scholarly journals Response to chronic sleep restriction, extension, and subsequent total sleep deprivation in humans: adaptation or preserved sleep homeostasis?

SLEEP ◽  
2018 ◽  
Vol 41 (7) ◽  
Author(s):  
Jelena Skorucak ◽  
Emma L Arbon ◽  
Derk-Jan Dijk ◽  
Peter Achermann
SLEEP ◽  
2020 ◽  
Author(s):  
Erika M Yamazaki ◽  
Caroline A Antler ◽  
Charlotte R Lasek ◽  
Namni Goel

Abstract Study Objectives The amount of recovery sleep needed to fully restore well-established neurobehavioral deficits from sleep loss remains unknown, as does whether the recovery pattern differs across measures after total sleep deprivation (TSD) and chronic sleep restriction (SR). Methods In total, 83 adults received two baseline nights (10–12-hour time in bed [TIB]) followed by five 4-hour TIB SR nights or 36-hour TSD and four recovery nights (R1–R4; 12-hour TIB). Neurobehavioral tests were completed every 2 hours during wakefulness and a Maintenance of Wakefulness Test measured physiological sleepiness. Polysomnography was collected on B2, R1, and R4 nights. Results TSD and SR produced significant deficits in cognitive performance, increases in self-reported sleepiness and fatigue, decreases in vigor, and increases in physiological sleepiness. Neurobehavioral recovery from SR occurred after R1 and was maintained for all measures except Psychomotor Vigilance Test (PVT) lapses and response speed, which failed to completely recover. Neurobehavioral recovery from TSD occurred after R1 and was maintained for all cognitive and self-reported measures, except for vigor. After TSD and SR, R1 recovery sleep was longer and of higher efficiency and better quality than R4 recovery sleep. Conclusions PVT impairments from SR failed to reverse completely; by contrast, vigor did not recover after TSD; all other deficits were reversed after sleep loss. These results suggest that TSD and SR induce sustained, differential biological, physiological, and/or neural changes, which remarkably are not reversed with chronic, long-duration recovery sleep. Our findings have critical implications for the population at large and for military and health professionals.


SLEEP ◽  
2017 ◽  
Vol 40 (suppl_1) ◽  
pp. A56-A57
Author(s):  
E Hennecke ◽  
D Lange ◽  
J Fronczek ◽  
A Bauer ◽  
D Aeschbach ◽  
...  

2013 ◽  
Vol 331 ◽  
pp. 66-77 ◽  
Author(s):  
Pooja Rajdev ◽  
David Thorsley ◽  
Srinivasan Rajaraman ◽  
Tracy L. Rupp ◽  
Nancy J. Wesensten ◽  
...  

SLEEP ◽  
2021 ◽  
Author(s):  
Jelena Skorucak ◽  
Nathan Weber ◽  
Mary A Carskadon ◽  
Chelsea Reynolds ◽  
Scott Coussens ◽  
...  

Abstract The high prevalence of chronic sleep restriction in adolescents underscores the importance of understanding how adolescent sleep is regulated under such conditions. One component of sleep regulation is a homeostatic process: if sleep is restricted, then sleep intensity increases. Our knowledge of this process is primarily informed by total sleep deprivation studies and has been incorporated in mathematical models of human sleep regulation. Several animal studies, however, suggest that adaptation occurs in chronic sleep restriction conditions, showing an attenuated or even decreased homeostatic response. We investigated the homeostatic response of adolescents to different sleep opportunities. Thirty-four participants were allocated to one of three groups with 5, 7.5 or 10 h of sleep opportunity per night for 5 nights. Each group underwent a protocol of 9 nights designed to mimic a school week between 2 weekends: 2 baseline nights (10 h sleep opportunity), 5 condition nights (5, 7.5 or 10 h), and two recovery nights (10 h). Measures of sleep homeostasis (slow-wave activity and slow-wave energy) were calculated from frontal and central EEG derivations and compared to predictions derived from simulations of the homeostatic process of the two-process model of sleep regulation. Only minor differences were found between empirical data and model predictions, indicating that sleep homeostasis is preserved under chronic sleep restriction in adolescents. These findings improve our understanding of effects of repetitive short sleep in adolescents.


SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A56-A56
Author(s):  
Mark McCauley ◽  
Peter McCauley ◽  
Hans Van Dongen

Abstract Introduction In commercial aviation and other operational settings where biomathematical models of fatigue are used for fatigue risk management, accurate prediction of recovery during rest periods following duty periods with sleep loss and/or circadian misalignment is critical. The recuperative potential of recovery sleep is influenced by a variety of factors, including long-term, allostatic effects of prior sleep/wake history. For example, recovery tends to be slower after sustained sleep restriction versus acute total sleep deprivation. Capturing such dynamics has proven to be challenging. Methods Here we focus on the dynamic biomathematical model of McCauley et al. (2013). In addition to a circadian process, this model features differential equations for sleep/wake regulation including a short-term sleep homeostatic process capturing change in the order of hours/days and a long-term allostatic process capturing change in the order of days/weeks. The allostatic process modulates the dynamics of the homeostatic process by shifting its equilibrium setpoint, which addresses recently observed phenomena such as reduced vulnerability to sleep loss after banking sleep. It also differentiates the build-up and recovery rates of fatigue under conditions of chronic sleep restriction versus acute total sleep deprivation; nonetheless, it does not accurately predict the disproportionately rapid recovery seen after total sleep deprivation. To improve the model, we hypothesized that the homeostatic process may also modulate the allostatic process, with the magnitude of this effect scaling as a function of time awake. Results To test our hypothesis, we added a parameter to the model to capture modulation by the homeostatic process of the allostatic process build-up during wakefulness and dissipation during sleep. Parameter estimation using previously published laboratory datasets of fatigue showed this parameter as significantly different from zero (p<0.05) and yielding a 10%–20% improvement in goodness-of-fit for recovery without adversely affecting goodness-of-fit for pre-recovery days. Conclusion Inclusion of a modulation effect of the allostatic process by the homeostatic process improved prediction accuracy in a variety of sleep loss and circadian misalignment scenarios. In addition to operational relevance for duty/rest scheduling, this finding has implications for understanding mechanisms underlying the homeostatic and allostatic processes of sleep/wake regulation. Support (if any) Federal Express Corporation


2020 ◽  
Vol 14 ◽  
Author(s):  
Luis A. De Jesús-Olmo ◽  
Norma Rodríguez ◽  
Marcelo Francia ◽  
Jonathan Alemán-Rios ◽  
Carlos J. Pacheco-Agosto ◽  
...  

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