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

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.

Download Full-text

Evidence that Homeostatic Sleep Regulation Depends on Ambient Illuminance Levels

10.20944/preprints201909.0129.v1 ◽

2019 ◽

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 ◽

Wave Activity ◽

Sleep Regulation ◽

Older Volunteers ◽

Sleep Homeostasis ◽

Subjective Sleepiness ◽

Dim Light

We examined whether the ambient illuminance during extended wakefulness modulates the homeostatic increase in human deep sleep [i.e. 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, 2800K), and once under either white light (WL: 250 lux, 2800K) or blue-enriched white light (BL: 250 lux, 9000K) 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.

Download Full-text

Effects of sleep deprivation in neonatal rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1998.275.1.r148 ◽

1998 ◽

Vol 275 (1) ◽

pp. R148-R157 ◽

Cited By ~ 14

Author(s):

Marcos G. Frank ◽

Roger Morrissette ◽

H. Craig Heller

Keyword(s):

Sleep Deprivation ◽

Slow Wave ◽

Slow Wave Sleep ◽

Sleep Time ◽

Postnatal Life ◽

Neonatal Rats ◽

Sleep Regulation ◽

Adult Rats ◽

Sleep Homeostasis ◽

Show Evidence

This investigation represents the first systematic study of sleep homeostasis in developing mammals that spans the preweaning and postweaning periods. Neonatal rats from 12 to 24 days of postnatal life ( P12– P24) were anesthetized with Metofane (methoxyflurane) and implanted with miniaturized electroencephalographic (EEG) and electromyographic electrodes. After 48 h of recovery, neonatal rats were sleep deprived for 3 h by either gentle handling or forced locomotion. We find that 3-h sleep deprivation produces dramatically different compensatory responses at different stages of postnatal development. In striking contrast to adult rats, sleep deprivation does not increase slow-wave sleep EEG delta (0.5–4.0 Hz) activity in rats younger than P24. However, P12– P20rats do show evidence of sleep regulation because they show compensatory increases in sleep time and sleep continuity during recovery. In P12 rats, ∼90% of total slow wave sleep time lost during the sleep-deprivation period was recovered during subsequent sleep. A similar recovery of active sleep time was observed in P20– P24rats. These findings suggest not only that sleep is regulated in neonatal rats but that the accumulation and/or discharge of sleep need changes dramatically between the third and fourth postnatal weeks.

Download Full-text

Reduced sleep pressure in young children with autism

SLEEP ◽

10.1093/sleep/zsz309 ◽

2019 ◽

Vol 43 (6) ◽

Cited By ~ 4

Author(s):

Ayelet Arazi ◽

Gal Meiri ◽

Dor Danan ◽

Analya Michaelovski ◽

Hagit Flusser ◽

...

Keyword(s):

Slow Wave ◽

Sleep Disturbances ◽

Slow Wave Sleep ◽

Sleep Onset ◽

Children With Autism ◽

Autism Spectrum ◽

Potential Contribution ◽

Sleep Regulation ◽

Children With Asd ◽

Sleep Homeostasis

Download Full-text

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.

Download Full-text

Changes in sleep quality of athletes under normobaric hypoxia equivalent to 2,000-m altitude: a polysomnographic study

Journal of Applied Physiology ◽

10.1152/japplphysiol.00315.2007 ◽

2007 ◽

Vol 103 (6) ◽

pp. 2005-2011 ◽

Cited By ~ 25

Author(s):

Masako Hoshikawa ◽

Sunao Uchida ◽

Takayuki Sugo ◽

Yasuko Kumai ◽

Yoshiteru Hanai ◽

...

Keyword(s):

Sleep Quality ◽

Slow Wave ◽

Slow Wave Sleep ◽

Sleep Stage ◽

Normobaric Hypoxia ◽

Fast Fourier Transformation ◽

Urinary Catecholamines ◽

Arterial Blood ◽

Subjective Sleepiness

This study evaluated the sleep quality of athletes in normobaric hypoxia at a simulated altitude of 2,000 m. Eight male athletes slept in normoxic condition (NC) and hypoxic conditions equivalent to those at 2,000-m altitude (HC). Polysomnographic recordings of sleep included the electroencephalogram (EEG), electrooculogram, chin surface electromyogram, and electrocardiogram. Thoracic and abdominal motion, nasal and oral airflow, and arterial blood oxygen saturation (SaO2) were also recorded. Standard visual sleep stage scoring and fast Fourier transformation analyses of the EEG were performed on 30-s epochs. Subjective sleepiness and urinary catecholamines were also monitored. Mean SaO2 decreased and respiratory disturbances increased with HC. The increase in respiratory disturbances was significant, but the increase was small and subclinical. The duration of slow-wave sleep (stage 3 and 4) and total delta power (<3 Hz) of the all-night non-rapid eye movement sleep EEG decreased for HC compared with NC. Subjective sleepiness and amounts of urinary catecholamines did not differ between the conditions. These results indicate that acute exposure to normobaric hypoxia equivalent to that at 2,000-m altitude decreased slow-wave sleep in athletes, but it did not change subjective sleepiness or amounts of urinary catecholamines.

Download Full-text

Sleep regulation in rats: effects of sleep deprivation, light, and circadian phase

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1986.251.6.r1037 ◽

1986 ◽

Vol 251 (6) ◽

pp. R1037-R1044 ◽

Cited By ~ 8

Author(s):

L. Trachsel ◽

I. Tobler ◽

A. A. Borbely

Keyword(s):

Sleep Deprivation ◽

Slow Wave Sleep ◽

Rest Period ◽

Activity Period ◽

Base Line ◽

Sleep Regulation ◽

Continuous Darkness ◽

Circadian Phase ◽

Sleep Homeostasis ◽

Pentobarbital Sodium Anesthesia

Sleep states and electroencephalographic (EEG) parameters were determined in unrestrained rats that had been implanted with electrodes under deep pentobarbital sodium anesthesia. Two base-line days with a light-dark cycle (LD) and 2 days under continuous darkness (DD) were followed by 24 h of sleep deprivation (SD) ending in the middle of the circadian activity period and by 2 recovery days in DD. In the base-line LD rest period, the amount of rapid-eye-movement sleep (REMS) and the EEG amplitude of non-REMS (NREMS) were lower than in the corresponding DD period. SD caused an immediate enhancement of REMS, NREMS, the slow-wave sleep (SWS) fraction of NREMS, and NREMS EEG amplitude. Although REMS, NREMS, and SWS showed a second peak at habitual light onset, they did not exceed base line. Subsequently, all parameters exhibited a marked negative rebound. We conclude that REMS and the EEG amplitude of NREMS are suppressed by light, amplitude and frequency parameters of NREMS are differently affected by light as well as by SD, and the short duration of the SD-induced increase of SWS may reflect a circadian influence on sleep homeostasis.

Download Full-text

Reduced sleep pressure in young children with autism

10.1101/706135 ◽

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.

Download Full-text

Evidence against a role for the growth hormone-releasing peptide axis in human slow-wave sleep regulation

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1998.274.5.e779 ◽

1998 ◽

Vol 274 (5) ◽

pp. E779-E784 ◽

Cited By ~ 7

Author(s):

Rodrigo Moreno-Reyes ◽

Myriam Kerkhofs ◽

Mireille L’Hermite-Balériaux ◽

Michael O. Thorner ◽

Eve Van Cauter ◽

...

Keyword(s):

Growth Hormone ◽

Slow Wave ◽

Slow Wave Sleep ◽

Growth Hormone Releasing Hormone ◽

Sleep Regulation ◽

Healthy Men ◽

Intravenous Injections ◽

Late Night ◽

The Third ◽

Upper Limit

A complex interrelationship exists between sleep and somatotropic activity. In humans, intravenous injections of growth hormone-releasing hormone (GHRH) given during sleep consistently stimulate slow-wave (SW) sleep, particularly when given in the latter part of the night. In the present study, the possible somnogenic effects induced under similar conditions by GH-releasing peptide (GHRP) were investigated in seven young healthy men. Bolus intravenous injections of GHRP-2 (1 μg/kg body wt) or saline, in randomized order, were given after 60 s of the third rapid-eye-movement period. All GHRP injections were immediately followed by transient prolactin elevations and by GH pulses of a magnitude within or around the upper limit of the physiological range. Except for a nonsignificant tendency to increased amounts of wakefulness during the 1st h after the injection, no effects of GHRP-2 administration on sleep were detected. There was in particular no enhancement of SW sleep. Thus, in contrast to GHRH, late-night single injections of GHRP-2 at a dosage resulting in similar GH elevations have no stimulatory effects on SW sleep. The present data provide evidence against the involvement of the GHRP axis in human SW sleep regulation.

Download Full-text

008 ARC Genotype Modulates Slow Wave Sleep Following Total Sleep Deprivation

SLEEP ◽

10.1093/sleep/zsab072.007 ◽

2021 ◽

Vol 44 (Supplement_2) ◽

pp. A4-A4

Author(s):

Brieann Satterfield ◽

Darian Lawrence-Sidebottom ◽

Michelle Schmidt ◽

Jonathan Wisor ◽

Hans Van Dongen

Keyword(s):

Individual Differences ◽

Sleep Deprivation ◽

Slow Wave ◽

Molecular Mechanisms ◽

Slow Wave Sleep ◽

Early Gene ◽

Total Sleep Deprivation ◽

Recovery Sleep ◽

Sleep Homeostasis ◽

Arc Gene

Abstract Introduction The activity-regulated cytoskeleton associated protein (ARC) gene is an immediate early gene that is involved in synaptic plasticity. Recent evidence from a rodent model suggests that Arc may also be involved in sleep homeostasis. However, little is known about the molecular mechanisms regulating the sleep homeostat. In humans, sleep homeostasis is manifested by a marked increase in slow wave sleep (SWS) following acute total sleep deprivation (TSD). There are large, trait individual differences in the magnitude of this SWS rebound effect. We sought to determine whether a single nucleotide polymorphism (SNP) of the ARC gene is associated with individual differences in SWS rebound following TSD. Methods 64 healthy normal sleepers (ages 27.2 ± 4.8y; 32 females) participated in one of two in-laboratory TSD studies. In each study, subjects had a baseline day with 10h sleep opportunity (TIB 22:00–08:00) which was followed by 38h TSD. The studies concluded with 10h recovery sleep opportunity (TIB 22:00–08:00). Baseline and recovery sleep were recorded polysomnographically and scored visually by a trained technician. Genomic DNA was extracted from whole blood. The ARC c.*742 + 58C>T non-coding SNP, rs35900184, was assayed using real-time PCR. Heterozygotes and T/T homozygotes were combined for analysis. The genotype effect on time in SWS was assessed using mixed-effects ANOVA with fixed effects for ARC genotype (C/C vs. T carriers), night (baseline vs. recovery), and their interaction, controlling for study. Results The genotype distribution in this sample – C/C: 41; C/T: 17; T/T: 6 – did not vary significantly from Hardy-Weinberg equilibrium. There was a significant interaction between ARC genotype and night (F1,62=7.27, p=0.009). Following TSD, T allele carriers exhibited 47.6min more SWS compared to baseline, whereas C/C homozygotes exhibited 62.3min more SWS compared to baseline. There was no significant difference in SWS between genotypes at baseline (F1,61=0.69, p=0.41). Conclusion ARC T allele carriers exhibited an attenuated SWS rebound following TSD compared to those homozygous for the C allele. This suggests that the ARC SNP is associated with trait individual differences related to sleep homeostasis, and may thus influence molecular mechanisms involved in long-term memory. Support (if any) ONR N00014-13-1-0302, NIH R21CA167691, and USAMRDC W81XWH-18-1-0100.

Download Full-text

Enhanced Slow Wave Sleep in Patients with Prolactinoma

The Journal of Clinical Endocrinology & Metabolism ◽

10.1210/jcem.83.8.5016 ◽

1998 ◽

Vol 83 (8) ◽

pp. 2706-2710 ◽

Cited By ~ 14

Author(s):

Ralf-Michael Frieboes ◽

Harald Murck ◽

Günter Karl Stalla ◽

Irina A. Antonijevic ◽

Axel Steiger

Keyword(s):

Slow Wave ◽

Rem Sleep ◽

Slow Wave Sleep ◽

Hormone Secretion ◽

Sleep Regulation ◽

Endocrine Diseases ◽

Term Administration ◽

Secondary Hypogonadism ◽

Bidirectional Interactions

abstract Bidirectional interactions between nocturnal hormone secretion and sleep regulation are well established. In particular, a link between PRL and rapid eye movement (REM) sleep has been hypothesized. Short-term administration of PRL and even long-term hyperprolactinemia in animals increases REM sleep. Furthermore, sleep disorders are frequent symptoms in patients with endocrine diseases. We compared the sleep electroencephalogram of seven drug-free patients with prolactinoma (mean PRL levels 1450 ± 1810 ng/mL; range between 146 and 5106 ng/mL) with that of matched controls. The patients had secondary hypogonadism but no other endocrine abnormalities. They spent more time in slow wave sleep than the controls (79.4 ± 54.4 min in patients vs. 36.6 ± 23.5 min in controls, P < 0.05). REM sleep variables did not differ between the samples. Our data suggest that chronic excessive enhancement of PRL levels exerts influences on the sleep electroencephalogram in humans. Our result, which seems to be in contrast to the enhanced REM sleep under hyperprolactinemia in rats, leads to the hypothesis that both slow wave sleep and REM sleep can be stimulated by PRL. These findings are in accordance with reports of good sleep quality in patients with prolactinoma, which is in contrast to that of patients with other endocrine diseases.

Download Full-text