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Sleep continuity and efficacy are essential for optimal cognitive functions. How sleep fragmentation (SF) impairs cognitive functioning, and especially cognitive fatigue (CF), remains elusive. We investigated the impact of induced SF on CF through the TloadDback task, measuring interindividual variability in working memory capacity. Sixteen participants underwent an adaptation polysomnography night and three consecutive nights, once in a SF condition induced by non-awakening auditory stimulations, once under restorative sleep (RS) condition, counterbalanced within-subject. In both conditions, participants were administered memory, vigilance, inhibition and verbal fluency testing, and for CF the TloadDback, as well as sleep questionnaires and fatigue and sleepiness visual analog scales were administered. Subjective fatigue increased and sleep architecture was altered after SF (reduced sleep efficiency, percentage of N3 and REM, number of NREM and REM phases) despite similar total sleep time. At the behavioral level, only inhibition deteriorated after SF, and CF similarly evolved in RS and SF conditions. In line with prior research, we show that SF disrupts sleep architecture and exerts a deleterious impact on subjective fatigue and inhibition. However, young healthy participants appear able to compensate for CF induced by three consecutive SF nights. Further studies should investigate SF effects in extended and/or pathological disruption settings.

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PurposeHypobaric hypoxic habitats are currently being touted as a potential solution to minimise decompression procedures in preparation for extra vehicular activities during future space missions. Since astronauts will live in hypoxic environments for the duration of such missions, the present study sought to elucidate the separate and combined effects of inactivity [simulated with the experimental bed rest (BR) model] and hypoxia on sleep characteristics in women.MethodsTwelve women (Age = 27 ± 3 year) took part in three 10-day interventions, in a repeated measures cross-over counterbalanced design: (1) normobaric normoxic BR (NBR), (2) normobaric hypoxic BR (HBR; simulated altitude of 4,000 m), and (3) normobaric hypoxic ambulatory (HAMB; 4,000 m) confinement, during which sleep was assessed on night 1 and night 10 with polysomnography. In addition, one baseline sleep assessment was performed. This baseline assessment, although lacking a confinement aspect, was included statistically as a fourth comparison (i.e., pseudo normobaric normoxic ambulatory; pNAMB) in the present study.ResultsHypoxia decreased sleep efficiency (p = 0.019), increased N1% sleep (p = 0.030), decreased N3 sleep duration (p = 0.003), and increased apnea hypopnea index (p < 0.001). BR impaired sleep maintenance, efficiency, and architecture [e.g., N2% sleep increased (p = 0.033)]. Specifically, for N3% sleep, the effects of partial pressure of oxygen and activity interacted. Hypoxia decreased N3% sleep both when active (pNAMB vs HAMB; p < 0.001) and inactive (NBR vs HBR; p = 0.021), however, this decrease was attenuated in the inactive state (–3.8%) compared to the active state (–10.2%).ConclusionA 10-day exposure to hypoxia and BR negatively impacted sleep on multiple levels as in macrostructure, microstructure and respiratory functioning. Interestingly, hypoxia appeared to have less adverse effects on sleep macrostructure while the participants were inactive (bed ridden) compared to when ambulatory. Data were missing to some extent (i.e., 20.8%). Therefore, multiple imputation was used, and our results should be considered as exploratory.