodes coincided with habitual wake-time. Slow-wave activity decreased and sleep spindle activity increased in the course of all sleep episodes. Slow-wave activity in non-REM sleep exhibited a low amplitude circadian modulation which did not parallel the circadian rhythm of sleep propensity. Sleep spindle activity showed a marked endogenous circadian rhythm; its crest coincident with the beginning of the habitual sleep episode. Analyses of the (nonadditive) interaction of the circadian and sleep-dependent components of sleep propensity and sleep structure revealed that the phase relation between the sleep-wake cycle and the circadian pacemaker during entrainment promotes the consolidation of sleep and wakefulness and facilitates the transitions between these vigilance states.
1,241 citations
Cites methods or result from "Ultrashort sleep-wake schedule ; II..."
...…bed time, confirms results obtained in recent experiments in which the confound of prior wakefulness was minimized (Klein et al., 1993; Dantz et al., 1994) and previous estimates (Weitzman et al., 1974; Carskadon and Dement, 1975; Webb and Agnew, 1975; Czeisler, 1978; Lavie, 1986; Zulley, 1990)....
[...]
...…of imposed 20, 90, 180, or 240 min rest-activity cycles that were then maintained for one to ten 24 hr days, focused primarily on the circadian variation in sleep propensity (Weitzman et al., 1974; Carskadon and Dement, 1975; Webb and Agnew, 1975; Czeisler, 1978; Lavie, 1986; Zulley, 1990)....
[...]
TL;DR: The evidence did not support a direct link between circadian-related fatigue influences and performance or safety outcomes and further research is needed to clarify the link.
607 citations
Cites background from "Ultrashort sleep-wake schedule ; II..."
...…probabilty of falling asleep and subjective ratings of sleepiness show a ronounced circadian rhythm, with maximum values occurring t about 06:00 (Lavie, 1986; Zulley, 1990; Åkerstedt and Folkard, 995) In light of this pattern in human sleep and wakefulness it is erhaps not surprising that a…...
[...]
TL;DR: Exogenous melatonin can act as soporific agent, a chronohypnotic, and/or a chronobiotic in order to treat sleep or circadian rhythm disorders.
Abstract: The circadian rhythm of pineal melatonin is the best marker of internal time under low ambient light levels. The endogenous melatonin rhythm exhibits a close association with the endogenous circadian component of the sleep propensity rhythm. This has led to the idea that melatonin is an internal sleep ‘facilitator’ in humans, and therefore useful in the treatment of insomnia and the readjustment of circadian rhythms. There is evidence that administration of melatonin is able: (i) to induce sleep when the homeostatic drive to sleep is insufficient; (ii) to inhibit the drive for wakefulness emanating from the circadian pacemaker; and (iii) induce phase shifts in the circadian clock such that the circadian phase of increased sleep propensity occurs at a new, desired time. Therefore, exogenous melatonin can act as soporific agent, a chronohypnotic, and/or a chronobiotic. We describe the role of melatonin in the regulation of sleep, and the use of exogenous melatonin to treat sleep or circadian rhythm disorders.
601 citations
TL;DR: Three kindreds with a profound phase advance of the sleep–wake, melatonin and temperature rhythms associated with a very short τ represent a well-characterized familial circadian rhythm variant in humans and provide a unique opportunity for genetic analysis of human circadian physiology.
Abstract: Biological circadian clocks oscillate with an approximately 24-hour period, are ubiquitous, and presumably confer a selective advantage by anticipating the transitions between day and night. The circadian rhythms of sleep, melatonin secretion and body core temperature are thought to be generated by the suprachiasmatic nucleus of the hypothalamus, the anatomic locus of the mammalian circadian clock. Autosomal semi-dominant mutations in rodents with fast or slow biological clocks (that is, short or long endogenous period lengths; tau) are associated with phase-advanced or delayed sleep-wake rhythms, respectively. These models predict the existence of familial human circadian rhythm variants but none of the human circadian rhythm disorders are known to have a familial tendency. Although a slight 'morning lark' tendency is common, individuals with a large and disabling sleep phase-advance are rare. This disorder, advanced sleep-phase syndrome, is characterized by very early sleep onset and offset; only two cases are reported in young adults. Here we describe three kindreds with a profound phase advance of the sleep-wake, melatonin and temperature rhythms associated with a very short tau. The trait segregates as an autosomal dominant with high penetrance. These kindreds represent a well-characterized familial circadian rhythm variant in humans and provide a unique opportunity for genetic analysis of human circadian physiology.
535 citations
TL;DR: In this article, the authors examined whether smartphone use depletes employees' regulatory resources and impairs their engagement at work the following day, and they found that smartphone use for work at night increased depletion the next morning via its effects on sleep.
476 citations
References
More filters
Book•
01 Jan 1968
11,993 citations
TL;DR: The model shows that the experimental data are consistent with the concept of a single circadian pacemaker in humans, which has implications for the understanding of sleep as a restorative process and its timing with respect to day and night.
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.
1,303 citations
TL;DR: Two- to threefold variations in sleep length were observed in 12 subjects living on self-selected schedules in an environment free of time cues and the duration of polygraphically recorded sleep episodes was highly correlated with the circadian phase of the body temperature rhythm at bedtime.
Abstract: Two- to threefold variations in sleep length were observed in 12 subjects living on self-selected schedules in an environment free of time cues. The duration of polygraphically recorded sleep episodes was highly correlated with the circadian phase of the body temperature rhythm at bedtime and not with the length of prior wakefulness. Furthermore, the rate of REM (rapid eye movement) sleep accumulation , REM latency, bedtime selection, and self-rated alertness assessments were also correlated with the body temperature rhythm.
887 citations
TL;DR: For half a century, "Sleep and Wakefulness" has been a valuable reference work on phases of the sleep cycle, experimental work on sleep and wakefulness, sleep disorders and their treatment, and such sleep-like states as hypnosis and hibernation.
805 citations
01 Jan 1979
TL;DR: Despite the fact that Cortisol, like many other hormones, is secreted in a highly variable sequence of episodes, a clear circadian pattern emerges in each curve, averaged from the data on n subjects, and there is perfect correspondence in phase and relative amplitude between the curves.
Abstract: As in other vertebrates, the human circadian system is characterized by a distinct temporal order of its components. This order is maintained by the coupling forces between various oscillators as well as by the entraining signals from the Zeitgebers (see Chapter 12). There is hardly a tissue or function that has not been shown to have some 24-hr variation. As an example, Figure 1 presents results of an experiment in which six subjects were held in groups of two on the same rigorous schedule. Although there were considerable interindi-vidual differences and also day-to-day variations, patterns like those shown in Figure 1 are satisfactorily reproducible. This reproducibility is again illustrated in Figure 2, which summarizes data on plasma Cortisol collected in six laboratories. To account for possible phase-controlling effects of sleep (see below), the curves are normalized with regard to the various sleep times of the subjects. Despite the fact that Cortisol, like many other hormones, is secreted in a highly variable sequence of episodes (see Chapter 12, Figure 1), a clear circadian pattern emerges in each curve, averaged from the data on n subjects, and there is perfect correspondence in phase and relative amplitude between the curves. It is noteworthy that two submaxima appear in all curves at about the same circadian phases. Presumably, they are not consequences of the usual meal timing but may represent a rhythm component interposed between the circadian domain and the episodes (cf. the discussion in Aschoff, 1979).
545 citations