Modeling Neurocognitive Decline and Recovery During Repeated Cycles of Extended Sleep and Chronic Sleep Deficiency

ABSTRACT Introduction Military operations often involve intense exposure to stressors combined with acute sleep deprivation, while military personnel also experience high prevalence of chronic sleep deficiency from insomnia and other sleep disorders. However, the impact of acute and chronic sleep deficiency on physiologic stressor responses is poorly understood. In a controlled laboratory study with normal sleepers and individuals with chronic sleep-onset insomnia, we measured responses to an acute stressor administered in a sleep deprivation condition or a control condition. Methods Twenty-two adults (aged 22-40 years; 16 females)—11 healthy normal sleepers and 11 individuals with sleep-onset insomnia—completed a 5-day (4-night) in-laboratory study. After an adaptation day and a baseline day, subjects were assigned to a 38-hour total sleep deprivation (TSD) condition or a control condition; the study ended with a recovery day. At 8:00 PM after 36 hours awake in the sleep deprivation condition or 12 hours awake in the control condition, subjects underwent a Maastricht Acute Stress Test (MAST). Salivary cortisol was measured immediately before the MAST at 8:00 PM, every 15 minutes after the MAST from 8:15 PM until 9:15 PM, and 30 minutes later at 9:45 PM. Baseline salivary cortisol was collected in the evening of the baseline day. Additionally, before and immediately upon completion of the MAST, self-report ratings of affect and pain were collected. Results The MAST elicited a stressor response in both normal sleepers and individuals with sleep-onset insomnia, regardless of the condition, as evidenced by increases in negative affect and pain ratings. Relative to baseline, cortisol levels increased immediately following the MAST, peaked 30 minutes later, and then gradually returned to pre-MAST levels. At the cortisol peak, there was a significant difference across groups and conditions, reflecting a pronounced blunting of the cortisol response in the normal sleepers in the TSD condition and the sleep-onset insomnia group in both the TSD and control conditions. Conclusions Blunted stressor reactivity as a result of sleep deficiency, whether acute or chronic, may reflect reduced resiliency attributable to allostatic load and may put warfighters at increased risk in high-stakes, rapid response scenarios.

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Young adults are more vulnerable to chronic sleep deficiency and recurrent circadian disruption than older adults

Scientific Reports ◽

10.1038/s41598-018-29358-x ◽

2018 ◽

Vol 8 (1) ◽

Cited By ~ 16

Author(s):

Kirsi-Marja Zitting ◽

Mirjam Y. Münch ◽

Sean W. Cain ◽

Wei Wang ◽

Arick Wong ◽

...

Keyword(s):

Older Adults ◽

Young Adults ◽

Circadian Disruption ◽

Sleep Deficiency ◽

Chronic Sleep

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Modeling the Influence of Chronic Sleep Restriction on Cortisol Circadian Rhythms, with Implications for Metabolic Disorders

Metabolites ◽

10.3390/metabo11080483 ◽

2021 ◽

Vol 11 (8) ◽

pp. 483

Author(s):

Rohit Rao ◽

Pramod Somvanshi Elizabeth B. Klerman ◽

Charles Marmar ◽

Francis J. Doyle

Keyword(s):

Mathematical Model ◽

Hpa Axis ◽

Subsequent Development ◽

Modern Society ◽

Circadian Rhythmicity ◽

Sleep Restriction ◽

Metabolic Complications ◽

Increased Risk ◽

Sleep Deficiency ◽

Chronic Sleep

Chronic sleep deficiency is prevalent in modern society and is associated with increased risk of metabolic and other diseases. While the mechanisms by which chronic sleep deficiency induces pathophysiological changes are yet to be elucidated, the hypothalamic–pituitary–adrenal (HPA) axis may be an important mediator of these effects. Cortisol, the primary hormone of the HPA axis, exhibits robust circadian rhythmicity and is moderately influenced by sleep and wake states and other physiology. Several studies have explored the effects of acute or chronic sleep deficiency (i.e., usually from self-selected chronic sleep restriction, CSR) on the HPA axis. Quantifying long-term changes in the circadian rhythm of cortisol under CSR in controlled conditions is inadequately studied due to practical limitations. We use a semi-mechanistic mathematical model of the HPA axis and the sleep/wake cycle to explore the influence of CSR on cortisol circadian rhythmicity. In qualitative agreement with experimental findings, model simulations predict that CSR results in physiologically relevant disruptions in the phase and amplitude of the cortisol rhythm. The mathematical model presented in this work provides a mechanistic framework to further explore how CSR might lead to HPA axis disruption and subsequent development of chronic metabolic complications.

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Chronic Sleep Reduction and School Performance

PsycEXTRA Dataset ◽

10.1037/e713082007-001 ◽

2007 ◽

Author(s):

Anne Marie Meijer ◽

Godfried L. H. Van Den Wittenboer

Keyword(s):

School Performance ◽

Chronic Sleep

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Residual, differential neurobehavioral deficits linger after multiple recovery nights following chronic sleep restriction or acute total sleep deprivation

SLEEP ◽

10.1093/sleep/zsaa224 ◽

2020 ◽

Author(s):

Erika M Yamazaki ◽

Caroline A Antler ◽

Charlotte R Lasek ◽

Namni Goel

Keyword(s):

Sleep Deprivation ◽

Response Speed ◽

Sleep Loss ◽

Sleep Restriction ◽

Total Sleep Deprivation ◽

Psychomotor Vigilance Test ◽

Recovery Sleep ◽

Time In Bed ◽

Neurobehavioral Deficits ◽

Chronic Sleep

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.

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Homeostatic Response to Sleep Restriction in Adolescents

SLEEP ◽

10.1093/sleep/zsab106 ◽

2021 ◽

Author(s):

Jelena Skorucak ◽

Nathan Weber ◽

Mary A Carskadon ◽

Chelsea Reynolds ◽

Scott Coussens ◽

...

Keyword(s):

Slow Wave ◽

Process Model ◽

Animal Studies ◽

Sleep Restriction ◽

Sleep Regulation ◽

Homeostatic Process ◽

Sleep Homeostasis ◽

High Prevalence ◽

Homeostatic Response ◽

Chronic Sleep

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.

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Fatigue As A Performance Shaping Factor In Human Reliability Analysis For Long-Duration Spaceflight

Proceedings of the Human Factors and Ergonomics Society Annual Meeting ◽

10.1177/1071181320641408 ◽

2020 ◽

Vol 64 (1) ◽

pp. 1681-1685

Author(s):

Ronald Boring ◽

Thomas Ulrich ◽

Torrey Mortenson ◽

David German

Keyword(s):

Reliability Analysis ◽

Meta Analysis ◽

Extended Period ◽

Human Reliability ◽

Human Reliability Analysis ◽

Space Applications ◽

Performance Shaping Factors ◽

Long Duration ◽

Starting Point ◽

Chronic Sleep

This paper provides background on the process to enhance human reliability analysis (HRA) for long-duration space applications. While short-duration missions largely mirror ground activities and fit well with existing HRA methods, new missions to the Moon or Mars entail a significantly longer duration of time in space for astronauts. This extended period in space presents opportunities to affect astronaut performance that require consideration of new performance shaping factors (PSFs). In the present paper, we conducted a meta-analysis on fatigue and developed a new PSF to account for chronic sleep deprivation associated with long-duration space missions. Fatigue provides a starting point for additional PSFs needed for space HRA.

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