Effects of activity of daily living and gender on circadian rhythms of the elderly in a nursing home

The objective of this study was to confirm the effects of ADL (Activity of Daily Living) and gender on circadian rhythms of the elderly in a nursing home. Twenty-one elderly volunteers, aged over 65 years, were divided in four groups depending on their ADL and gender: subjects with almost no problem in ADL (H males, H females) and those who were almost bedridden (L males, L females). Oral temperature, heart rate, blood pressure, time of sleep and wake, subjective sleepiness, overall feeling and vitality were measured every 4 hours during the day continuously for six days. The circadian rhythm was calculated by using the least squares fit of cosine function. Subjective sleep quality was also surveyed. In the sleep/wake rhythm, the mesor was significantly higher in L males compared to the other groups and the amplitude was significantly lower in L females compared to other groups. The subjective sleepiness was higher in L males compared to the other groups and L females showed a higher sleepiness compared to H females. No significant difference among the group was observed in subjective sleep quality. In conclusion, these results indicate that the subjective sleepiness and sleep/wake rhythm differ depending on ADL and gender, although no significant difference was observed in physiological parameters. ADL and gender based difference in subjective sleepiness and sleep/wake rhythm should be taken into account with regard to the care of the elderly in nursing homes.     

The Effect of Activity on the Waking Temperature Rhythm in Humans

Nine healthy female subjects were studied when exposed to the natural light-dark cycle, but living for 17 “days” on a 27h day (9h sleep, 18h wake). Since the circadian endogenous oscillator cannot entrain to this imposed period, forced desynchronization between the sleep/activity cycle and the endogenous circadian temperature rhythm took place. This enabled the effects of activity on core temperature to be assessed at different endogenous circadian phases and at different stages of the sleep/activity cycle. Rectal temperature was measured at 6-minute intervals, and the activity of the nondominant wrist was summed at 1-minute intervals. Each waking span was divided into overlapping 3h sections, and each section was submitted to linear regression analysis between the rectal temperatures and the total activity in the previous 30 minutes. From this analysis were obtained the gradient (of the change in rectal temperature produced by a unit change in activity) and the intercept (the rectal temperature predicted when activity was zero). The gradients were subjected to a two-factor analysis of variance (ANOVA) (circadian phase/ time awake). There was no significant effect of time awake, but circadian phase was highly significant statistically. Post hoc tests (Newman-Keuls) indicated that gradients around the temperature peak were significantly less than those around its trough. The intercepts formed a sinusoid that, for the group, showed a mesor (±SE) of 36.97 (±0.12) and amplitude (95% confidence interval) of 0.22°C (0.12°C, 0.32°C). We conclude that this is a further method for removing masking effects from circadian temperature rhythm data in order to assess its endogenous component, a method that can be used when subjects are able to live normally. We suggest also that the decreased effect of activity on temperature when the endogenous circadian rhythm and activity are at their peak will reduce the possibility of hyperthermia.     

Are age differences in sleep due to phase differences in the output of the circadian timing system?

Our aim was to evaluate whether age-related changes in the phase of the output of the circadian timing system (CTS) can explain age differences in habitual bedtime/wake time and in sleep consolidation parameters. Analyses focused on a group of healthy elderly people (older than 70 years) with no sleep problems and with similar subjective sleep quality as a young control group. The 2-week sleep diary data and 24h laboratory temperature recordings were examined for 70 subjects (22 young men [YM], 19 old men [OM], 29 old women [OW]). Polysomnographic (PSG) sleep data recorded during temperature data acquisition were also available for 62 subjects. These analyses made use of our recently developed technique to demask temperature rhythm data. As expected, compared to the young subjects, older subjects showed earlier habitual bedtime and wake time, more disturbed sleep, and a tendency for an earlier minimum of the circadian temperature rhythm. Despite sleep consolidation differences, the groups showed very similar habitual phase-angle differences (interval between the time occurrence of the fitted temperature minimum and habitual wake time). Both elderly and young subjects woke up on average 3h after the temperature minimum. After controlling for the effects of age group, habitual bedtime and wake time were related to clock time phase of the circadian temperature rhythm, with an earlier phase associated with earlier habitual bedtime and wake time. None of the sleep consolidation parameters were linked to the temperature phase angle. In conclusion, sleep consolidation changes associated with healthy aging do not appear to be related to changes in the phase-angle difference between the output signal from the CTS and sleep.     

Forced Desynchrony of Orcadian Rhythms of Body Temperature and Activity in Rats

The daily rhythm in body temperature is thought to be the result of the direct effects of activity and the effects of an endogenous circadian clock. Forced desynchrony (FD) is a tool used in human circadian rhythm research to disentangle endogenous and activity-related effects on daily rhythms. In the present study, we applied an FD protocol to rats. We subjected 8 rats for 5 days to a 20h forced activity cycle consisting of lOh of forced wakefulness and lOh for rest and sleep. The procedure aimed to introduce a lOh sleep/ lOh wake cycle, which period was different from the endogenous circadian (about 24h) rhythm. Of the variation in the raw body temperature data, 68-77% could be explained by a summation of estimated endogenous circadian cycle and forced activity cycle components of body temperature. Free-running circadian periods of body temperature during FD were similar to free-running periods measured in constant conditions. The applied forced activity cycle reduced clock-related circadian modulation of activity. This reduction of circadian modulation of activity did not affect body temperature. Also, the effects of the forced activity on body temperature were remarkably small.     

Masking effects of posture and sleep onset on core body temperature have distinct circadian rhythms: results from a 90-min/day protocol

Both recumbency and sleep affect core body temperature (CBT). To characterize their circadian effects and interactions, the authors examined the bedtime temperature drops (TDs) of nine men and eight women (aged 20 to 30) who repeated 90-min sleep-wake cycles over 2.5 days. While awake, subjects were exposed to 50 to 250 lux; while asleep, lights were off. Electroencephalogram-monitored time inbed lasted 30 min during each cycle. Cosinor nonlinear mixed-effects regressions modeled the circadian rhythm of TDs. The circadian maximum of TDs occurred approximately 4 h before the time of circadian CBT minimum, in a model that included the effects of baseline expected CBT, deviations from baseline CBT, time in study, and gender-dependent 24- and 12-h adjustments. Rates of temperature drops were faster during initial periods of lying awake than during periods of initially sleeping. Both rates followed separate circadian rhythms. The circadian maximum of TDs was located near customary nocturnal bedtimes, suggesting its role in fostering sleep during a normal bedtime routine. The apparent deceleration of temperature dropping at sleep onset supports the notion that the sleep onset period has complicated circadian neuroregulatory dynamics. These findings confirm the need for nonlinear models of temperature responses to postural changes and sleep that incorporate circadian variability in these masking effects.     

Dueling Hypotheses: Circatidal Versus Circalunidian Battle Basics–Second Engagement

The daily rhythm in body temperature is thought to be the result of the direct effects of activity and the effects of an endogenous circadian clock. Forced desynchrony (FD) is a tool used in human circadian rhythm research to disentangle endogenous and activity-related effects on daily rhythms. In the present study, we applied an FD protocol to rats. We subjected 8 rats for 5 days to a 20h forced activity cycle consisting of lOh of forced wakefulness and lOh for rest and sleep. The procedure aimed to introduce a lOh sleep/ lOh wake cycle, which period was different from the endogenous circadian (about 24h) rhythm. Of the variation in the raw body temperature data, 68–77% could be explained by a summation of estimated endogenous circadian cycle and forced activity cycle components of body temperature. Free-running circadian periods of body temperature during FD were similar to free-running periods measured in constant conditions. The applied forced activity cycle reduced clock-related circadian modulation of activity. This reduction of circadian modulation of activity did not affect body temperature. Also, the effects of the forced activity on body temperature were remarkably small.     

Regression Models for the Estimation of Orcadian Rhythms in the Presence of Effects Due to Masking

The estimation of human circadian rhythms from experimental data is complicated by the presence of “masking” effects associated with the sleep-wake cycle. The observed rhythm may include a component due to masking, as well as the endogenous component linked to a circadian pacemaker. In situations where the relationship between the sleep-wake cycle and the circadian rhythm is not constant, it may be possible to obtain individual estimates of these two components, but methods commonly used for the estimation of circadian rhythms, such as the cosinor analysis, spectral analysis, average waveforms and complex demodulation, have not generally been adapted to identify the modulations that arise from masking. The estimates relate to the observed rhythms, and the amplitudes and acrophases do not necessarily refer to the endogenous rhythm.

In this paper methods are discussed for the separation of circadian and masking effects using regression models that incorporate a sinusoidal circadian variation together with functions of time since sleep and time during sleep. The basic model can be extended to include a time-varying circadian rhythm and estimates are available for the amplitude and phase at a given time, together with their joint confidence intervals and tests for changes in amplitude and acrophase between any two selected times. Modifications of these procedures are discussed to allow for non-sinusoidal circadian rhythms, non-additivity of the circadian and time-since-sleep effects and the breakdown of the usual assumptions concerning the residual errors.

This approach enables systematic masking effects associated with the sleep-wake cycle to be separated from the circadian rhythm, and it has applications to the analysis of data from experiments where the sleep-wake cycle is not synchronized with the circadian rhythm, for example after time-zone transitions or during irregular schedules of work and rest.     

Contribution of circadian physiology and sleep homeostasis to age-related changes in human sleep

The circadian pacemaker and sleep homeostasis play pivotal roles in vigilance state control. It has been hypothesized that age-related changes in the human circadian pacemaker, as well as sleep homeostatic mechanisms, contribute to the hallmarks of age-related changes in sleep, that is, earlier wake time and reduced sleep consolidation. Assessments of circadian parameters in healthy young (∼20-30 years old) and older people (∼65-75 years old)—in the absence of the confounding effects of sleep, changes in posture, and light exposure—have demonstrated that an earlier wake time in older people is accompanied by about a 1h advance of the rhythms of core body temperature and melatonin. In addition, older people wake up at an earlier circadian phase of the body temperature and plasma melatonin rhythm. The amplitude of the endogenous circadian component of the core body temperature rhythm assessed during constant routine and forced desynchrony protocols is reduced by 20-30% in older people. Recent assessments of the intrinsic period of the human circadian pacemaker in the absence of the confounding effects of light revealed no age-related reduction of this parameter in both sighted and blind individuals. Wake maintenance and sleep initiation are not markedly affected by age except that sleep latencies are longer in older people when sleep initiation is attempted in the early morning. In contrast, major age-related reductions in the consolidation and duration of sleep occur at all circadian phases. Sleep of older people is particularly disrupted when scheduled on the rising limb of the temperature rhythm, indicating that the sleep of older people is more susceptible to arousal signals genernpated by the circadian pacemaker. Sleep-homeostatic mechanisms, as assayed by the sleep-deprivation-induced increase of EEG slow-wave activity (SWA), are operative in older people, although during both baseline sleep and recovery sleep SWA in older people remains at lower levels. The internal circadian phase advance of awakening, as well as the age-related reduction in sleep consolidation, appears related to an age-related reduction in the promotion of sleep by the circadian pacemaker during the biological night in combination with a reduced homeostatic pressure for sleep. Early morning light exposure associated with this advance of awakening in older people could reinforce the advanced circadian phase. Quantification of the interaction between sleep homeostasis and circadian rhythmicity contributes to understanding age-related changes in sleep timing and quality. (Chronobiology International, 17(3), 285-311, 2000)     

The Adjustment of the Circadian Rhythm of Body Temperature to Simulated Time-Zone Transitions: A Comparison of the Effect of Using Raw Versus Unmasked Data

Deep body temperature and sleep/activity diaries data were recorded during control days and for 6 days after simulated time zone transitions of 8 h to the east (six subjects) or west (seven subjects). Circadian rhythms were assessed by cosinor analysis of both raw data (the conventional method) and purified data (corrected for the effects of sleep and activity). Analysis of raw data gives misleading information about the phase and amplitude of the rhythms due to the masking effects of the exogenous component. Use of purified data indicates that during the process of adjustment after an eastward shift (a) phase changes are more erratic than after a shift to the west; (b) no marked decrease in the amplitude of the rhythms is evident; and (c) no clear evidence exists that the circadian rhythm breaks up temporarily. The masking effect was less after the time zone transition if sleep maintenance was poor.     

The Adjustment of the Circadian Rhythm of Body Temperature to Simulated Time-Zone Transitions: A Comparison of the Effect of Using Raw Versus Unmasked Data

Deep body temperature and sleep/activity diaries data were recorded during control days and for 6 days after simulated time zone transitions of 8 h to the east (six subjects) or west (seven subjects). Circadian rhythms were assessed by cosinor analysis of both raw data (the conventional method) and purified data (corrected for the effects of sleep and activity). Analysis of raw data gives misleading information about the phase and amplitude of the rhythms due to the masking effects of the exogenous component. Use of purified data indicates that during the process of adjustment after an eastward shift (a) phase changes are more erratic than after a shift to the west; (b) no marked decrease in the amplitude of the rhythms is evident; and (c) no clear evidence exists that the circadian rhythm breaks up temporarily. The masking effect was less after the time zone transition if sleep maintenance was poor.     

Uncovering Different Masking Factors on Wrist Skin Temperature Rhythm in Free-Living Subjects

Most circadian rhythms are controlled by a major pacemaker located in the hypothalamic suprachiasmatic nucleus. Some of these rhythms, called marker rhythms, serve to characterize the timing of the internal temporal order. However, these variables are susceptible to masking effects as the result of activity, body position, light exposure, environmental temperature and sleep. Recently, wrist skin temperature (WT) has been proposed as a new index for evaluating circadian system status. In light of previous evidence suggesting the important relationship between WT and core body temperature regulation, the aim of this work was to purify the WT pattern in order to obtain its endogenous rhythm with the application of multiple demasking procedures. To this end, 103 subjects (18–24 years old) were recruited and their WT, activity, body position, light exposure, environmental temperature and sleep were recorded under free-living conditions for 1 week. WT demasking by categories or intercepts was applied to simulate a “constant routine” protocol (awakening, dim light, recumbent position, low activity and warm environmental temperature). Although the overall circadian pattern of WT was similar regardless of the masking effects, its amplitude was the rhythmic parameter most affected by environmental conditions. The acrophase and mesor were determined to be the most robust parameters for characterizing this rhythm. In addition, a circadian modulation of the masking effect was found for each masking variable. WT rhythm exhibits a strong endogenous component, despite the existence of multiple external influences. This was evidenced by simultaneously eliminating the influence of activity, body position, light exposure, environmental temperature and sleep. We therefore propose that it could be considered a valuable and minimally-invasive means of recording circadian physiology in ambulatory conditions.     

CONTRIBUTION OF CIRCADIAN PHYSIOLOGY AND SLEEP HOMEOSTASIS TO AGE-RELATED CHANGES IN HUMAN SLEEP

The circadian pacemaker and sleep homeostasis play pivotal roles in vigilance state control. It has been hypothesized that age-related changes in the human circadian pacemaker, as well as sleep homeostatic mechanisms, contribute to the hallmarks of age-related changes in sleep, that is, earlier wake time and reduced sleep consolidation. Assessments of circadian parameters in healthy young (～20–30 years old) and older people (～65–75 years old)—in the absence of the confounding effects of sleep, changes in posture, and light exposure—have demonstrated that an earlier wake time in older people is accompanied by about a 1h advance of the rhythms of core body temperature and melatonin. In addition, older people wake up at an earlier circadian phase of the body temperature and plasma melatonin rhythm. The amplitude of the endogenous circadian component of the core body temperature rhythm assessed during constant routine and forced desynchrony protocols is reduced by 20–30% in older people. Recent assessments of the intrinsic period of the human circadian pacemaker in the absence of the confounding effects of light revealed no age-related reduction of this parameter in both sighted and blind individuals. Wake maintenance and sleep initiation are not markedly affected by age except that sleep latencies are longer in older people when sleep initiation is attempted in the early morning. In contrast, major age-related reductions in the consolidation and duration of sleep occur at all circadian phases. Sleep of older people is particularly disrupted when scheduled on the rising limb of the temperature rhythm, indicating that the sleep of older people is more susceptible to arousal signals genernpated by the circadian pacemaker. Sleep-homeostatic mechanisms, as assayed by the sleep-deprivation–induced increase of EEG slow-wave activity (SWA), are operative in older people, although during both baseline sleep and recovery sleep SWA in older people remains at lower levels. The internal circadian phase advance of awakening, as well as the age-related reduction in sleep consolidation, appears related to an age-related reduction in the promotion of sleep by the circadian pacemaker during the biological night in combination with a reduced homeostatic pressure for sleep. Early morning light exposure associated with this advance of awakening in older people could reinforce the advanced circadian phase. Quantification of the interaction between sleep homeostasis and circadian rhythmicity contributes to understanding age-related changes in sleep timing and quality. (Chronobiology International, 17(3), 285–311, 2000)     

The development of new purification methods to assess the circadian rhythm of body temperature in Mongolian gerbils

Six Mongolian gerbils were studied for 8-10d while housed in separate cages in a 12:12h light-dark (L-D) cycle (lights on at 07:00h). Recordings of body temperature, heart rate, and spontaneous activity were made throughout. The temperature and heart rate rhythms were “purified” to take into account the effects of activity, and then the rhythm of temperature was further purified to take into account other masking influences (“non-activity masking effects” or NAME,). The methods employed in the purification processes involved linear regression analysis or analysis of covariance, the latter using functions of activity and NAME as covariates. From these methods, it was possible to obtain not only an estimate of the endogenous component of the temperature rhythm but also a measure of circadian changes in the sensitivity of temperature to masking effects.

Even though all purification methods removed many of the effects of spontaneous activity from the temperature record, there remained temperature fluctuations at the L-D and D-L transitions that appeared to be independent of activity. The NAME was of only very marginal value in the purification process. Comparison of the purification methods indicated that the linear methods were inferior (both from a biological viewpoint and when the results were compared mathematically) to those that allowed the rate of rise of temperature due to increasing amounts of activity to become progressively less. The sensitivity of temperature and heart rate to the masking effects of activity showed a circadian rhythm, with sensitivities in the resting phase being greater than those in the active phase. These findings are compatible with the view that thermoregulatory reflexes are induced by spontaneous activity of sufficient amount, and that there is a circadian rhythm in the body temperature at which these reflexes are initiated and in their effectiveness.     

Purification of Masked Temperature data from Humans: Some Preliminary Observations on a Comparison of the use of an Activity Diary, Wrist Actimetry, and Heart Rate Monitoring

Fourteen ambulatory subjects, varying in their amount of habitual physical activity, were studied for 24h during a total of 25 “typical” days. Rectal temperature was recorded every 6 minutes, an activity diary was filled in every half hour, and wrist activity and heart rate were monitored every minute. Actimetry and heart rate data generally showed close parallelism with each other and with the masking effects on body temperature. Psychological stressors such as public speaking produced a greater effect on heart rate and body temperature than on wrist movement, while typing produced high values for wrist movement, but affected heart rate and temperature much less. When data for the circadian rhythm of body temperature were purified, the diary, actimetry, and measurement of heart rate were all useful in reducing masking effects, but the present evidence indicates that heart rate can be more successful than actimetry-as judged by the closeness of the purified data to a sinusoid. This superiority of heart rate monitoring over wrist activity as a method of purification might be because core temperature can be increased by stressor-induced thermogenesis, as well as by physical activity, and because wrist movement can, with some activities, give an inaccurate estimate of the factors that contribute to whole-body thermogenesis.     

Disruptions in sleep–wake cycles in community-dwelling cancer patients receiving palliative care and their correlates

Significant disruptions in sleep–wake cycles have been found in advanced cancer patients in prior research. However, much remains to be known about specific sleep–wake cycle variables that are impaired in patients with a significantly altered performance status. More studies are also needed to explore the extent to which disrupted sleep–wake cycles are related to physical and psychological symptoms, time to death, maladaptive sleep behaviors, quality of life and 24-h light exposure. This study conducted in palliative cancer patients was aimed at characterizing patients’ sleep–wake cycles using various circadian parameters (i.e. amplitude, acrophase, mesor, up-mesor, down-mesor, rhythmicity coefficient). It also aimed to compare rest–activity rhythm variables of participants with a performance status of 2 vs. 3 on the Eastern Cooperative Oncology Group scale (ECOG) and to evaluate the relationships of sleep–wake cycle parameters with several possible correlates. The sample was composed of 55 community-dwelling cancer patients receiving palliative care with an ECOG of 2 or 3. Circadian parameters were assessed using an actigraphic device for seven consecutive 24-h periods. A light recording and a daily pain diary were completed for the same period. A battery of self-report scales was also administered. A dampened circadian rhythm, a low mean activity level, an early mean time of peak activity during the day, a late starting time of activity during the morning and an early time of decline of activity during the evening were observed. In addition, a less rhythmic sleep–wake cycle was associated with a shorter time to death (from the first home visit) and with a lower 24-h light exposure. Sleep–wake cycles are markedly disrupted in palliative cancer patients, especially, near the end of life. Effective non-pharmacological interventions are needed to improve patients’ circadian rhythms, including perhaps bright light therapy.     

Alterations of locomotor activity rhythm and sleep parameters in patients with advanced glaucoma

The aim of this study was to evaluate the effect of advanced glaucoma on locomotor activity rhythms and related sleep parameters. Nine normal subjects and nine age-matched patients with bilateral advanced primary open-angle glaucoma, >10 yrs since diagnosis, were included in this observational, prospective, case-control study. Patients were required to record the timing and duration of their sleep and daily activities, and wore an actigraph on the wrist of the nondominant arm for 20 d. Activity rhythm period, MESOR (24-h time-series mean), amplitude (one-half peak-to-trough variation), and acrophase (peak time), plus long sleep episodes during the wake state, sleep duration, efficiency, and latency, as well as mean activity score, wake minutes, and mean wake episodes during the sleep interval were assessed in controls and glaucomatous patients. Glaucomatous patients exhibited significant decrease in nighttime sleep efficiency, and significant increase in the mean activity score, wake minutes, and mean wake episode during the night. These results suggest that alterations of circadian physiology could be a risk to the quality of life of patients with glaucoma.     

Alterations of the characteristics of the circadian rest-activity rhythm of cancer in-patients

The aim of the present study was to evaluate the characteristics of the circadian rest-activity rhythm of cancer patients. Thirty-one in-patients, consisting of 19 males and 12 females, were randomly selected from the Regional Cancer Center, Pandit Jawaharlal Nehru Medical College, Raipur, India. The rest-activity rhythm was studied non-invasively by wrist actigraphy, and compared with 35 age-matched apparently healthy subjects (22 males and 13 females). All subjects wore an Actiwatch (AW64, Mini Mitter Co. Inc., USA) for at least 4-7 consecutive days. Fifteen-second epoch length was selected for gathering actigraphy data. In addition, several sleep parameters, such as time in bed, assumed sleep, actual sleep time, actual wake time, sleep efficiency, sleep latency, sleep bouts, wake bouts, and fragmentation index, were also recorded. Data were analyzed using several statistical techniques, such as cosinor rhythmometry, spectral analysis, ANOVA, Duncan's multiple-range test, and t-test. Dichotomy index (I相似文献   

The Shape of the Endogenous Circadian Rhythm of Rectal Temperature in Humans

Fourteen healthy subjects have been studied in an isolation unit while living on a 30h “day” (20h awake, 10h asleep) for 14 (solar) days but while aware of real time. Waking activities were sedentary and included reading, watching television, and so forth. Throughout, regular recordings of rectal temperature were made, and in a subgroup of 6 subjects, activity was measured by a wrist accelerometer. Temperature data have been subjected to cosinor analysis after “purification,” a method that enables the endogenous (clock-driven) and exogenous (activity-driven) components of the circadian rhythm to be assessed. Moreover, the protocol enables effects due to the circadian rhythm and time-since-waking to be separated. Results showed that activity was slightly affected by the endogenous temperature rhythm. Also, the masking effects on body temperature exerted by the exogenous factors appeared to be less than average in the hours before and just after the peak of the endogenous temperature rhythm. This has the effect of producing a temperature plateau rather than a peak during the daytime. The implications of this for mental performance and sleep initiation are discussed. (Chronobiology International, 13(4), 261-271, 1996)     

An endogenous circadian rhythm in sleep inertia results in greatest cognitive impairment upon awakening during the biological night

Sleep inertia is the impaired cognitive performance immediately upon awakening, which decays over tens of minutes. This phenomenon has relevance to people who need to make important decisions soon after awakening, such as on-call emergency workers. Such awakenings can occur at varied times of day or night, so the objective of the study was to determine whether or not the magnitude of sleep inertia varies according to the phase of the endogenous circadian cycle. Twelve adults (mean, 24 years; 7 men) with no medical disorders other than mild asthma were studied. Following 2 baseline days and nights, subjects underwent a forced desynchrony protocol composed of seven 28-h sleep/wake cycles, while maintaining a sleep/wakefulness ratio of 1:2 throughout. Subjects were awakened by a standardized auditory stimulus 3 times each sleep period for sleep inertia assessments. The magnitude of sleep inertia was quantified as the change in cognitive performance (number of correct additions in a 2-min serial addition test) across the first 20 min of wakefulness. Circadian phase was estimated from core body temperature (fitted temperature minimum assigned 0 degrees ). Data were segregated according to: (1) circadian phase (60 degrees bins); (2) sleep stage; and (3) 3rd of the night after which awakenings occurred (i.e., tertiary 1, 2, or 3). To control for any effect of sleep stage, the circadian rhythm of sleep inertia was initially assessed following awakenings from Stage 2 (62% of awakening occurred from this stage; n = 110). This revealed a significant circadian rhythm in the sleep inertia of cognitive performance (p = 0.007), which was 3.6 times larger during the biological night (circadian bin 300 degrees , approximately 2300-0300 h in these subjects) than during the biological day (bin 180 degrees , approximately 1500-1900 h). The circadian rhythm in sleep inertia was still present when awakenings from all sleep stages were included (p = 0.004), and this rhythm could not be explained by changes in underlying sleep drive prior to awakening (changes in sleep efficiency across circadian phase or across the tertiaries), or by the proportion of the varied sleep stages prior to awakenings. This robust endogenous circadian rhythm in sleep inertia may have important implications for people who need to be alert soon after awakening.     

Measuring Phase Shifts in Humans Following a Simulated Time‐Zone Transition: Agreement Between Constant Routine and Purification Methods

Twelve healthy participants were studied in an Isolation Unit. For the first 7 (control) days, subjects lived on UK time. Then the clock was advanced by 8 h, mimicking an eastward time‐zone transition, and for days 8 to 12, participants lived on this new local time. Two constant routines (participants were not allowed to sleep, were restricted in movement, and ate regular, identical snacks) were undertaken, during the control days (days 3 to 4) and at the end of the experiment (days 11 to 12). Rectal temperature and activity were measured throughout, with activity used to correct the measured temperatures for the direct (masking) effects of the sleep‐wake cycle. Phase changes of the temperature rhythm between the constant routines were assessed by cross‐correlation and cosinor analysis. During days 8 to 10, the measured temperatures and those that had been corrected (purified) for masking were assessed by the same two methods, and the shifts were extrapolated to predict the values expected during the second constant routine. Individuals differed widely in the phase shifts of the temperature rhythm, but the correlations between the changes measured by constant routines and those estimated by the purification methods were high (r=0.771 to 0.903), and the differences between them were not significantly different from zero (p>0.24). Phase shifts of the measured (masked) temperature rhythm were poorer predictors of the shift obtained from the constant routines (r≤0.605; mean±SD of differences >3±4.5 h). Limitations of the methods due to the variability of results are discussed, but we conclude that the mean phase shifts obtained from purified, but not raw, temperature data show acceptable agreement with those found using our version of the constant routine.