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.     

Duration of Sleep Inertia after Napping during Simulated Night Work and in Extended Operations

Due to the mixed findings of previous studies, it is still difficult to provide guidance on how to best manage sleep inertia after waking from naps in operational settings. One of the few factors that can be manipulated is the duration of the nap opportunity. The aim of the present study was to investigate the magnitude and time course of sleep inertia after waking from short (20-, 40- or 60-min) naps during simulated night work and extended operations. In addition, the effect of sleep stage on awakening and duration of slow wave sleep (SWS) on sleep inertia was assessed. Two within-subject protocols were conducted in a controlled laboratory setting. Twenty-four healthy young men (Protocol 1: n?=?12, mean age?=?25.1 yrs; Protocol 2: n?=?12, mean age?=?23.2 yrs) were provided with nap opportunities of 20-, 40-, and 60-min (and a control condition of no nap) ending at 02:00?h after ～20?h of wakefulness (Protocol 1 [P1]: simulated night work) or ending at 12:00?h after ～30?h of wakefulness (Protocol 2 [P2]: simulated extended operations). A 6-min test battery, including the Karolinska Sleepiness Scale (KSS) and the 4-min 2-Back Working Memory Task (WMT), was repeated every 15?min the first hour after waking. Nap sleep was recorded polysomnographically, and in all nap opportunities sleep onset latency was short and sleep efficiency high. Mixed-model analyses of variance (ANOVA) for repeated measures were calculated and included the factors time (time post-nap), nap opportunity (duration of nap provided), order (order in which the four protocols were completed), and the interaction of these terms. Results showed no test x nap opportunity effect (i.e., no effect of sleep inertia) on KSS. However, WMT performance was impaired (slower reaction time, fewer correct responses, and increased omissions) on the first test post-nap, primarily after a 40- or 60-min nap. In P2 only, performance improvement was evident 45?min post-awakening for naps of 40?min or more. In ANOVAs where sleep stage on awakening was included, the test x nap opportunity interaction was significant, but differences were between wake and non-REM Stage 1/Stage 2 or wake and SWS. A further series of ANOVAs showed no effect of the duration of SWS on sleep inertia. The results of this study demonstrate that no more than 15?min is required for performance decrements due to sleep inertia to dissipate after nap opportunities of 60?min or less, but subjective sleepiness is not a reliable indicator of this effect. Under conditions where sleep is short, these findings also suggest that SWS, per se, does not contribute to more severe sleep inertia. When wakefulness is extended and napping occurs at midday (i.e., P2), nap opportunities of 40- and 60-min have the advantage over shorter duration sleep periods, as they result in performance benefits ～45?min after waking.     

EFFECTS OF ARTIFICIAL DAWN ON SUBJECTIVE RATINGS OF SLEEP INERTIA AND DIM LIGHT MELATONIN ONSET

The timing of work and social requirements has a negative impact on performance and well-being of a significant proportion of the population in our modern society due to a phenomenon known as social jetlag. During workdays, in the early morning, late chronotypes, in particular, suffer from a combination of a nonoptimal circadian phase and sleep deprivation. Sleep inertia, a transient period of lowered arousal after awakening, therefore, becomes more severe. In the present home study, the authors tested whether the use of an alarm clock with artificial dawn could reduce complaints of sleep inertia in people having difficulties in waking up early. The authors also examined whether these improvements were accompanied by a shift in the melatonin rhythm. Two studies were performed: Study 1: three conditions (0, 50, and 250 lux) and Study 2: two conditions (0 lux and self-selected dawn-light intensity). Each condition lasted 2 weeks. In both studies, the use of the artificial dawn resulted in a significant reduction of sleep inertia complaints. However, no significant shift in the onset of melatonin was observed after 2 weeks of using the artificial dawn of 250 lux or 50 lux compared to the control condition. A multilevel analysis revealed that only the presence of the artificial dawn, rather than shift in the dim light melatonin onset or timing of sleep offset, is related to the observed reduction of sleep inertia complaints. Mechanisms other than shift of circadian rhythms are needed to explain the positive results on sleep inertia of waking up with a dawn signal. (Author correspondence: m.c.gimenez@rug.nl)     

Duration of sleep inertia after napping during simulated night work and in extended operations

Due to the mixed findings of previous studies, it is still difficult to provide guidance on how to best manage sleep inertia after waking from naps in operational settings. One of the few factors that can be manipulated is the duration of the nap opportunity. The aim of the present study was to investigate the magnitude and time course of sleep inertia after waking from short (20-, 40- or 60-min) naps during simulated night work and extended operations. In addition, the effect of sleep stage on awakening and duration of slow wave sleep (SWS) on sleep inertia was assessed. Two within-subject protocols were conducted in a controlled laboratory setting. Twenty-four healthy young men (Protocol 1: n = 12, mean age = 25.1 yrs; Protocol 2: n = 12, mean age = 23.2 yrs) were provided with nap opportunities of 20-, 40-, and 60-min (and a control condition of no nap) ending at 02:00 h after ～20 h of wakefulness (Protocol 1 [P1]: simulated night work) or ending at 12:00 h after ～30 h of wakefulness (Protocol 2 [P2]: simulated extended operations). A 6-min test battery, including the Karolinska Sleepiness Scale (KSS) and the 4-min 2-Back Working Memory Task (WMT), was repeated every 15 min the first hour after waking. Nap sleep was recorded polysomnographically, and in all nap opportunities sleep onset latency was short and sleep efficiency high. Mixed-model analyses of variance (ANOVA) for repeated measures were calculated and included the factors time (time post-nap), nap opportunity (duration of nap provided), order (order in which the four protocols were completed), and the interaction of these terms. Results showed no test x nap opportunity effect (i.e., no effect of sleep inertia) on KSS. However, WMT performance was impaired (slower reaction time, fewer correct responses, and increased omissions) on the first test post-nap, primarily after a 40- or 60-min nap. In P2 only, performance improvement was evident 45 min post-awakening for naps of 40 min or more. In ANOVAs where sleep stage on awakening was included, the test x nap opportunity interaction was significant, but differences were between wake and non-REM Stage 1/Stage 2 or wake and SWS. A further series of ANOVAs showed no effect of the duration of SWS on sleep inertia. The results of this study demonstrate that no more than 15 min is required for performance decrements due to sleep inertia to dissipate after nap opportunities of 60 min or less, but subjective sleepiness is not a reliable indicator of this effect. Under conditions where sleep is short, these findings also suggest that SWS, per se, does not contribute to more severe sleep inertia. When wakefulness is extended and napping occurs at midday (i.e., P2), nap opportunities of 40- and 60-min have the advantage over shorter duration sleep periods, as they result in performance benefits ～45 min after waking.     

Comparing Sleep‐Loss Sleepiness and Sleep Inertia: Lapses Make the Difference

To compare the behavioral effects of sleep‐loss sleepiness (performance impairment due to sleep loss) and sleep inertia (period of impaired performance that follows awakening), mean response latencies and number of lapses from a visual simple reaction‐time task were analyzed. Three experimental conditions were designed to manipulate sleepiness and sleep‐inertia levels: uninterrupted sleep, partial sleep reduction, and total sleep deprivation. Each condition included two consecutive nights (the first always a night of uninterrupted sleep, and the second either a night of uninterrupted sleep, a night when sleep was reduced to 3 h, or a night of total sleep deprivation), as well as two days in which performance was assessed at 10 different time points (08:00, 08:30, 09:00, 09:30, 10:00, 11:00, 14:00, 17:00, 20:00, and 23:00 h). From 08:00 to 09:00 h, reaction times in the partial sleep‐reduction and total sleep‐deprivation conditions were at a similar level and were slower than those observed in the uninterrupted sleep condition. In the same time period, the frequency of lapses in the total sleep‐deprivation condition was higher than in the partial sleep‐reduction condition, while this latter condition never differed from the uninterrupted sleep condition. The results indicate that both sleep inertia and sleep‐loss sleepiness lead to an increase in response latencies, but only extreme sleepiness leads to an increase in lapse frequency. We conclude that while reaction times slow as a result of both sleep inertia and sleep‐loss sleepiness, lapses appear to be a specific feature of sleep‐loss sleepiness.     

Can stress act as a sleep inertia countermeasure when on-call?

The nature of on-call work is such that workers can be called and required to respond immediately after being woken. However, due to sleep inertia, impaired performance immediately upon waking is typical. We investigated the impact of a preceding stressor (an alarm/mobilisation procedure) on sleepiness and performance upon waking. Healthy, adult males (n = 16) attended the sleep laboratory for four consecutive nights which included two, counterbalanced on-call sleeps where participants were woken at 04:00 h by (a) an alarm/mobilisation procedure (Alarm) or (b) gently by a researcher (Control). Following waking was a 2-h testing session comprising the repeated administration of the Karolinska Sleepiness Scale (KSS) and 5-min Psychomotor Vigilance Task (PVT). Results from within-subjects analysis of variance in both the Control and Alarm conditions showed that for subjective sleepiness (KSS) there was a significant fixed effect of time (p = 0.012), with participants becoming less sleepy as time post-wake increased. In terms of PVT performance outcomes, in neither the Alarm or Control conditions were there measurable signs of sleep inertia with performance remaining stable across the 2-h testing period. Based on previous research measuring impact of sleep inertia when woken near the circadian nadir, performance findings in particular were unexpected. We propose that stress caused by study procedures (i.e. finger pricks using lancets) unrelated to the simulated wake-up protocols may have countered any impact of sleep inertia on performance.     

Sleep initiation and initial sleep intensity: interactions of homeostatic and circadian mechanisms

Sleep initiation and sleep intensity in humans show a dissimilar time course. The propensity of sleep initiation (PSI), as measured by the multiple sleep latency test, remains at a relatively constant level throughout the habitual period of waking or exhibits a midafternoon peak. When waking is extended into the sleep period, PSI rises rapidly within a few hours. In contrast, sleep intensity, as measured by electroencephalographic slow-wave activity during naps, shows a gradual increase during the period of habitual waking. In the two-process model of sleep regulation, it corresponds to the rising limb of the homeostatic Process S. We propose that PSI is determined by the difference between Process S and the threshold H defining sleep onset, which is modulated by the circadian process C. In contrast to a previous version of the model, the parameters of H (amplitude, phase, skewness) differ from those of threshold L, which defines sleep termination. The present model is able to simulate the time course of PSI under baseline conditions as well as following recovery sleep after extended sleep deprivation. The simulations suggest that during the regular period of waking, a circadian process counteracts the increasing sleep propensity induced by a homeostatic process. Data obtained in the rat indicate that during the circadian period of predominant waking, a circadian process prevents a major intrusion of sleep.     

Sleepiness and Sleep in a Simulated “Six Hours On/Six Hours Off” Sea Watch System

Ships are operated around the clock using rapidly rotating shift schedules called sea watch systems. Sea watch systems may cause fatigue, in the same way as other irregular working time arrangements. The present study investigated subjective sleepiness and sleep duration in connection with a 6 h on/6 h off duty system. The study was performed in a bridge simulator, very similar to those found on ships. Twelve officers divided into two groups participated in the study that lasted 66 h. Half of the subjects started with the 06:00–12:00 h watch and the other half with the 12:00–18:00 h watch. The subjects alternated between off‐duty and on‐duty for the remainder of the experimental period. Approximately halfway through the experiment, the 12:00–18:00 h watch was divided into two 3 h watches/off‐duty periods. The effect of this was to reverse the on‐duty/off‐duty pattern between the two groups. This enabled all subjects to work the four possible watches (00:00–06:00 h, 06:00–12:00 h, 12:00–18:00 h, and 18:00–24:00 h) in an order that was essentially counterbalanced between groups. Ratings of sleepiness (Karolinska Sleepiness Scale; KSS) were obtained every 30 min during on‐duty periods and if subjects were awake during off‐duty periods. The subjectively rated duration of sleep was recorded after each off‐duty period that preceded watch periods when KSS was rated. The results showed that the average level of sleepiness was significantly higher during the 00:00–06:00 h watch compared to the 12:00–18:00 h and 18:00–24:00 h watches, but not to the 06:00–12:00 h watch. Sleepiness also progressed significantly from the start toward the end of each watch, with the exception of the 06:00‐12:00 h watch, when levels remained approximately stable. There were no differences between groups (i.e., the order between watches). Sleep duration during the 06:00–12:00 h off‐duty period (3 h 29 min) was significantly longer than during the 12:00–18:00 h period (1 h 47 min) and the 18:00–24:00 h period (2 h 7 min). Sleep during the 00:00–06:00 h period (4 h 23 min) was longer than all sleep periods except the 06:00–12:00 h period. There were no differences between groups. In spite of sufficient opportunities for sleep, sleep was on the average around 1–1 h 30 min shorter than the 7–7 h 30 min that is considered “normal” during a 24 h period. This is probably a consequence of the difficulty to sleep during daytime due to the alerting effects of the circadian rhythm. Also, sleepiness during the night and early mornings reached high levels, which may be explained by a combination of working close to or during the circadian trough of alertness and the relatively short sleep periods obtained. An initial suppression of sleepiness was observed during all watches, except for the 06:00–12:00 h watch. This suppression may be explained by the “masking effect” exerted by the relative high levels of activity required when taking over the responsibility of the ship. Toward the end of watches, the levels of sleepiness progressively increased to relatively high levels, at least during the 00:00–06:00 h watch. Presumably, initially high levels of activity are replaced by routine and even boredom.     

CONTRIBUTION OF CORE BODY TEMPERATURE,PRIOR WAKE TIME,AND SLEEP STAGES TO COGNITIVE THROUGHPUT PERFORMANCE DURING FORCED DESYNCHRONY

Shiftworkers are often required to sleep at inappropriate phases of their circadian timekeeping system, with implications for the dynamics of ultradian sleep stages. The independent effects of these changes on cognitive throughput performance are not well understood. This is because the effects of sleep on performance are usually confounded with circadian factors that cannot be controlled under normal day/night conditions. The aim of this study was to assess the contribution of prior wake, core body temperature, and sleep stages to cognitive throughput performance under conditions of forced desynchrony (FD). A total of 11 healthy young adult males resided in a sleep laboratory in which day/night zeitgebers were eliminated and ambient room temperature, lighting levels, and behavior were controlled. The protocol included 2 training days, a baseline day, and 7?×?28-h FD periods. Each FD period consisted of an 18.7-h wake period followed by a 9.3-h rest period. Sleep was assessed using standard polysomnography. Core body temperature and physical activity were assessed continuously in 1-min epochs. Cognitive throughput was measured by a 5-min serial addition and subtraction (SAS) task and a 90-s digit symbol substitution (DSS) task. These were administered in test sessions scheduled every 2.5?h across the wake periods of each FD period. On average, sleep periods had a mean (± standard deviation) duration of 8.5 (±1.2) h in which participants obtained 7.6 (±1.4) h of total sleep time. This included 4.2 (±1.2) h of stage 1 and stage 2 sleep (S1–S2 sleep), 1.6 (±0.6) h of slow-wave sleep (SWS), and 1.8 (±0.6) h of rapid eye movement (REM) sleep. A mixed-model analysis with five covariates indicated significant fixed effects on cognitive throughput for circadian phase, prior wake time, and amount of REM sleep. Significant effects for S1–S2 sleep and SWS were not found. The results demonstrate that variations in core body temperature, time awake, and amount of REM sleep are associated with changes in cognitive throughput performance. The absence of significant effect for SWS may be attributable to the truncated range of sleep period durations sampled in this study. However, because the mean and variance for SWS were similar to REM sleep, these results suggest that cognitive throughput may be more sensitive to variations in REM sleep than SWS. (Author correspondence: david.darwent@unisa.edu.au)     

Post-Sleep Inertia Performance Benefits of Longer Naps in Simulated Nightwork and Extended Operations

Operational settings involving shiftwork or extended operations require periods of prolonged wakefulness, which in conjunction with sleep loss and circadian factors, can have a negative impact on performance, alertness, and workplace safety. Napping has been shown to improve performance and alertness after periods of prolonged wakefulness and sleep loss. Longer naps may not only result in longer-lasting benefits but also increase the risk of sleep inertia immediately upon waking. The time course of performance after naps of differing durations is thus an important consideration in weighing the benefits and risks of napping in workplace settings. The objective of this study was to evaluate the effectiveness of nap opportunities of 20, 40, or 60 min for maintaining alertness and performance 1.5–6 h post-nap in simulated nightwork (P1) or extended operations (P2). Each protocol included 12 participants in a within-subjects design in a controlled laboratory environment. After a baseline 8 h time-in-bed, healthy young males (P1 mean age 25.1 yr; P2 mean age 23.2 yr) underwent either ≈20 h (P1) or ≈30 h (P2) of sleep deprivation on four separate occasions, followed by nap opportunities of 0, 20, 40, and 60 min. Sleep on the baseline night and during the naps was recorded polysomnographically. During the nap opportunities, sleep onset latency was short and sleep efficiency was high. A greater proportion of slow-wave sleep (SWS) was obtained in nap opportunities of 40 and 60 min compared with 20 min. Rapid eye movement (REM) sleep occurred infrequently. A subjective sleepiness rating (Karolinska Sleepiness Scale, KSS), 2-Back Working Memory Task (WMT), and Psychomotor Vigilance Task (PVT) were completed 1.5, 2, 2.5, 3, 4, 5, and 6 h post-nap. The slowest 10% of PVT responses were significantly faster after 40 and 60 min naps compared with a 20 min (P1) or no (P2) nap. There were significantly fewer PVT lapses after 40 and 60 min naps compared with no nap (P2), and after 60 min naps compared with 20 min naps (P1). Participants felt significantly less sleepy and made more correct responses and fewer omissions on the WMT after 60 min naps compared with no nap (P2). Subjective sleepiness and WMT performance were not related to the amount of nap-time spent in SWS. However, PVT response speed was significantly slower when time in SWS was <10 min compared with 20–29.9 min. In conclusion, in operationally relevant scenarios, nap opportunities of 40 and 60 min show more prolonged benefits 1.5–6 h post-nap, than a 20 min or no nap opportunity. Benefits were more apparent when the homeostatic pressure for sleep was high and post-nap performance testing occurred across the afternoon (P2). For sustained improvement in cognitive performance, naps of 40–60 min are recommended. (Author correspondence: t.l.signal@massey.ac.nz)     

Daytime naps in darkness phase shift the human circadian rhythms of melatonin and thyrotropin secretion

To systematically determine the effects of daytime exposure to sleep in darkness on human circadian phase, four groups of subjects participated in 4-day studies involving either no nap (control), a morning nap (0900-1500), an afternoon nap (1400-2000), or an evening nap (1900-0100) in darkness. Except during the scheduled sleep/dark periods, subjects remained awake under constant conditions, i.e., constant dim light exposure (36 lx), recumbence, and caloric intake. Blood samples were collected at 20-min intervals for 64 h to determine the onsets of nocturnal melatonin and thyrotropin secretion as markers of circadian phase before and after stimulus exposure. Sleep was polygraphically recorded. Exposure to sleep and darkness in the morning resulted in phase delays, whereas exposure in the evening resulted in phase advances relative to controls. Afternoon naps did not change circadian phase. These findings indicate that human circadian phase is dependent on the timing of darkness and/or sleep exposure and that strategies to treat circadian misalignment should consider not only the timing and intensity of light, but also the timing of darkness and/or sleep.     

Sleep Architecture When Sleeping at an Unusual Circadian Time and Associations with Insulin Sensitivity

Circadian misalignment affects total sleep time, but it may also affect sleep architecture. The objectives of this study were to examine intra-individual effects of circadian misalignment on sleep architecture and inter-individual relationships between sleep stages, cortisol levels and insulin sensitivity. Thirteen subjects (7 men, 6 women, age: 24.3±2.5 y; BMI: 23.6±1.7 kg/m²) stayed in a time blinded respiration chamber during three light-entrained circadian cycles (3x21h and 3x27h) resulting in a phase advance and a phase delay. Sleep was polysomnographically recorded. Blood and salivary samples were collected to determine glucose, insulin and cortisol concentrations. Intra-individually, a phase advance decreased rapid eye movement (REM) sleep and slow-wave sleep (SWS), increased time awake, decreased sleep and REM sleep latency compared to the 24h cycle. A phase delay increased REM sleep, decreased stage 2 sleep, increased time awake, decreased sleep and REM sleep latency compared to the 24h cycle. Moreover, circadian misalignment changed REM sleep distribution with a relatively shorter REM sleep during the second part of the night. Inter-individually, REM sleep was inversely associated with cortisol levels and HOMA-IR index. Circadian misalignment, both a phase advance and a phase delay, significantly changed sleep architecture and resulted in a shift in rem sleep. Inter-individually, shorter REM sleep during the second part of the night was associated with dysregulation of the HPA-axis and reduced insulin sensitivity. Trial Registration: International Clinical Trials Registry Platform NTR2926 http://apps.who.int/trialsearch/     

Circadian clock resetting by sleep deprivation without exercise in Syrian hamsters: dark pulses revisited

Circadian rhythms in Syrian hamsters can be phase shifted by procedures that stimulate wheel running ("exercise") in the mid-subjective day (the hamster's usual sleep period). The authors recently demonstrated that keeping hamsters awake by gentle handling, without continuous running, is sufficient to mimic this effect. Here, the authors assessed whether wakefulness, independent of wheel running, also mediates phase shifts to dark pulses during the midsubjective day in hamsters free-running in constant light (LL). With running wheels locked during a 3 h dark pulse on day 3 of LL, hamsters (N = 16) averaged only 43+/-15 min of spontaneous wake time and phase shifted only 24+/-43 min. When wheels were open during a dark pulse, two hamsters remained awake, ran continuously, and showed phase advance shifts of 7.3 h and 8.7 h, respectively, whereas the other hamsters were awake <60 min and shifted only 45+/-38 min. No animals stayed awake for 3 h without running. Additional time in LL (10 and 20 days) did not potentiate the waking or phase shift response to dark pulses. When all hamsters were sleep deprived with wheels locked during a dark pulse, phase advance shifts averaged 261+/-110 min and ranged up to 7.3 h. These shifts are large compared to those previously observed in response to the 3 h sleep deprivation procedure. Additional tests revealed that this potentiated shift response is dependent on LL prior to sleep deprivation but not LL after sleep deprivation. A final sleep deprivation test showed that a small part of the potentiation may be due to suppression of spontaneous wheel running by LL. These results indicate that some correlate of waking, other than continuous running, mediates the phase-shifting effect of dark pulses in the mid-subjective day. The mechanism by which LL potentiates shifting remains to be determined. The lack of effect of subsequent LL on the magnitude of shifts to sleep deprivation in the dark suggests that LL reduces responsivity to light by processes that take >3 h of dark to reverse.     

Sleepiness and sleep in a simulated "six hours on/six hours off" sea watch system

Ships are operated around the clock using rapidly rotating shift schedules called sea watch systems. Sea watch systems may cause fatigue, in the same way as other irregular working time arrangements. The present study investigated subjective sleepiness and sleep duration in connection with a 6 h on/6 h off duty system. The study was performed in a bridge simulator, very similar to those found on ships. Twelve officers divided into two groups participated in the study that lasted 66 h. Half of the subjects started with the 06:00-12:00 h watch and the other half with the 12:00-18:00 h watch. The subjects alternated between off-duty and on-duty for the remainder of the experimental period. Approximately halfway through the experiment, the 12:00-18:00 h watch was divided into two 3 h watches/off-duty periods. The effect of this was to reverse the on-duty/off-duty pattern between the two groups. This enabled all subjects to work the four possible watches (00:00-06:00 h, 06:00-12:00 h, 12:00-18:00 h, and 18:00-24:00 h) in an order that was essentially counterbalanced between groups. Ratings of sleepiness (Karolinska Sleepiness Scale; KSS) were obtained every 30 min during on-duty periods and if subjects were awake during off-duty periods. The subjectively rated duration of sleep was recorded after each off-duty period that preceded watch periods when KSS was rated. The results showed that the average level of sleepiness was significantly higher during the 00:00-06:00 h watch compared to the 12:00-18:00 h and 18:00-24:00 h watches, but not to the 06:00-12:00 h watch. Sleepiness also progressed significantly from the start toward the end of each watch, with the exception of the 06:00-12:00 h watch, when levels remained approximately stable. There were no differences between groups (i.e., the order between watches). Sleep duration during the 06:00-12:00 h off-duty period (3 h 29 min) was significantly longer than during the 12:00-18:00 h period (1 h 47 min) and the 18:00-24:00 h period (2 h 7 min). Sleep during the 00:00-06:00 h period (4 h 23 min) was longer than all sleep periods except the 06:00-12:00 h period. There were no differences between groups. In spite of sufficient opportunities for sleep, sleep was on the average around 1-1 h 30 min shorter than the 7-7 h 30 min that is considered “normal” during a 24 h period. This is probably a consequence of the difficulty to sleep during daytime due to the alerting effects of the circadian rhythm. Also, sleepiness during the night and early mornings reached high levels, which may be explained by a combination of working close to or during the circadian trough of alertness and the relatively short sleep periods obtained. An initial suppression of sleepiness was observed during all watches, except for the 06:00-12:00 h watch. This suppression may be explained by the “masking effect” exerted by the relative high levels of activity required when taking over the responsibility of the ship. Toward the end of watches, the levels of sleepiness progressively increased to relatively high levels, at least during the 00:00-06:00 h watch. Presumably, initially high levels of activity are replaced by routine and even boredom.     

Timing and consolidation of human sleep, wakefulness, and performance by a symphony of oscillators

Daily rhythms in sleep and waking performance are generated by the interplay of multiple external and internal oscillators. These include the light-dark and social cycles, a circadian hypothalamic oscillator oscillating virtually independently of behavior, and a homeostatic oscillator driven primarily by sleep-wake behavior. Both internal oscillators contribute to variation in many aspects of sleep and wakefulness (e.g., sleep timing and duration, REM sleep, non-REM sleep, REM density, sleep spindles, slow-wave sleep, electroencephalographic oscillations during wakefulness and sleep, and performance parameters, including attention and memory). The relative contribution of the oscillators varies greatly between these variables. Sleep and performance cannot be predicted by either oscillator independently but critically depend on their phase relationship and amplitude. The homeostatic oscillator feeds back onto the central pacemaker or its outputs. Thus, the amplitude of observed circadian variation in sleep and performance depends on how long we have been asleep or awake. During entrainment to external 24-h cycles, the opposing interplay between circadian and homeostatic changes in sleep propensity consolidates sleep and wakefulness. Some physiological correlates and mediators of both the circadian process (e.g., melatonin and hypocretin rhythms) and the homeostat (e.g., EEG, slow-wave activity, and adenosine release) have been established, offering targets for the development of countermeasures for circadian sleep and performance disorders. Interindividual differences in sleep timing, duration, and morning or evening preference are associated with changes of circadian or sleep homeostatic processes or both. Molecular genetic correlates, including polymorphisms in clock genes, of some of these interindividual differences are emerging.     

Morning Sleep Inertia in Alertness and Performance: Effect of Cognitive Domain and White Light Conditions

The transition from sleep to wakefulness entails a temporary period of reduced alertness and impaired performance known as sleep inertia. The extent to which its severity varies with task and cognitive processes remains unclear. We examined sleep inertia in alertness, attention, working memory and cognitive throughput with the Karolinska Sleepiness Scale (KSS), the Psychomotor Vigilance Task (PVT), n-back and add tasks, respectively. The tasks were administered 2 hours before bedtime and at regular intervals for four hours, starting immediately after awakening in the morning, in eleven participants, in a four-way cross-over laboratory design. We also investigated whether exposure to Blue-Enhanced or Bright Blue-Enhanced white light would reduce sleep inertia. Alertness and all cognitive processes were impaired immediately upon awakening (p<0.01). However, alertness and sustained attention were more affected than cognitive throughput and working memory. Moreover, speed was more affected than accuracy of responses. The light conditions had no differential effect on performance except in the 3-back task (p<0.01), where response times (RT) at the end of four hours in the two Blue-Enhanced white light conditions were faster (200 ms) than at wake time. We conclude that the effect of sleep inertia varies with cognitive domain and that it’s spectral/intensity response to light is different from that of sleepiness. That is, just increasing blue-wavelength in light may not be sufficient to reduce sleep inertia. These findings have implications for critical professions like medicine, law-enforcement etc., in which, personnel routinely wake up from night-time sleep to respond to emergency situations.     

Sleep Deprivation in the Dark Period Does Not Impair Memory in OF1 Mice

There is increasing evidence that sleep facilitates memory acquisition and consolidation. Moreover, the sleep-wake history preceding memory acquisition and retention as well as circadian timing may be important. We showed previously that sleep deprivation (SD) following learning in OF1 mice impaired their performance on an object recognition task. The learning task was scheduled at the end of the 12 h dark period and the test 24 h later. To investigate the influence of the prominent circadian sleep-wake distribution typical for rodents, we now scheduled the learning task at the beginning of the dark period. Wakefulness following immediately after the learning task was attained either by gentle interference (SD; n?=?20) or by spontaneous wheel running (RW; n?=?20). Two control groups were used: one had no RW throughout the experiment (n?=?23), while the other group's wheel was blocked immediately after acquisition (n?=?16), thereby preventing its use until testing. Recognition memory, defined as the difference in exploration of a novel and of familiar objects, was assessed 24 h later during the test phase. Motor activity and RW use were continuously recorded. Remarkably, performance on the object recognition task was not influenced by the protocols; the waking period following acquisition did not impair memory, independent of the method inducing wakefulness (i.e., sleep deprivation or spontaneous running). Thus, all groups explored the novel object significantly longer than the familiar ones during the test phase. Interestingly, neither the amount of rest lost during the SD interventions nor the amount of rest preceding acquisition influenced performance. However, the total amount of rest obtained by the control and SD mice subjected to acquisition at “dark offset” correlated positively (r?=?0.66) with memory at test, while no such relationship occurred in the corresponding groups tested at dark onset. Neither the amount of running nor intermediate rest correlated with performance at test in the RW group. We conclude that interfering with sleep during the dark period does not affect object recognition memory consolidation.     

Estimates on the Duration of Sleep and Wakefulness Made in Isolation

Fifteen subjects who lived singly in an isolation unit without temporal cues were asked to note every day after awakening how many hours they thought they had slept, and in the evening before retiring how many hours they had been awake. These estimates of the duration of sleep and wakefulness were compared with the intervals between two signals given by the subjects by pressing a button at the time of waking up and when turning off their bedside reading lamp. The results can be summarized as follows: (a) the daily estimated durations of sleep and wakefulness were positively correlated with the actual durations in all but one subject; (b) sleep and wake times were better estimated in the presence of a light-dark cycle even if the subjects were not entrained by the zeitgeber; (c) for both episodes, there was a consistent trend from an overestimation of relatively short to an underestimation of long durations; (d) with equal durations in the two episodes, sleep was estimated to be shorter than wake time; (e) the most accurate estimates centered around 10.5 h of sleep and 13.5 h of wake time; (f) the sleep and wake times added up to 24 h in subjects who did not deliberately “compensate” for relatively long sleep estimates with a short wake estimate, with the full cycle being adjusted to 24 h.     

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.