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 × 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 × circadian phase × prior wake interaction. 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 × 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 × circadian phase × prior wake interaction. 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.
Authors: J Waterhouse; D Weinert; D Minors; S Folkard; D Owens; G Atkinson; I Macdonald; N Sytnik; P Tucker; T Reilly Journal: Chronobiol Int Date: 2000-07 Impact factor: 2.877
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Authors: C A Czeisler; J F Duffy; T L Shanahan; E N Brown; J F Mitchell; D W Rimmer; J M Ronda; E J Silva; J S Allan; J S Emens; D J Dijk; R E Kronauer Journal: Science Date: 1999-06-25 Impact factor: 47.728
Authors: Peter McCauley; Leonid V Kalachev; Daniel J Mollicone; Siobhan Banks; David F Dinges; Hans P A Van Dongen Journal: Sleep Date: 2013-12-01 Impact factor: 5.849
Authors: Youngsoo Kim; David Elmenhorst; Robert E Strecker; Andreas Bauer; Angela Weisshaupt; Franziska Wedekind; Tina Kroll; Robert W McCarley Journal: J Sleep Res Date: 2015-04-21 Impact factor: 3.981