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Study Objectives: To investigate the relative contributions of the homeostatic and circadian processes on sleep regulation under conditions of severe sleep restriction. Design: The 13-day laboratory based study consisted of 3 x 24-h baseline days (8 h sleep opportunity, 16 h wake) followed by 7 x 28-h forced desynchrony days (4.7 h sleep opportunity, 23.3 h wake). Setting: The study was conducted in a time isolation unit at the Centre for Sleep Research, University of South Australia. Participants: Fourteen healthy, nonsmoking males, aged 21.8 +/- 3.8 (mean +/- SD) years participated in the study. Interventions: N/A Measurements: Sleep was measured using standard polysomnography. Core body temperature (CBT) was recorded continuously using a rectal thermistor. Each epoch of sleep was assigned a circadian phase based on the CBT data (6 x 60-degree bins) and an elapsed time into sleep episode (2 x 140-min intervals). Results: The percentage of SWS decreased with elapsed time into the sleep episode. However, no change in the percentage of REM sleep was observed with sleep progression. Whilst there was a circadian modulation of REM sleep, the amplitude of the circadian variation was smaller than expected. Sleep efficiency remained high throughout the sleep episode and across all circadian phases. Conclusions: Previous forced desynchrony studies have demonstrated a strong circadian influence on sleep, in the absence of sleep restriction. The current study suggests that in the presence of high homeostatic pressure, the circadian modulation of sleep, in particular sleep efficiency and to a lesser extent, REM sleep, are reduced. Refereed/Peer-reviewed

Conclusions: The performance consequence of sleep restriction in our study was prominent during the biological night, even when the prior wake duration was short, and this performance consequence was in forms of waking state instability. This result is likely due to acute homeostatic sleep pressure remaining high despite the sleep episode. Study Objectives: The homeostatic-circadian regulation of neurobehavioral functioning is not well understood in that the role of sleep dose in relation to prior wake and circadian phase remains largely unexplored. The aim of the present study was to examine the neurobehavioral impact of sleep dose at different combinations of prior wake and circadian phase. Design: A between-participant design involving 2 forced desynchrony protocols varying in sleep dose. Both protocols comprised 7 repetitions of a 28-h sleep/wake cycle. The sleep dose in a standard protocol was 9.33 h per 28-h day and 4.67 h in a sleep-restricted protocol. Setting: A time-isolation laboratory at the Centre for Sleep Research, the University of South Australia. Participants: A total of 27 young healthy males participated in the study with 13 in the standard protocol (age 22.5+- 2.2 y) and 14 in the sleep-restricted protocol (age 21.8 +-3.8 y). Interventions: Wake periods during both protocols were approximately 4 h delayed each 28-h day relative to the circadian system, allowing performance testing at different combinations of prior wake and circadian phase. The manipulation in sleep dose between the 2 protocols, therefore, allowed the impact of sleep dose on neurobehavioral performance to be examined at various combinations of prior wake and circadian phase. Measurements and Results: Neurobehavioral function was assessed using the psychomotor vigilance task (PVT). There was a sleep dose x circadian phase interaction effect on PVT performance such that sleep restriction resulted in slower and more variable response times, predominantly during the biological night. This interaction was not altered by prior wakefulness, as indicated by a nonsignificant sleep dose x circadian phase x prior wake interaction. Refereed/Peer-reviewed

Study Objectives: The state instability hypothesis posits that increasing sleep drive brings about escalating state instability in attention, making neurobehavioral performance increasingly variable. This hypothesis predicts that performance variability is a function of prior wake, circadian phase, and time on task. These predictions have been supported when wakefulness is beyond the habitual wake period. Our study aimed to test these predictions within the habitual wake period. Design: A 12-calendar-day 28-h forced desynchrony protocol consisting of 7 repetitions of a 28-h sleep/wake cycle, with two-thirds time awake and one-third time in bed. Each wake period included 7 equally spaced 1-h testing sessions. Setting: A time-isolation sleep laboratory. Participants: Thirteen young healthy males. Interventions: Wake periods during the protocol were 4 h delayed each 28-h "day" relative to the circadian system, such that they were distributed across the whole circadian cycle. This allowed performance testing at different combinations of prior wake of a habitual length (i.e., < 18 h) and circadian phase. Measurements and Results: Performance variability was indexed by standard deviation of response times within a 10-min psychomotor vigilance task. We found that response times became more variable with increasing wakefulness and towards circadian nadir, i.e., when sleep drive was increasing. These changes in response time variability were however not dependent on time on task, which is likely due to the modest level of sleep drive in our study. Conclusions: The state instability hypothesis, as an explanation for the responsiveness of neurobehavioral performance to increasing sleep drive, is supported during the habitual wake period. Refereed/Peer-reviewed