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The circadian system of man: results of experiments under temporal isolation. Front Cover. Rütger A. Wever. Springer-Verlag, - Science - pages.
Table of contents
- Melatonin and Human Chronobiology
- Special order items
- Plasticity of the Intrinsic Period of the Human Circadian Timing System
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Melatonin and Human Chronobiology
Positive Reinforcement. Internal Validity. Registered Student Login. The pattern of cyclical body cycles in humans and other species, which are governed by internal "biological clocks", and last approximately 24 hours. Some biological cycles reach high points at different times of the day. These cycles are approximately 24 hours in length.
The body's "biological clock" can be set and reset by light, travel and other stimuli. Cycles with peaks and low points have been identified for numerous variables, including sleep, blood sugar level, and body temperature. Results from research have indicated that circadian rhythms result in people being physiologically ready to fall asleep easiest at a particular time each day, and that the actual time varies from person to person.
People tend to fall asleep when their body temperature starts to drop, and wake up as it begins to rise again. Studies have also indicated that when people are cut off from exposure to the light-dark cycle, circadian rhythms tend to remain close to the same. The DSPD subject had a spontaneous period length tau of The latter results in significantly disturbed sleep, even when DSPD patients are permitted to sleep and wake at their preferred times.
Delayed sleep phase disorder in temporal isolation. SLEEP ;30 9 Yet, once asleep, DSPD patients frequently report satisfactory sleep, and when permitted to sleep on a self-selected schedule, their sleep is reported to be of normal duration and quality, though, as discussed later, the limited objective data do not generally support this characterization. Several theories have been offered regarding the pathophysiology of the disorder, all of which hypothesize a reduced capacity to achieve the daily phase advance required to entrain the endogenous clock to the hour day.
One assumption underlying such hypotheses is that individuals with DSPD have an abnormally long spontaneous period length, or tau.
Special order items
Thus, the question remains as to whether an abnormally long spontaneous period length may contribute to the constellation of symptoms that define DSPD. We describe the sleep and body temperature rhythms of an individual with DSPD studied in temporal isolation. The DSPD subject was a year-old male graduate student who reported a lifelong history of very late bedtimes and an inability to awaken refreshed until the early afternoon.
Physical and psychiatric screenings revealed no pathology. As part of an ongoing study to assess circadian rhythmicity in older vs younger individuals, data were obtained from 3 healthy normal subjects close to the DSPD subject's age 2 females, aged 19 and 26, and a male, aged All were compensated for participation.
Following enrollment in the study, subjects maintained daily sleep logs for 2 consecutive weeks while living at home and continuing their usual daily activities. They then underwent a laboratory session that continued for 23 consecutive days and nights. Throughout their stay in the lab, subjects lived in a studio apartment that was shielded from any cues to time of day. Illumination was provided by desk and floor lamps situated around the apartment. Illumination in different areas of the apartment ranged from 10 lux to lux, with a typical level e.
The first 2 nights in the lab were used for adaptation and to screen for sleep disorders i. This was followed by a 4-day entrainment period, during which sleep and rising times, as well as meal times, were circumscribed. For the next 17 days, subjects were permitted to self-select bedtimes and wake times and to eat meals at their discretion. Subjects were allowed to engage in activities of their choice, with the exception of strenuous exercise, and they were not permitted to nap. Sleep was recorded polygraphically on the adaptation and entrainment nights.
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EEG, EOG, and EMG were recorded continuously throughout the free-run portion except when subjects showered , via a telemetry system Biosentry, Torrance, CA that permitted freedom of movement around the isolation apartment. Body core temperature was also recorded continuously, in 2-minute epochs, using a rectal thermistor, connected to an ambulatory data storage device Minilogger, Minimitter, Inc. Bend, OR. Closed-circuit TV permitted observation of subjects throughout the laboratory session, and an intercom system permitted communication when necessary.
Sleep records were scored in second epochs using standard criteria. Summary sleep measures were obtained by averaging data from sleep episodes recorded on 15 of the day free-run period for the DSPD subject data from 2 days were not available due to equipment malfunction and from 48 of 54 free-run sleep episodes for the normal controls. Data from the first night were not used because subjects had circumscribed bedtimes.
Raw body temperature data were edited for artifact e. Curve-fitting techniques using a harmonic regression model were used to estimate parameters of the temperature rhythm, including the daily minimum tmin. Linear regression on the daily time of tmin was used to calculate spontaneous period length tau.
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All comparisons were made using one-way and two-way for halves of the night analyses ANOVA, with the exception of sleep onset latency. All P values are based on two-tailed tests of significance. The DSPD subject's home sleep log confirmed his report of very late sleep and waking times. His mean estimated sleep latency was 50 minutes, resulting in an average sleep period time of 9. On all but one day, the subject used an alarm clock to awaken.
The day on which an alarm clock was not used, the subject reported a bedtime of and an awakening time of That the subject's circadian system was delayed was verified further by temperature data obtained during the entrainment portion of the lab session. Because his scheduled wake time in the lab was , the subject's temperature minimum was masked by rising from bed i. For the entire day interval, the subject exhibited an average tau of This is compared to an average tau of Timing of spontaneous sleep periods bars and daily temperature minima inverted triangles for the subject with DSPD dark and for a normal year-old male subject light gray , across 17 days of temporal isolation.
The DSPD subject exhibited a spontaneous period length tau of The figure also shows the altered phase relationship between sleep and body temperature in the DSPD subject see text and Figure 2 for details. As shown in Figure 2 , the phase relationship between the subject's sleep and body temperature was also altered relative to normal subjects. Whereas, the average phase angle between sleep onset and tmin was 1.
Plasticity of the Intrinsic Period of the Human Circadian Timing System
Conversely, sleep offset occurred more closely to tmin in the DSPD subject than in the normal subjects 5. Average phase relationship between the timing of spontaneous sleep open bars and the minimum of body temperature tmin; vertical line for the DSPD subject top and for three similarly-aged control subjects studied under identical conditions. Shown are average intervals and standard error from sleep onset to tmin 3. Table 1 shows the comparison of sleep between the DSPD subject and the 3 comparison subjects.
Based on data averaged over 14 sleep periods for the DSPD subject and 47 sleep episodes for the comparison subjects, the DSPD subject exhibited a significantly longer sleep onset latency, significantly greater wake time after sleep onset WASO , significantly less stage 2 sleep and significantly poorer sleep efficiency. To our knowledge, this is the first report of a documented case of DSPD studied under conditions in which spontaneous period length tau could be measured. The results suggest that the phase disturbances that characterize DSPD under entrained conditions may be the consequence of a fundamental abnormality of the circadian timing system.
For the subject studied here, this was reflected not only in a long tau , but also in an altered phase relationship between the timing of sleep and the circadian rhythm of body core temperature. Although the latter finding has been reported previously in patients studied in entrained conditions, 6 , 7 that such an alteration was also observed in temporal isolation supports the notion that the etiology of DSPD goes beyond simply a reduced capacity to achieve and maintain the appropriate phase relationship between sleep timing and the hour day.
Rather, the disorder may also reflect a fundamental inability of the endogenous circadian timing system to maintain normal internal phase relationships among physiological systems, and to properly adjust those internal relationships within the confines of the hour day. In normal subjects, the phase relationship between sleep and temperature changes in temporal isolation relative to that observed under entrained conditions 8 : in isolation, tmin tends to occur toward the beginning of sleep.
Under entrained conditions, tmin occurs, instead, toward the end of the sleep period, a change in phase angle of several hours. A comparison of our findings with those from DSPD patients studied in entrainment 6 , 7 suggests that those with DSPD may have a reduced capacity to achieve such a change in phase angle in response to entrainment. Our findings further suggest, possibly as a consequence of these altered internal phase relationships, that the quality of sleep in DSPD may be substantially poorer than that of normal subjects, even when bedtimes and wake times are self-selected.
Our DSPD subject exhibited an average sleep onset latency twice that of the 3 control subjects and almost twice the amount of wakefulness after sleep onset WASO as control subjects, resulting in significantly poorer sleep efficiency. Also, the temporal distribution of slow wave sleep was significantly altered in the DSPD subject. This finding may suggest that, in addition to abnormal circadian clock function, DSPD may be characterized by alteration s in the homeostatic regulation of sleep, as well. Specifically, the rate with which Process S 9 is depleted during sleep may be slowed.