Time-of-Day Mediates the Influences of Extended Wake and Sleep Restriction on Simulated Driving

Although a nonlinear time-of-day and prior wake interaction on performance has been well documented, two recent studies have aimed to incorporate the influences of sleep restriction into this paradigm. Through the use of sleep-restricted forced desynchrony protocols, both studies reported a time-of-day?×?sleep restriction interaction, as well as a time-of-day?×?prior wake?×?sleep dose three-way interaction. The current study aimed to investigate these interactions on simulated driving performance, a more complex task with ecological validity for the problem of fatigued driving. The driving performance of 41 male participants (mean?±?SD: 22.8 ±2.2 yrs) was assessed on a 10-min simulated driving task with the standard deviation of lateral position (SDLAT) measured. Using a between-group design, participants were subjected to either a control condition of 9.33?h of sleep/18.66?h of wake, a moderate sleep-restriction (SR) condition of 7?h of sleep/21?h of wake, or a severe SR condition of 4.66?h of sleep/23.33?h of wake. In each condition, participants were tested at 2.5-h intervals after waking across 7?×?28-h d of forced desynchrony. Driving sessions occurred at nine doses of prior wake, within six divisions of the circadian cycle based on core body temperature (CBT). Mixed-models analyses of variance (ANOVAs) revealed significant main effects of time-of-day, prior wake, sleep debt, and sleep dose on SDLAT. Additionally, significant two-way interactions of time-of-day?×?prior wake and time-of-day?×?sleep debt, as well as significant three-way interactions of time-of-day?×?prior wake?×?sleep debt and time-of-day?×?sleep debt?×?sleep dose were observed. Although limitations such as the presence of practice effects and large standard errors are noted, the study concludes with three findings. The main effects demonstrate that extending wake, reducing sleep, and driving at poor times of day all significantly impair driving performance at an individual level. In addition to this, combining either extended wake or a sleep debt with the early morning hours greatly decreases driving performance. Finally, operating under the influence of a reduced sleep dose can greatly decrease performance at all times of the day. (Author correspondence: raymond.matthews@unisa.edu.au)     

Sleep restriction masks the influence of the circadian process on sleep propensity

Previous forced desynchrony studies have highlighted the close relationship between the circadian rhythms of core body temperature (CBT) and sleep propensity. In particular, these studies have shown that a "forbidden zone" for sleep exists on the rising limb of the CBT rhythm. In these previous studies, the length of the experimental day was either ultrashort (90 min), short (20 h), or long (28 h), and the ratio of sleep to wake was normal (i.e., 1:2). The aim of the current study was to examine the relative effects of the circadian and homeostatic processes on sleep propensity using a 28-h forced desynchrony protocol in which the ratio of sleep to wake was substantially lower than normal (i.e., 1:5). Twenty-seven healthy males lived in a time-isolation sleep laboratory for 11 consecutive days. Participants completed either a control (n = 13) or sleep restriction (n = 14) condition. In both conditions, the protocol consisted of 2 × 24-h baseline days followed by 8 × 28-h forced desynchrony days. On forced desynchrony days, the control group had 9.3 h in bed and 18.7 h of wake, and the sleep restriction group had 4.7 h in bed and 23.3 h of wake. For all participants, each 30-s epoch of time in bed was scored as sleep or wake based on standard polysomnography recordings, and was also assigned a circadian phase (360° = 24 h) based on a cosine equation fitted to continuously recorded CBT data. For each circadian phase (i.e., 72 × 5° bins), sleep propensity was calculated as the percentage of epochs spent in bed scored as sleep. For the control group, there was a clear circadian rhythm in sleep propensity, with a peak of 98.5% at 5° (~05:20 h), a trough of 64.9% at 245° (~21:20 h), and an average of 82.3%. In contrast, sleep propensity for the sleep restriction group was relatively high at all circadian phases, with an average of 96.7%. For this group, the highest sleep propensity (99.0%) occurred at 60° (~09:00 h), and the lowest sleep propensity (91.3%) occurred at 265° (~22:40 h). As has been shown previously, these current data indicate that with a normal sleep-to-wake ratio, the effect of the circadian process on sleep propensity is pronounced, such that a forbidden zone for sleep exists at a phase equivalent to evening time for a normally entrained individual. However, these current data also indicate that when the ratio of sleep to wake is substantially lower than normal, this circadian effect is masked. In particular, sleep propensity is very high at all circadian phases, including those that coincide with the forbidden zone for sleep. This finding suggests that if the homeostatic pressure for sleep is sufficiently high, then the circadian drive for wakefulness can be overridden. In future studies, it will be important to determine whether or not this masking effect occurs with less severe sleep restriction, e.g., with a sleep-to-wake ratio of 1:3.     

The effects of a split sleep–wake schedule on neurobehavioural performance and predictions of performance under conditions of forced desynchrony

Extended wakefulness, sleep loss, and circadian misalignment are factors associated with an increased accident risk in shiftwork. Splitting shifts into multiple shorter periods per day may mitigate these risks by alleviating prior wake. However, the effect of splitting the sleep–wake schedule on the homeostatic and circadian contributions to neurobehavioural performance and subjective assessments of one’s ability to perform are not known. Twenty-nine male participants lived in a time isolation laboratory for 13?d, assigned to one of two 28-h forced desynchrony (FD) schedules. Depending on the assigned schedule, participants were provided the same total time in bed (TIB) each FD cycle, either consolidated into a single period (9.33?h TIB) or split into two equal halves (2?×?4.67?h TIB). Neurobehavioural performance was regularly assessed with a psychomotor vigilance task (PVT) and subjectively-assessed ability was measured with a prediction of performance on a visual analogue scale. Polysomnography was used to assess sleep, and core body temperature was recorded to assess circadian phase. On average, participants obtained the same amount of sleep in both schedules, but those in the split schedule obtained more slow wave sleep (SWS) on FD days. Mixed-effects ANOVAs indicated no overall difference between the standard and split schedules in neurobehavioural performance or predictions of performance. Main effects of circadian phase and prior wake were present for both schedules, such that performance and subjective ratings of ability were best around the circadian acrophase, worst around the nadir, and declined with increasing prior wake. There was a schedule by circadian phase interaction for all neurobehavioural performance metrics such that performance was better in the split schedule than the standard schedule around the nadir. There was no such interaction for predictions of performance. Performance during the standard schedule was significantly better than the split schedule at 2?h of prior wake, but declined at a steeper rate such that the schedules converged by 4.5–7?h of prior wake. Overall, the results indicate that when the total opportunity for sleep per day is satisfactory, a split sleep–wake schedule is not detrimental to sleep or performance. Indeed, though not reflected in subjective assessments of performance capacity, splitting the schedule may be of some benefit, given its reduction of neurobehavioural impairment at night and its association with increased SWS. Therefore, for some industries that require operations to be sustained around the clock, implementing a split work–rest schedule may be of assistance.     

Sleep Restriction Masks the Influence of the Circadian Process on Sleep Propensity

Previous forced desynchrony studies have highlighted the close relationship between the circadian rhythms of core body temperature (CBT) and sleep propensity. In particular, these studies have shown that a “forbidden zone” for sleep exists on the rising limb of the CBT rhythm. In these previous studies, the length of the experimental day was either ultrashort (90?min), short (20?h), or long (28?h), and the ratio of sleep to wake was normal (i.e., 1:2). The aim of the current study was to examine the relative effects of the circadian and homeostatic processes on sleep propensity using a 28-h forced desynchrony protocol in which the ratio of sleep to wake was substantially lower than normal (i.e., 1:5). Twenty-seven healthy males lived in a time-isolation sleep laboratory for 11 consecutive days. Participants completed either a control (n?=?13) or sleep restriction (n?=?14) condition. In both conditions, the protocol consisted of 2?×?24-h baseline days followed by 8?×?28-h forced desynchrony days. On forced desynchrony days, the control group had 9.3?h in bed and 18.7?h of wake, and the sleep restriction group had 4.7?h in bed and 23.3?h of wake. For all participants, each 30-s epoch of time in bed was scored as sleep or wake based on standard polysomnography recordings, and was also assigned a circadian phase (360°?=?24?h) based on a cosine equation fitted to continuously recorded CBT data. For each circadian phase (i.e., 72?×?5° bins), sleep propensity was calculated as the percentage of epochs spent in bed scored as sleep. For the control group, there was a clear circadian rhythm in sleep propensity, with a peak of 98.5% at 5° (～05:20?h), a trough of 64.9% at 245° (～21:20?h), and an average of 82.3%. In contrast, sleep propensity for the sleep restriction group was relatively high at all circadian phases, with an average of 96.7%. For this group, the highest sleep propensity (99.0%) occurred at 60° (～09:00?h), and the lowest sleep propensity (91.3%) occurred at 265° (～22:40?h). As has been shown previously, these current data indicate that with a normal sleep-to-wake ratio, the effect of the circadian process on sleep propensity is pronounced, such that a forbidden zone for sleep exists at a phase equivalent to evening time for a normally entrained individual. However, these current data also indicate that when the ratio of sleep to wake is substantially lower than normal, this circadian effect is masked. In particular, sleep propensity is very high at all circadian phases, including those that coincide with the forbidden zone for sleep. This finding suggests that if the homeostatic pressure for sleep is sufficiently high, then the circadian drive for wakefulness can be overridden. In future studies, it will be important to determine whether or not this masking effect occurs with less severe sleep restriction, e.g., with a sleep-to-wake ratio of 1:3. (Author correspondence: charli.sargent@cqu.edu.au)     

THE INFLUENCE OF CIRCADIAN PHASE AND PRIOR WAKE ON NEUROMUSCULAR FUNCTION

Previous forced desynchrony (FD) studies have shown that neurobehavioral function is affected by circadian phase and duration of prior wakefulness. There is some evidence that neuromuscular function may also be affected by circadian phase and prior wake, but these effects have not been systematically investigated. This study examined the effects of circadian phase and prior wake on two measures of neuromuscular function—postural balance (PB) and maximal grip strength (MGS)—using a 28-h FD protocol. Eleven male participants (mean?±?SD: 22.7?±?2.5 yr) lived in a sound-attenuated, light- and temperature-controlled time-isolation laboratory for 12 days. Following two training days and a baseline day, participants were scheduled to seven 28-h FD days, with the ratio between sleep opportunity and wake spans kept constant (i.e., 9.3?h sleep period and 18.7?h wake period). PB was measured during 1?min of quiet standing on a force platform. MGS of the dominant hand was measured using a dynamometer. These two measures were obtained every 2.5?h during wake. Core body temperature was continuously recorded with rectal thermistors to determine circadian phase. For both measures of neuromuscular function, individual data points were assigned a circadian phase and a level of prior wake. Data were analyzed by repeated-measures analysis of variance (ANOVA) with two within-subjects factors: circadian phase (six phases) and prior wake (seven levels). For MGS, there was a main effect of circadian phase, but no main effect of prior wake. For PB, there were no main effects of circadian phase or prior wake. There were no interactions between circadian phase and prior wake for MGS or PB. The significant effect of circadian phase on muscle strength is in agreement with previous reports in the literature. In terms of prior wake, both MGS and PB remained relatively stable across wake periods, indicating that neuromuscular function may be more robust than neurobehavioral function when the duration of wakefulness is within a normal range (i.e., 18.7?h). (Author correspondence: charli.sargent@unisa.edu.au)     

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)     

Effects of Artificial Dawn and Morning Blue Light on Daytime Cognitive Performance,Well-being,Cortisol and Melatonin Levels

Light exposure elicits numerous effects on human physiology and behavior, such as better cognitive performance and mood. Here we investigated the role of morning light exposure as a countermeasure for impaired cognitive performance and mood under sleep restriction (SR). Seventeen participants took part of a 48h laboratory protocol, during which three different light settings (separated by 2?wks) were administered each morning after two 6-h sleep restriction nights: a blue monochromatic LED (light-emitting diode) light condition (BL; 100?lux at 470?nm for 20?min) starting 2?h after scheduled wake-up time, a dawn-simulating light (DsL) starting 30?min before and ending 20?min after scheduled wake-up time (polychromatic light gradually increasing from 0 to 250?lux), and a dim light (DL) condition for 2?h beginning upon scheduled wake time (<8?lux). Cognitive tasks were performed every 2?h during scheduled wakefulness, and questionnaires were administered hourly to assess subjective sleepiness, mood, and well-being. Salivary melatonin and cortisol were collected throughout scheduled wakefulness in regular intervals, and the effects on melatonin were measured after only one light pulse. Following the first SR, analysis of the time course of cognitive performance during scheduled wakefulness indicated a decrease following DL, whereas it remained stable following BL and significantly improved after DsL. Cognitive performance levels during the second day after SR were not significantly affected by the different light conditions. However, after both SR nights, mood and well-being were significantly enhanced after exposure to morning DsL compared with DL and BL. Melatonin onset occurred earlier after morning BL exposure, than after morning DsL and DL, whereas salivary cortisol levels were higher at wake-up time after DsL compared with BL and DL. Our data indicate that exposure to an artificial morning dawn simulation light improves subjective well-being, mood, and cognitive performance, as compared with DL and BL, with minimal impact on circadian phase. Thus, DsL may provide an effective strategy for enhancing cognitive performance, well-being, and mood under mild sleep restriction.     

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.     

Revisiting spontaneous internal desynchrony using a quantitative model of sleep physiology

Early attempts to characterize free-running human circadian rhythms generated three notable results: 1) observed circadian periods of 25 hours (considerably longer than the now established 24.1- to 24.2-hour average intrinsic circadian period) with sleep delayed to later circadian phases than during entrainment; 2) spontaneous internal desynchrony of circadian rhythms and sleep/wake cycles--the former with an approximately 24.9-hour period, and the latter with a longer (28-68 hour) or shorter (12-20 hour) period; and 3) bicircadian (48-50 hour) sleep/wake cycles. All three results are reproduced by Kronauer et al.'s (1982) coupled oscillator model, but the physiological basis for that phenomenological model is unclear. We use a physiologically based model of hypothalamic and brain stem nuclei to investigate alternative physiological mechanisms that could underlie internal desynchrony. We demonstrate that experimental observations can be reproduced by changes in two pathways: promotion of orexinergic (Orx) wake signals, and attenuation of the circadian signal reaching hypothalamic nuclei. We reason that delayed sleep is indicative of an additional wake-promoting drive, which may be of behavioral origin, associated with removal of daily schedules and instructions given to participants. We model this by increasing Orx tone during wake, which reproduces the observed period lengthening and delayed sleep. Weakening circadian input to the ventrolateral preoptic nucleus (possibly mediated by the dorsomedial hypothalamus) causes desynchrony, with observed sleep/wake cycle period determined by degree of Orx up-regulation. During desynchrony, sleep/wake cycles are driven by sleep homeostasis, yet sleep bout length maintains circadian phase dependence. The model predicts sleep episodes are shortest when started near the temperature minimum, consistent with experimental findings. The model also correctly predicts that it is possible to transition to bicircadian rhythms from either a synchronized or desynchronized state. Our findings suggest that feedback from behavioral choices to physiology could play an important role in spontaneous internal desynchrony.     

Recovery of cognitive performance from sleep debt: do a short rest pause and a single recovery night help?

We studied the recovery of multitask performance and sleepiness from acute partial sleep deprivation through rest pauses embedded in performance sessions and an 8 h recovery sleep opportunity the following night. Sixteen healthy men, aged 19-22 yrs, participated in normal sleep (two successive nights with 8 h sleep) and sleep debt (one 2 h night sleep followed by an 8 h sleep the following night) conditions. In both conditions, the participants performed four 70 min multitask sessions, with every other one containing a 10 min rest pause with light neck-shoulder exercise. The multitask consisted of four simultaneously active subtasks, with the level of difficulty set in relation to each participant's ability. Physiological sleepiness was assessed with continuous electroencephalography/electro-oculography recordings during themultitask sessions, and subjective sleepiness was self-rated with the Karolinska Sleepiness Scale. Results showed that multitask performance and physiological and subjective sleepiness were impaired by the sleep debt ( p > .001). The rest pause improved performance and subjective sleepiness for about 15 min, regardless of the amount of prior sleep ( p > .01-.05). Following recovery sleep, all outcome measures showed marked improvement ( p < .001), but they failed to reach the levels observed in the control condition ( p < .001-.05). A correlation analysis showed the participants whose multitask performance deteriorated the most following the night of sleep loss tended to be the same persons whose performance was most impaired following the night of the recovery sleep ( p < .001). Taken together, our results suggest that a short rest pause with light exercise is not an effective countermeasure in itself for sleep debt-induced impairments when long-term effects are sought. In addition, it seems that shift arrangements that lead to at least a moderate sleep debt should be followed by more than one recovery night to ensure full recovery. Persons whose cognitive performance is most affected by sleep debt are likely to require the most sleep to recover.     

Recovery of Cognitive Performance from Sleep Debt: Do a Short Rest Pause and a Single Recovery Night Help?

We studied the recovery of multitask performance and sleepiness from acute partial sleep deprivation through rest pauses embedded in performance sessions and an 8 h recovery sleep opportunity the following night. Sixteen healthy men, aged 19–22 yrs, participated in normal sleep (two successive nights with 8 h sleep) and sleep debt (one 2 h night sleep followed by an 8 h sleep the following night) conditions. In both conditions, the participants performed four 70 min multitask sessions, with every other one containing a 10 min rest pause with light neck‐shoulder exercise. The multitask consisted of four simultaneously active subtasks, with the level of difficulty set in relation to each participant's ability. Physiological sleepiness was assessed with continuous electroencephalography/electro‐oculography recordings during the multitask sessions, and subjective sleepiness was self‐rated with the Karolinska Sleepiness Scale. Results showed that multitask performance and physiological and subjective sleepiness were impaired by the sleep debt (p>.001). The rest pause improved performance and subjective sleepiness for about 15 min, regardless of the amount of prior sleep (p>.01–.05). Following recovery sleep, all outcome measures showed marked improvement (p<.001), but they failed to reach the levels observed in the control condition (p<.001–.05). A correlation analysis showed the participants whose multitask performance deteriorated the most following the night of sleep loss tended to be the same persons whose performance was most impaired following the night of the recovery sleep (p<.001). Taken together, our results suggest that a short rest pause with light exercise is not an effective countermeasure in itself for sleep debt‐induced impairments when long‐term effects are sought. In addition, it seems that shift arrangements that lead to at least a moderate sleep debt should be followed by more than one recovery night to ensure full recovery. Persons whose cognitive performance is most affected by sleep debt are likely to require the most sleep to recover.     

Interactive mathematical models of subjective alertness and cognitive throughput in humans

The authors present here mathematical models in which levels of subjective alertness and cognitive throughput are predicted by three components that interact with one another in a nonlinear manner. These components are (1) a homeostatic component (H) that falls in a sigmoidal manner during wake and rises in a saturating exponential manner at a rate that is determined by circadian phase during sleep; (2) a circadian component (C) that is a function of the output of our mathematical model of the effect of light on the circadian pacemaker, with the amplitude further regulated by the level of H; and (3) a sleep inertia component (W) that rises in a saturating exponential manner after waketime. The authors first construct initial models of subjective alertness and cognitive throughput based on the results of sleep inertia studies, sleep deprivation studies initiated across all circadian phases, 28-h forced desynchrony studies, and alertness and performance dose response curves to sleep. These initial models are then refined using data from nearly one hundred fifty 30- to 50-h sleep deprivation studies in which subjects woke at their habitual times. The interactive three-component models presented here are able to predict even the fine details of neurobehavioral data from sleep deprivation studies and, after further validation, may provide a powerful tool for the design of safe shift work and travel schedules, including those in which people are exposed to unusual patterns of light.     

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.     

It’s not just what you eat but when: The impact of eating a meal during simulated shift work on driving performance

Shiftworkers have impaired performance when driving at night and they also alter their eating patterns during nightshifts. However, it is unknown whether driving at night is influenced by the timing of eating. This study aims to explore the effects of timing of eating on simulated driving performance across four simulated nightshifts. Healthy, non-shiftworking males aged 18–35 years (n = 10) were allocated to either an eating at night (n = 5) or no eating at night (n = 5) condition. During the simulated nightshifts at 1730, 2030 and 0300 h, participants performed a 40-min driving simulation, 3-min Psychomotor Vigilance Task (PVT-B), and recorded their ratings of sleepiness on a subjective scale. Participants had a 6-h sleep opportunity during the day (1000–1600 h). Total 24-h food intake was consistent across groups; however, those in the eating at night condition ate a large meal (30% of 24-h intake) during the nightshift at 0130 h. It was found that participants in both conditions experienced increased sleepiness and PVT-B impairments at 0300 h compared to 1730 and 2030 h (p < 0.001). Further, at 0300 h, those in the eating condition displayed a significant decrease in time spent in the safe zone (p < 0.05; percentage of time within 10 km/h of the speed limit and 0.8 m of the centre of the lane) and significant increases in speed variability (p < 0.001), subjective sleepiness (p < 0.01) and number of crashes (p < 0.01) compared to those in the no eating condition. Results suggest that, for optimal performance, shiftworkers should consider restricting food intake during the night.     

Post Learning Sleep Improves Cognitive-Emotional Decision-Making: Evidence for a ‘Deck B Sleep Effect’ in the Iowa Gambling Task

The Iowa Gambling Task (IGT) is widely used to assess real life decision-making impairment in a wide variety of clinical populations. Our study evaluated how IGT learning occurs across two sessions, and whether a period of intervening sleep between sessions can enhance learning. Furthermore, we investigate whether pre-sleep learning is necessary for this improvement. A 200-trial version of the IGT was administered at two sessions separated by wake, sleep or sleep and wake (time-of-day control). Participants were categorized as learners and non-learners based on initial performance in session one. In session one, participants initially preferred the high-frequency reward decks B and D, however, a subset of learners decreased choice from negative expected value ‘bad’ deck B and increased choices towards with a positive expected value ‘good’ decks (decks C and D). The learners who had a period of sleep (sleep and sleep/wake control conditions) between sessions showed significantly larger reduction in choices from deck B and increase in choices from good decks compared to learners that had intervening wake. Our results are the first to show that post-learning sleep can improve performance on a complex decision-making task such as the IGT. These results provide new insights into IGT learning and have important implications for understanding the neural mechanisms of “sleeping on” a decision.     

Effects of two nights partial sleep deprivation on an evening submaximal weightlifting performance; are 1 h powernaps useful on the day of competition?

We have investigated the effects that sleep restriction (3-h sleep during two consecutive nights) have on an evening (17:00 h) submaximal weightlifting session; and whether this performance improves following a 1-h post-lunch powernap. Fifteen resistance-trained males participated in this study. Before the experimental protocol commenced, 1RM bench press and inclined leg press and normative habitual sleep were recorded. Participants were familiarised with the testing protocol, then completed three experimental conditions with two nights of prescribed sleep: (i) Normal (N): retire at 23:00 h and wake at 06:30 h, (ii) partial sleep-deprivation (SD): retire at 03:30 h and wake at 06:30 h and (iii) partial sleep-deprivation with nap (SD_N): retire at 03:30 h and wake at 06:30 h with a 1-h nap at 13:00 h. Each condition was separated by at least 7 days and the order of administration was randomised and counterbalanced. Rectal (T_rec) and mean skin (T_s) temperatures, Profile of Mood Scores, subjective tiredness, alertness and sleepiness values were measured at 08:00, 11:00, 14:00 and 17:00 h on the day of the weightlifting session. Following the final temperature measurements at 17:00 h, participants completed a 5-min active warm-up before a ‘strength’ protocol. Participants performed three repetitions of right-hand grip strength, then three repetitions at each incremental load (40%, 60% and 80% of 1RM) for bench press and inclined leg press, with a 5-min recovery in between each repetition. A linear encoder was attached perpendicular to the movement, to the bar used for the exercises. Average power (AP), average force (AF), peak velocity (PV), distance (D) and time-to-peak velocity (tPV) were measured (MuscleLab software) during the concentric phase of the movements for each lift. Data were analysed using general linear models with repeated measures. The main findings were that SD reduced maximal grip (2.7%), bench press (11.2% AP, 3.3% AF and 9.4% PV) and leg press submaximal values (5.7% AP) with a trend for a reduction in AF (3.3% P = 0.06). Furthermore, RPE increased for measures of grip strength, leg and bench press during SD. Following a 1-h powernap (SD_N), values of grip and bench press improved to values similar in N, as did tiredness, alertness and sleepiness. There was a main effect for “load” on the bar for both bench and leg press where AP, AF, tPV values increased with load (P < 0.05) and PV decreased from the lightest to the heaviest load for both bench and leg press. An interaction of “load and condition” was present in leg press only, where the rate of change of AP is greater in the N than SD and SD_N conditions. In addition, for PV and tPV the rate of change was greater for SD_N than N or SD condition values. In summary, SD had a negative effect on grip strength and some components of bench and inclined leg press. The use of a 1-h power nap that ended 3 h before the “strength” assessment had a positive effect on weightlifting performance, subjective mood and ratings of tiredness.     

Plasticity of the intrinsic period of the human circadian timing system

Human expeditions to Mars will require adaptation to the 24.65-h Martian solar day-night cycle (sol), which is outside the range of entrainment of the human circadian pacemaker under lighting intensities to which astronauts are typically exposed. Failure to entrain the circadian time-keeping system to the desired rest-activity cycle disturbs sleep and impairs cognitive function. Furthermore, differences between the intrinsic circadian period and Earth's 24-h light-dark cycle underlie human circadian rhythm sleep disorders, such as advanced sleep phase disorder and non-24-hour sleep-wake disorders. Therefore, first, we tested whether exposure to a model-based lighting regimen would entrain the human circadian pacemaker at a normal phase angle to the 24.65-h Martian sol and to the 23.5-h day length often required of astronauts during short duration space exploration. Second, we tested here whether such prior entrainment to non-24-h light-dark cycles would lead to subsequent modification of the intrinsic period of the human circadian timing system. Here we show that exposure to moderately bright light ( approximately 450 lux; approximately 1.2 W/m(2)) for the second or first half of the scheduled wake episode is effective for entraining individuals to the 24.65-h Martian sol and a 23.5-h day length, respectively. Estimations of the circadian periods of plasma melatonin, plasma cortisol, and core body temperature rhythms collected under forced desynchrony protocols revealed that the intrinsic circadian period of the human circadian pacemaker was significantly longer following entrainment to the Martian sol as compared to following entrainment to the 23.5-h day. The latter finding of after-effects of entrainment reveals for the first time plasticity of the period of the human circadian timing system. Both findings have important implications for the treatment of circadian rhythm sleep disorders and human space exploration.     

Alertness and psychomotor performance levels of marine pilots on an irregular work roster

ABSTRACT

Fatigue is recognized as an important safety concern in the transportation industry. In this study, our goal was to investigate how circadian and sleep–wake dependent factors influence St-Lawrence River pilots’ sleep–wake cycle, alertness and psychomotor performance levels at work. A total of 18 male St-Lawrence River ship pilots were recruited to a 16–21-day field study. Pilots’ chronotype, sleepiness and insomnia levels were documented using standardized questionnaires. Their sleep–wake cycle was documented by a sleep–wake log and wrist-worn activity monitoring. Subjective alertness and objective psychomotor performances were assessed ~5×/day for each work and rest day. Ship transits were distributed throughout the 24-h day and lasted on average (± SEM) 5.93 ± 0.67 h. Main sleep periods occurred mainly at night, and objectively lasted 6.04 ± 1.02 h before work days. When going to bed at the end of work days, pilots subjectively reported sleeping 7.64 ± 1.64 h in the prior 24 h. Significant diurnal and wake-dependent effects were observed for subjective alertness and objective psychomotor performance, with minimum levels occurring between 09:00 and 10:00. Thus, despite their irregular work schedule, ship pilots presented, as a group, a diurnal variation of alertness and psychomotor performance indicative of a day-oriented circadian system. Important inter-individual differences were observed on psychomotor performance mesor and phase. In individuals, earlier phases in psychomotor performance were correlated with earlier chronotype. This study indicates that both circadian and homeostatic processes modulate alertness and psychomotor performance levels with worst levels reached when long shifts ended in the morning. This work has potential applications as it indicates fatigue countermeasures considering both processes are scientifically based.     

A unique,fast-forwards rotating schedule with 12-h long shifts prevents chronic sleep debt

Sleep debt – together with circadian misalignment – is considered a central factor for adverse health outcomes associated with shift work. Here, we describe in detail sleep-wake behavior in a fast-forward rotating 12-h shift schedule, which involves at least 24 hours off after each shift and thus allows examining the role of immediate recovery after shift-specific sleep debt. Thirty-five participants at two chemical plants in Germany were chronotyped using the Munich ChronoType Questionnaire for Shift-Workers (MCTQ^Shift) and wore actimeters throughout the two-week study period. From these actimetry recordings, we computed sleep and nap duration, social jetlag (a measure of circadian misalignment), and the daily timing of activity and sleep (center of gravity and mid-sleep, respectively). We observed that the long off-work periods between each shift create a fast alternation between shortened (mean ± standard deviation, 5h 17min ± 56min) and extended (8h 25min ± 72min) sleep episodes resulting in immanent reductions of sleep debt. Additionally, extensive napping of early chronotypes (up to 3 hours before the night shift) statistically compensated short sleep durations after the night shift. Partial rank correlations showed chronotype-dependent patterns of sleep and activity that were similar to those previously described in 8-h schedules; however, sleep before the day shift did not differ between chronotypes. Our findings indicate that schedules preventing a build-up of chronic sleep debt may reduce detrimental effects of shift work irrespective of shift duration. Prospective studies are needed to further elucidate the relationship between sleep, the circadian system, and health and safety hazards.     

Identification of human plasma metabolites exhibiting time-of-day variation using an untargeted liquid chromatography-mass spectrometry metabolomic approach

Although daily rhythms regulate multiple aspects of human physiology, rhythmic control of the metabolome remains poorly understood. The primary objective of this proof-of-concept study was identification of metabolites in human plasma that exhibit significant 24-h variation. This was assessed via an untargeted metabolomic approach using liquid chromatography-mass spectrometry (LC-MS). Eight lean, healthy, and unmedicated men, mean age 53.6 (SD ± 6.0) yrs, maintained a fixed sleep/wake schedule and dietary regime for 1 wk at home prior to an adaptation night and followed by a 25-h experimental session in the laboratory where the light/dark cycle, sleep/wake, posture, and calorific intake were strictly controlled. Plasma samples from each individual at selected time points were prepared using liquid-phase extraction followed by reverse-phase LC coupled to quadrupole time-of-flight MS analysis in positive ionization mode. Time-of-day variation in the metabolites was screened for using orthogonal partial least square discrimination between selected time points of 10:00 vs. 22:00 h, 16:00 vs. 04:00 h, and 07:00 (d 1) vs. 16:00 h, as well as repeated-measures analysis of variance with time as an independent variable. Subsequently, cosinor analysis was performed on all the sampled time points across the 24-h day to assess for significant daily variation. In this study, analytical variability, assessed using known internal standards, was low with coefficients of variation <10%. A total of 1069 metabolite features were detected and 203 (19%) showed significant time-of-day variation. Of these, 34 metabolites were identified using a combination of accurate mass, tandem MS, and online database searches. These metabolites include corticosteroids, bilirubin, amino acids, acylcarnitines, and phospholipids; of note, the magnitude of the 24-h variation of these identified metabolites was large, with the mean ratio of oscillation range over MESOR (24-h time series mean) of 65% (95% confidence interval [CI]: 49-81%). Importantly, several of these human plasma metabolites, including specific acylcarnitines and phospholipids, were hitherto not known to be 24-h variant. These findings represent an important baseline and will be useful in guiding the design and interpretation of future metabolite-based studies.