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 Reassessing the validity of slow-wave dynamics as a proxy for NREM sleep homeostasis

2019 ◽  
Author(s):  
Jeffrey Hubbard ◽  
Thomas C. Gent ◽  
Marieke M. B. Hoekstra ◽  
Yann Emmenegger ◽  
Valerie Mongrain ◽  
...  
Keyword(s):  
Slow Wave ◽  
Muscle Tone ◽  
Nrem Sleep ◽  
Sleep Regulation ◽  
Homeostatic Process ◽  
Wave Dynamics ◽  
Sleep Homeostasis ◽  
Human Experiments ◽  
And Function ◽  
Initial Power

AbstractSleep-wake driven changes in NREM sleep (NREMS) EEG delta (δ: ∼0.75-4.5Hz) power are widely used as proxy for a sleep homeostatic process. We noted frequency increases in δ-waves in sleep-deprived (SD) mice, prompting us to re-evaluate how slow-wave characteristics relate to prior sleep-wake history. We discovered two types of δ-waves; one responding to SD with high initial power and fast, discontinuous decay (δ2: ∼2.5-3.5Hz) and another unrelated to time-spent-awake with slow, linear decays (δ1: ∼0.75-1.75Hz). Human experiments confirmed this δ-band heterogeneity. Similar to SD, silencing of centromedial thalamus neurons boosted δ2-waves, specifically. δ2-dynamics paralleled that of temperature, muscle tone, heart-rate, and neuronal UP/DOWN state lengths, all reverting to characteristic NREMS levels within the first recovery hour. Thus, prolonged waking seems to necessitate a physiological recalibration before typical NREMS can be reinstated. These short-lasting δ2-dynamics challenge accepted models of sleep regulation and function based on the merged δ-band as sleep-need proxy.

Circadian Rhythms and Homeostatic Mechanisms for Sleep Regulation

2021 ◽  
pp. 65-86
Author(s):  
Cassie J. Hilditch ◽  
Erin E. Flynn-Evans
Keyword(s):  
Circadian Rhythm ◽  
Circadian Rhythms ◽  
Process Model ◽  
Modern Society ◽  
Current Evidence ◽  
Sleep Regulation ◽  
Sleep Homeostasis ◽  
Short And Long Term ◽  
Homeostatic Mechanisms

This chapter examines circadian rhythms and homeostatic mechanisms for sleep regulation. It reviews the current evidence describing the two-process model of sleep regulation and how to assess disruption to either of these sleep drives. This chapter also reviews the role of the photic and non-photic resetting of the circadian rhythm and describes how some aspects of modern society can cause sleep and circadian disruption. Further, this chapter describes how misalignment between the circadian rhythm and sleep homeostasis, such as occurs during jet lag and shift-work, can lead to sleep disruption. The short- and long-term consequences of circadian misalignment are also reviewed.

scholarly journals Differential modulation of NREM sleep regulation and EEG topography by chronic sleep restriction in mice

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Bowon Kim ◽  
Eunjin Hwang ◽  
Robert E. Strecker ◽  
Jee Hyun Choi ◽  
Youngsoo Kim
Keyword(s):  
Nrem Sleep ◽  
Brain Regions ◽  
Sleep Eeg ◽  
Sleep Restriction ◽  
Electrode Arrays ◽  
Sleep Regulation ◽  
Amplitude Analysis ◽  
Delta Power ◽  
Eeg Topography ◽  
Chronic Sleep

AbstractCompensatory elevation in NREM sleep EEG delta power has been typically observed following prolonged wakefulness and widely used as a sleep homeostasis indicator. However, recent evidence in human and rodent chronic sleep restriction (CSR) studies suggests that NREM delta power is not progressively increased despite of accumulated sleep loss over days. In addition, there has been little progress in understanding how sleep EEG in different brain regions responds to CSR. Using novel high-density EEG electrode arrays in the mouse model of CSR where mice underwent 18-h sleep deprivation per day for 5 consecutive days, we performed an extensive analysis of topographical NREM sleep EEG responses to the CSR condition, including period-amplitude analysis of individual slow waves. As previously reported in our analysis of REM sleep responses, we found different patterns of changes: (i) progressive decrease in NREM sleep duration and consolidation, (ii) persistent enhancement in NREM delta power especially in the frontal and parietal regions, and (iii) progressive increases in individual slow wave slope and frontal fast oscillation power. These results suggest that multiple sleep-wake regulatory systems exist in a brain region-specific manner, which can be modulated independently, especially in the CSR condition.

scholarly journals Glymphatic Dysfunction: A Bridge Between Sleep Disturbance and Mood Disorders

2021 ◽  
Vol 12 ◽  
Author(s):  
Tao Yan ◽  
Yuefeng Qiu ◽  
Xinfeng Yu ◽  
Linglin Yang
Keyword(s):  
Sleep Disturbance ◽  
Mood Disorders ◽  
Process Model ◽  
Water Channel ◽  
Sleep Regulation ◽  
Sleep Homeostasis ◽  
Close Relationship ◽  
Mechanism Of Interaction ◽  
Glymphatic Pathway ◽  
Dynamic Fluctuation

Mounting evidence demonstrates a close relationship between sleep disturbance and mood disorders, including major depression disorder (MDD) and bipolar disorder (BD). According to the classical two-process model of sleep regulation, circadian rhythms driven by the light–dark cycle, and sleep homeostasis modulated by the sleep–wake cycle are disrupted in mood disorders. However, the exact mechanism of interaction between sleep and mood disorders remains unclear. Recent discovery of the glymphatic system and its dynamic fluctuation with sleep provide a plausible explanation. The diurnal variation of the glymphatic circulation is dependent on the astrocytic activity and polarization of water channel protein aquaporin-4 (AQP4). Both animal and human studies have reported suppressed glymphatic transport, abnormal astrocytes, and depolarized AQP4 in mood disorders. In this study, the “glymphatic dysfunction” hypothesis which suggests that the dysfunctional glymphatic pathway serves as a bridge between sleep disturbance and mood disorders is proposed.

scholarly journals Reduced sleep pressure in young children with autism

2019 ◽  
Author(s):  
Ayelet Arazi ◽  
Gal Meiri ◽  
Dor Danan ◽  
Analya Michaelovski ◽  
Hagit Flusser ◽  
...  
Keyword(s):  
Slow Wave ◽  
Sleep Disturbances ◽  
Sleep Onset ◽  
Children With Autism ◽  
Autism Spectrum ◽  
Wave Activity ◽  
Slow Wave Activity ◽  
Sleep Regulation ◽  
Children With Asd ◽  
Sleep Homeostasis

AbstractStudy ObjectivesSleep disturbances and insomnia are highly prevalent in children with Autism Spectrum Disorder (ASD). Sleep homeostasis, a fundamental mechanism of sleep regulation that generates pressure to sleep as a function of wakefulness, has not been studied in children with ASD so far, and its potential contribution to their sleep disturbances remains unknown. Here, we examined whether slow wave activity (SWA), a measure that is indicative of sleep pressure, differs in children with ASD.MethodsIn this case-control study, we compared overnight electroencephalogram (EEG) recordings that were performed during Polysomnography (PSG) evaluations of 29 children with ASD and 23 typically developing children.ResultsChildren with ASD exhibited significantly weaker SWA power, shallower SWA slopes, and a decreased proportion of slow wave sleep in comparison to controls. This difference was largest during the first two hours following sleep onset and decreased gradually thereafter. Furthermore, SWA power of children with ASD was significantly, negatively correlated with the time of their sleep onset in the lab and at home, as reported by parents.ConclusionsThese results suggest that children with ASD may have a dysregulation of sleep homeostasis that is manifested in reduced sleep pressure. The extent of this dysregulation in individual children was apparent in the amplitude of their SWA power, which was indicative of the severity of their individual sleep disturbances. We, therefore, suggest that disrupted homeostatic sleep regulation may contribute to sleep disturbances in children with ASD.Statement of significanceSleep disturbances are apparent in 40-80% of children with autism. Homeostatic sleep regulation, a mechanism that increases the pressure to sleep as a function of prior wakefulness, has not been studied in children with autism. Here, we compared Polysomnography exams of 29 children with autism and 23 matched controls. We found that children with autism exhibited reduced slow-wave-activity power and shallower slopes, particularly during the first two hours of sleep. This suggests that they develop less pressure to sleep. Furthermore, the reduction in slow-wave-activity was associated with the severity of sleep disturbances as observed in the laboratory and as reported by parents. We, therefore, suggest that disrupted homeostatic sleep regulation may contribute to sleep disturbances of children with autism.

scholarly journals Bright morning light advances the human circadian system without affecting NREM sleep homeostasis

1989 ◽  
Vol 256 (1) ◽  
pp. R106-R111 ◽  
Author(s):  
D. J. Dijk ◽  
D. G. Beersma ◽  
S. Daan ◽  
A. J. Lewy
Keyword(s):  
Rem Sleep ◽  
Process Model ◽  
Sleep Onset ◽  
Light Condition ◽  
Bright Light ◽  
Circadian Pacemaker ◽  
Sleep Regulation ◽  
Plasma Melatonin ◽  
Sleep Homeostasis ◽  
Dim Light

Eight male subjects were exposed to either bright light or dim light between 0600 and 0900 h for 3 consecutive days each. Relative to the dim light condition, the bright light treatment advanced the evening rise in plasma melatonin and the time of sleep termination (sleep onset was held constant) for an average approximately 1 h. The magnitude of the advance of the plasma melatonin rise was dependent on its phase in dim light. The reduction in sleep duration was at the expense of rapid-eye-movement (REM) sleep. Spectral analysis of the sleep electroencephalogram (EEG) revealed that the advance of the circadian pacemaker did not affect EEG power densities between 0.25 and 15.0 Hz during either non-REM or REM sleep. The data show that shifting the human circadian pacemaker by 1 h does not affect non-REM sleep homeostasis. These findings are in accordance with the predictions of the two-process model of sleep regulation.

112 Chronic sleep restriction disrupts slow-wave sleep homeostatic regulation and damages monoaminergic structures in the rat brain

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A46-A46
Author(s):  
Mikhail Guzeev ◽  
Nikita Kurmazov ◽  
Valentina Simonova ◽  
Daria Belan ◽  
Ksenia Lapshina ◽  
...  
Keyword(s):  
Slow Wave ◽  
Slow Wave Sleep ◽  
Cognitive Disorders ◽  
Emotional Behavior ◽  
Sleep Restriction ◽  
High Tech ◽  
Integrative Physiology ◽  
Delta Power ◽  
Monoaminergic Structures ◽  
Chronic Sleep

Abstract Introduction The neurophysiological mechanisms underlying long-term neurological and cognitive disorders associated with chronic sleep restriction (CSR) are not fully understood. Here we evaluated how the sleep-wake cycle changes during and after a period of sleep restriction in rats, and whether CSR results in neurodegeneration in monoaminergic brain structures. Methods For CSR, 7-8-month-old Wistar rats underwent cycles of 3 h of sleep deprivation (SD) and 1 h of sleep opportunity (SO) continuously for 5 days on the orbital shaker. Telemetric sleep recordings were made before, during, and after CSR. Neurodegeneration in brain monoaminergic structures was assessed immunohistochemically. Results During SD, wakefulness comprised 85% of the total registration time; the remaining time was represented by drowsiness with low EEG delta power. Rapid eye movement sleep (REMS) was absent. During CSR, slow-wave sleep (SWS) and REMS were reduced by 62% and 57%. Total SWS time during SO periods increased on the first CSR day, but decreased to the baseline by the fifth CSR day. SWS EEG delta power (a measure of sleep intensity) decreased gradually from the first to the fifth CSR day. REMS total time remained elevated during all SO periods. During the first recovery day after CSR, SWS did not change, but REMS increased by 30%. No changes in total sleep time were found on the second recovery day but sleep intensity was decreased. In 14 days after CSR, all sleep parameters returned to the baseline. We revealed a loss of 24% of noradrenergic locus coeruleus neurons, 29% and 17% of dopaminergic neurons in the substantia nigra, the ventral tegmental area as well as in their striatal terminals. Conclusion We consider CSR as a damaging factor leading to a gradual suppression of homeostatic mechanisms governing sleep recovery. CSR can provoke neurodegeneration in monoaminergic structures involved in the regulation of emotional behavior, sleep, and autonomic functions. Support (if any) Ministry of Science and Higher Education of the Russian Federation grant (No. 075-15-2020-916 dated November 13, 2020) for the establishment and development of the Pavlovsky Center “Integrative Physiology for Medicine, High-Tech Healthcare and Stress Resilience Technologies”.

Time course of EEG power density during long sleep in humans

1990 ◽  
Vol 258 (3) ◽  
pp. R650-R661 ◽  
Author(s):  
D. J. Dijk ◽  
D. P. Brunner ◽  
A. A. Borbely
Keyword(s):  
Slow Wave ◽  
Process Model ◽  
Time Course ◽  
Slow Wave Sleep ◽  
Nrem Sleep ◽  
Sleep Stages ◽  
Base Line ◽  
Sleep Regulation ◽  
Recovery Sleep ◽  
Electroencephalogram Eeg

In nine subjects sleep was recorded under base-line conditions with a habitual bedtime (prior wakefulness 16 h; lights off at 2300 h) and during recovery from sleep deprivation with a phase-advanced bedtime (prior wakefulness 36 h; lights off at 1900 h). The duration of phase-advanced recovery sleep was greater than 12 h in all subjects. Spectral analysis of the sleep electroencephalogram (EEG) revealed that slow-wave activity (SWA; 0.75-4.5 Hz) in non-rapid-eye-movement (NREM) sleep was significantly enhanced during the first two NREM-REM sleep cycles of displaced recovery sleep. The sleep stages 3 and 4 (slow-wave sleep) and SWA decreased monotonically over the first three and four NREM-REM cycles of, respectively, base-line and recovery sleep. The time course of SWA in base-line and recovery sleep could be adequately described by an exponentially declining function with a horizontal asymptote. The results are in accordance with the two-process model of sleep regulation in which it is assumed that SWA rises as a function of the duration of prior wakefulness and decreases exponentially as a function of prior sleep. We conclude that the present data do not provide evidence for a 12.5-h sleep-dependent rhythm of deep NREM sleep.

scholarly journals Evidence That Homeostatic Sleep Regulation Depends on Ambient Lighting Conditions during Wakefulness

2019 ◽  
Vol 1 (4) ◽  
pp. 517-531 ◽  
Author(s):  
Christian Cajochen ◽  
Carolin Reichert ◽  
Micheline Maire ◽  
Luc J. M. Schlangen ◽  
Christina Schmidt ◽  
...  
Keyword(s):  
Slow Wave ◽  
White Light ◽  
Slow Wave Sleep ◽  
Age Groups ◽  
Sleep Regulation ◽  
Older Volunteers ◽  
Lighting Conditions ◽  
Ambient Lighting ◽  
Sleep Homeostasis ◽  
Subjective Sleepiness

We examined whether ambient lighting conditions during extended wakefulness modulate the homeostatic response to sleep loss as indexed by. slow wave sleep (SWS) and electroencephalographic (EEG) slow-wave activity (SWA) in healthy young and older volunteers. Thirty-eight young and older participants underwent 40 hours of extended wakefulness [i.e., sleep deprivation (SD)] once under dim light (DL: 8 lux, 2800 K), and once under either white light (WL: 250 lux, 2800 K) or blue-enriched white light (BL: 250 lux, 9000 K) exposure. Subjective sleepiness was assessed hourly and polysomnography was quantified during the baseline night prior to the 40-h SD and during the subsequent recovery night. Both the young and older participants responded with a higher homeostatic sleep response to 40-h SD after WL and BL than after DL. This was indexed by a significantly faster intra-night accumulation of SWS and a significantly higher response in relative EEG SWA during the recovery night after WL and BL than after DL for both age groups. No significant differences were observed between the WL and BL condition for these two particular SWS and SWA measures. Subjective sleepiness ratings during the 40-h SD were significantly reduced under both WL and BL compared to DL, but were not significantly associated with markers of sleep homeostasis in both age groups. Our data indicate that not only the duration of prior wakefulness, but also the experienced illuminance during wakefulness affects homeostatic sleep regulation in humans. Thus, working extended hours under low illuminance may negatively impact subsequent sleep intensity in humans.

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