scholarly journals Decoupling of Sleepiness from Sleep Time and Intensity during Chronic Sleep Restriction: Evidence for a Role of the Adenosine System

SLEEP ◽  
2012 ◽  
Vol 35 (6) ◽  
pp. 861-869 ◽  
Author(s):  
Youngsoo Kim ◽  
Yunren Bolortuya ◽  
Lichao Chen ◽  
Radhika Basheer ◽  
Robert W. McCarley ◽  
...  
Keyword(s):  
Sleep Time ◽  
Sleep Restriction ◽  
Chronic Sleep

scholarly journals Sleep allostasis in chronic sleep restriction: The role of the norepinephrine system

2013 ◽  
Vol 1531 ◽  
pp. 9-16 ◽  
Author(s):  
Youngsoo Kim ◽  
Lichao Chen ◽  
Robert W. McCarley ◽  
Robert E. Strecker
Keyword(s):  
Sleep Restriction ◽  
Norepinephrine System ◽  
Chronic Sleep

scholarly journals Metabolic Disturbances Induced by Sleep Restriction as Potential Triggers for Alzheimer’s Disease

2021 ◽  
Vol 15 ◽  
Author(s):  
Jesús Enrique García-Aviles ◽  
Rebeca Méndez-Hernández ◽  
Mara A. Guzmán-Ruiz ◽  
Miguel Cruz ◽  
Natalí N. Guerrero-Vargas ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Deficit ◽  
Amyloid Β ◽  
Sleep Restriction ◽  
Amyloid Β Peptide ◽  
Metabolic Disturbances ◽  
The Brain ◽  
Chronic Sleep

Sleep has a major role in learning, memory consolidation, and metabolic function. Although it is known that sleep restriction increases the accumulation of amyloid β peptide (Aβ) and the risk to develop Alzheimer’s disease (AD), the mechanism behind these effects remains unknown. In this review, we discuss how chronic sleep restriction induces metabolic and cognitive impairments that could result in the development of AD in late life. Here, we integrate evidence regarding mechanisms whereby metabolic signaling becomes disturbed after short or chronic sleep restriction in the context of cognitive impairment, particularly in the accumulation of Aβ in the brain. We also discuss the role of the blood-brain barrier in sleep restriction with an emphasis on the transport of metabolic signals into the brain and Aβ clearance. This review presents the unexplored possibility that the alteration of peripheral metabolic signals induced by sleep restriction, especially insulin resistance, is responsible for cognitive deficit and, subsequently, implicated in AD development.

Time-of-day modulation of homeostatic and allostatic sleep responses to chronic sleep restriction in rats

2012 ◽  
Vol 302 (12) ◽  
pp. R1411-R1425 ◽  
Author(s):  
S. Deurveilher ◽  
B. Rusak ◽  
K. Semba
Keyword(s):  
Eye Movement ◽  
Recovery Period ◽  
Sleep Time ◽  
Time Of Day ◽  
Male Rats ◽  
Sleep Restriction ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Delta Power ◽  
Chronic Sleep

To study sleep responses to chronic sleep restriction (CSR) and time-of-day influences on these responses, we developed a rat model of CSR that takes into account the polyphasic sleep patterns in rats. Adult male rats underwent cycles of 3 h of sleep deprivation (SD) and 1 h of sleep opportunity (SO) continuously for 4 days, beginning at the onset of the 12-h light phase (“3/1” protocol). Electroencephalogram (EEG) and electromyogram (EMG) recordings were made before, during, and after CSR. During CSR, total sleep time was reduced by ∼60% from baseline levels. Both rapid eye movement sleep (REMS) and non-rapid eye movement sleep (NREMS) during SO periods increased initially relative to baseline and remained elevated for the rest of the CSR period. In contrast, NREMS EEG delta power (a measure of sleep intensity) increased initially, but then declined gradually, in parallel with increases in high-frequency power in the NREMS EEG. The amplitude of daily rhythms in NREMS and REMS amounts was maintained during SO periods, whereas that of NREMS delta power was reduced. Compensatory responses during the 2-day post-CSR recovery period were either modest or negative and gated by time of day. NREMS, REMS, and EEG delta power lost during CSR were not recovered by the end of the second recovery day. Thus the “3/1” CSR protocol triggered both homeostatic responses (increased sleep amounts and intensity during SOs) and allostatic responses (gradual decline in sleep intensity during SOs and muted or negative post-CSR sleep recovery), and both responses were modulated by time of day.

scholarly journals 0220 Role Of CRF Signaling In The Disruption Of Sleep Homeostasis During Chronic Sleep Restriction

SLEEP ◽  
2018 ◽  
Vol 41 (suppl_1) ◽  
pp. A86-A86
Author(s):  
S Kumar ◽  
K Hsieh ◽  
D McGinty ◽  
R Szymusiak
Keyword(s):  
Sleep Restriction ◽  
Sleep Homeostasis ◽  
Chronic Sleep

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

SLEEP ◽  
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.

Homeostatic Response to Sleep Restriction in Adolescents

SLEEP ◽  
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.

scholarly journals O010 The role of dysfunctional beliefs and attitudes about sleep in the association between daily sleep and affect in adolescents and emerging adults

2021 ◽  
Vol 2 (Supplement_1) ◽  
pp. A5-A5
Author(s):  
E Chachos ◽  
L Shen ◽  
S Maskevich ◽  
Y Yap ◽  
J Stone ◽  
...  
Keyword(s):  
Positive Affect ◽  
Emerging Adults ◽  
Sleep Duration ◽  
Cognitive Vulnerability ◽  
Sleep Time ◽  
Dysfunctional Beliefs ◽  
Low Dimensions ◽  
Modifiable Factor ◽  
Beliefs And Attitudes

Abstract Introduction Sleep and affect are closely related. Late adolescence and emerging adulthood are associated with unique sleep patterns and risk for mood disturbances. This daily study examined whether dysfunctional beliefs and attitudes about sleep (DBAS), a modifiable cognitive vulnerability factor, moderated daily sleep-affect associations. Methods 421 community adolescents (n=205, 54.1% females, M±SDage=16.9±0.87) and emerging adults (n=216, 73.1% females, M±SDage=21.31±1.73) self-reported sleep and affect (adapted 12-item PANAS) and wore an actigraphy device for 7–28 days, providing >5000 daily observations. Linear mixed models tested whether DBAS moderated daily associations between self-reported and actigraphic sleep duration (total sleep time), sleep efficiency, and next-day affect on between and within-person levels. Both valence (positive/negative) and arousal (high/low) dimensions of affect were examined. Covariates included age, gender, ethnicity, day of week, and previous-day affect. Results DBAS significantly moderated associations between average sleep and next-day positive, but not negative, affect. Individuals with higher DBAS had significantly lower high arousal positive affect as average sleep duration (actigraphic: p=.002; self-reported: p=.014) and efficiency (actigraphic: p=.014) decreased. Similar moderation was found for average self-reported sleep duration and low arousal positive affect (p=.032). No significant results emerged on the within-person level. Previous-day affect significantly predicted next-day affect across models and outcomes (all p<.001). Discussion Adolescents and emerging adults with more negative views about sleep may experience dampened positive affect in shorter, or poorer, sleep periods. DBAS may constitute a modifiable factor increasing affective vulnerability on a global but not day-to-day level, and a therapeutic target for sleep-related affect disturbances in youths.

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