Homeostatic Changes in Slow Wave Sleep during Recovery Sleep Following Restricted Nocturnal Sleep and Partial Slow Wave Sleep Recovery during an Afternoon Nap

Sleepwalking has been conceptualized as deregulation between slow-wave sleep and arousal, with its occurrence in predisposed patients increasing following sleep deprivation. Recent evidence showed autonomic changes before arousals and somnambulistic episodes, suggesting that autonomic dysfunctions may contribute to the pathophysiology of sleepwalking. We investigated cardiac autonomic modulation during slow-wave sleep in sleepwalkers and controls during normal and recovery sleep following sleep deprivation. Fourteen adult sleepwalkers (5M; 28.1 ± 5.8 years) and 14 sex- and age-matched normal controls were evaluated by video-polysomnography for one baseline night and during recovery sleep following 25 h of sleep deprivation. Autonomic modulation was investigated with heart rate variability during participants' slow-wave sleep in their first and second sleep cycles. 5-min electrocardiographic segments from slow-wave sleep were analyzed to investigate low-frequency (LF) and high-frequency (HF) components of heart rate spectral decomposition. Group (sleepwalkers, controls) X condition (baseline, recovery) ANOVAs were performed to compare LF and HF in absolute and normalized units (nLF and nHF), and LF/HF ratio. When compared to controls, sleepwalkers' recovery slow-wave sleep showed lower LF/HF ratio and higher nHF during the first sleep cycle. In fact, compared to baseline recordings, sleepwalkers, but not controls, showed a significant decrease in nLF and LF/HF ratio as well as increased nHF during recovery slow-wave sleep during the first cycle. Although non-significant, similar findings with medium effect sizes were observed for absolute values (LF, HF). Patterns of autonomic modulation during sleepwalkers' recovery slow-wave sleep suggest parasympathetic dominance as compared to baseline sleep values and to controls. This parasympathetic predominance may be a marker of abnormal neural mechanisms underlying, or interfere with, the arousal processes and contribute to the pathophysiology of sleepwalking.

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Blocking of Central Nervous Mineralocorticoid Receptors Counteracts Inhibition of Pituitary-Adrenal Activity in Human Sleep*

The Journal of Clinical Endocrinology & Metabolism ◽

10.1210/jcem.82.4.3856 ◽

1997 ◽

Vol 82 (4) ◽

pp. 1106-1110

Author(s):

Jan Born ◽

Dirk Steinbach ◽

Christoph Dodt ◽

Horst-Lorenz Fehm

Keyword(s):

Slow Wave ◽

Slow Wave Sleep ◽

Mineralocorticoid Receptors ◽

Placebo Administration ◽

Nocturnal Sleep ◽

Healthy Men ◽

Regulatory Influence ◽

Human Sleep ◽

The Subject

Abstract Pituitary-adrenal activity has been found to be inhibited during early nocturnal sleep in humans. This inhibition was supposed to reflect a regulatory influence of hippocampal cells characterized by the expression of mineralocorticoid receptors (MR). Pituitary adrenal responsiveness to bolus injections of CRH (50 μg) was examined in each of nine healthy men on four occasions: CRH was injected either during early nocturnal sleep or at the same time of night while the subject was kept awake. Both of these conditions were run after pretreatment with the selective MR antagonist, canrenoate (2 × 200 mg, 0800 and 1700 h, preceding the experimental night) and after placebo administration. After placebo, sleep reduced ACTH and cortisol secretory responses to CRH to about 65% of the size observed during wakefulness (P < 0.05). After canrenoate, ACTH and cortisol secretory responses during sleep and wakefulness did not differ and were comparable with those obtained in placebo-treated subjects during wakefulness. Compared with placebo, canrenoate also distinctly reduced the time spent in slow-wave sleep (P < 0.005). The findings confirm an inhibition of pituitary-adrenal responsiveness during early sleep. The inhibition disappearance after blockage of MR suggests that sleep exerts this influence via central nervous MR-expressing cells. These cells seem to be simultaneously involved in the generation of slow-wave sleep.

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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.

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Antihypertensive medication prior to nocturnal sleep reduces the risk of new-onset type 2 diabetes in hypertensive patients: a role for slow-wave sleep?

Diabetologia ◽

10.1007/s00125-015-3791-5 ◽

2015 ◽

Vol 59 (2) ◽

pp. 390-391 ◽

Cited By ~ 2

Author(s):

Christian Benedict

Keyword(s):

Type 2 Diabetes ◽

Slow Wave ◽

Antihypertensive Medication ◽

Slow Wave Sleep ◽

Nocturnal Sleep ◽

Hypertensive Patients ◽

Onset Type ◽

New Onset

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Time course of EEG power density during long sleep in humans

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1990.258.3.r650 ◽

1990 ◽

Vol 258 (3) ◽

pp. R650-R661 ◽

Cited By ~ 10

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.

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Stable inter-individual differences in slow-wave sleep during nocturnal sleep and naps

Sleep and Biological Rhythms ◽

10.1111/j.1479-8425.2010.00454.x ◽

2010 ◽

Vol 8 (4) ◽

pp. 239-244 ◽

Cited By ~ 5

Author(s):

Philippa GANDER ◽

Leigh SIGNAL ◽

Hans PA VAN DONGEN ◽

Diane MULLER ◽

Margo VAN DEN BERG

Keyword(s):

Individual Differences ◽

Slow Wave ◽

Slow Wave Sleep ◽

Nocturnal Sleep

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Effect of Night Exercise during 27-Hr. Total Sleep Deprivation on the Subsequent Sleep

Perceptual and Motor Skills ◽

10.2466/pms.1985.60.3.915 ◽

1985 ◽

Vol 60 (3) ◽

pp. 915-924

Author(s):

Kazuya Matsumoto ◽

Yoshio Saito ◽

Kouichi Furumi ◽

Masao Abe

Keyword(s):

Sleep Deprivation ◽

Slow Wave ◽

Slow Wave Sleep ◽

Sleep Stage ◽

Sleep Onset ◽

Bicycle Ergometer ◽

Night Sleep ◽

Total Sleep Deprivation ◽

Exercise Condition ◽

Recovery Sleep

This study was designed to determine the effects from loading and nonloading of night physical exercise during 27-hr. total sleep deprivation on the subsequent sleep. Subjects were 6 healthy male students. They cycled on the bicycle ergometer at 50% of VO2 max for 10 min., and then rested for 20 min.; repeated this schedule 14 times during the night (00:00 to 08:00). The standard polysomnograms were recorded during day sleep after exercise and during the following recovery-night sleep. When night exercise was not imposed, the sleep recordings were made during the day sleep (day sleep after no exercise), after the 27-hr. total sleep deprivation and following recovery night sleep. Stage 3 and Stage 4 sleep latencies were significantly shortened in the exercise condition as compared with those on baseline night and the no-exercise condition. The mean amount of slow-wave sleep was in the order of baseline < no exercise < exercise, each increase being significant. Stage 2 sleep, however, significantly decreased. The rectal temperature during sleep was significantly higher in the early half of day sleep after exercise than in that without exercise. The self-rating of the sleep depth and rapidness of sleep onset were only significantly better for both conditions compared with that for baseline night. There were no significant differences on any sleep parameters between the exercise conditions after recovery sleep. Results suggest that the increase in slow-wave sleep during day sleep after night exercise may be ascribed to the effects of both the exercise and the total sleep deprivation. The results support the hypothesis that increase in slow-wave sleep was part of recovery from fatigue.

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Slow-Wave Sleep in Daytime and Nocturnal Sleep: An Estimate of the Time Course of "Process S"

Journal of Biological Rhythms ◽

10.1177/074873048600100404 ◽

1986 ◽

Vol 1 (4) ◽

pp. 303-308 ◽

Cited By ~ 19

Author(s):

John B. Knowles ◽

Alistair W. MacLean ◽

Laura Salem ◽

Charles Vetere ◽

Margot Coulter

Keyword(s):

Slow Wave ◽

Time Course ◽

Slow Wave Sleep ◽

Nocturnal Sleep

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Topographical changes in N1-P2 amplitude upon awakening from recovery sleep after slow-wave sleep deprivation

Clinical Neurophysiology ◽

10.1016/s1388-2457(02)00146-3 ◽

2002 ◽

Vol 113 (8) ◽

pp. 1183-1190 ◽

Cited By ~ 11

Author(s):

Michele Ferrara ◽

Luigi De Gennaro ◽

Fabio Ferlazzo ◽

Giuseppe Curcio ◽

Riccardo Cristiani ◽

...

Keyword(s):

Sleep Deprivation ◽

Slow Wave ◽

Slow Wave Sleep ◽

Recovery Sleep

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129 Greater NREM Sleep Rebound in Response to Experimental Sleep Disturbance Associated with Higher Inflammatory Resolution in Humans

SLEEP ◽

10.1093/sleep/zsab072.128 ◽

2021 ◽

Vol 44 (Supplement_2) ◽

pp. A52-A53

Author(s):

Larissa Engert ◽

Marc Dubourdeau ◽

Rammy Dang ◽

Janet Mullington ◽

Monika Haack

Keyword(s):

Sleep Disturbance ◽

Slow Wave ◽

Rem Sleep ◽

Sleep Disturbances ◽

Slow Wave Sleep ◽

Sleep Onset ◽

Nrem Sleep ◽

Low Grade ◽

German Research Foundation ◽

Recovery Sleep

Abstract Introduction Sleep disturbances deteriorate immune function by not only affecting pro-inflammatory pathways, but also inflammatory resolution pathways, which actively terminate inflammation. It is assumed that slow wave sleep (SWS) amount and slow wave activity (SWA) convey the immune-supportive functions of sleep. We investigated whether changes in SWS induced by experimental sleep disturbance followed by recovery sleep predict changes in inflammatory resolution mediators. Methods The randomized controlled within-subjects trial (N=24, 20-42 years, 12 women) consisted of two 19-day in-hospital protocols (experimental sleep disturbance/control). After three nights of baseline sleep (8h/night), participants in the experimental sleep disturbance condition were exposed to three cycles of three nights of disturbed sleep (delayed sleep-onset, hourly sleep disruption, advanced sleep-offset) followed by one night of 8h-recovery sleep. The protocol ended with three nights of recovery sleep. In the control condition, participants had uninterrupted sleep (8h/night). Sleep (PSG) and resolvin lipid mediators in plasma (1100h, LC-MS/MS) were assessed at baseline, during the last cycle of sleep disturbance, and during/after the first and third night of final recovery sleep. Data were analyzed using generalized linear mixed models and Pearson/Spearman correlations. Results As expected, SWS amount decreased during experimental sleep disturbance and increased during the first recovery sleep night (p<.001). Similarly, resolvin (Rv) D2 and RvD3 decreased during sleep disturbance and RvD2 increased with subsequent recovery sleep (p<.001). The SWS response did not correlate with the resolvin response to sleep disturbance or to recovery sleep. However, the NREM sleep response correlated with the resolvin response during the third recovery sleep night, i.e., a greater NREM response was associated with a greater RvD2 and RvD3 response (r=.68, p=.002; r=.58, p=.012). In contrast, a greater REM sleep response was associated with a lower resolvin response (r=−.63, p=.005; r=−.66, p=.003). Conclusion These data suggest that during recovery from sleep disturbance, NREM rather than REM sleep promotes inflammatory resolution, thereby acting as the sleep state that protects against low-grade systemic inflammation, which has been frequently observed as a consequence of sleep disturbances. Analysis whether SWA is related to inflammatory resolution is in progress. Support (if any) NIH/NINDS R01-NS091177; NIH/NCRR UL1-RR02758, M01-RR01032; German Research Foundation (DFG) EN1291/1-1.

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