Performance and sleepiness following moderate sleep disruption and slow wave sleep deprivation

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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Slow Wave Sleep During a Brief Nap is Related to Reduced Cognitive Deficits During Sleep Deprivation

SLEEP ◽

10.1093/sleep/zsab152 ◽

2021 ◽

Author(s):

Michelle E Stepan ◽

Erik M Altmann ◽

Kimberly M Fenn

Keyword(s):

Sleep Deprivation ◽

Cognitive Processing ◽

Slow Wave ◽

Slow Wave Sleep ◽

Vigilance Task ◽

Attention Task ◽

Performance Deficits ◽

Impaired Performance ◽

Short Period ◽

Set Up

Abstract Sleeping for a short period (i.e., napping) may help mitigate impairments in cognitive processing caused by sleep deprivation, but there is limited research on effects of brief naps in particular. Here, we tested the effect of a brief nap opportunity (30- or 60-min) during a period of sleep deprivation on two cognitive processes with broad scope, placekeeping and vigilant attention. In the evening, participants (N = 280) completed a placekeeping task (UNRAVEL) and a vigilant attention task (Psychomotor Vigilance Task [PVT]) and were randomly assigned to either stay awake overnight or sleep at home. Sleep-deprived participants were randomly assigned to receive either no nap opportunity, a 30-min opportunity, or a 60-min opportunity. Participants who napped were set up with polysomnography. The next morning, sleep participants returned, and all participants completed UNRAVEL and the PVT. Sleep deprivation impaired performance on both tasks, but nap opportunity did not reduce the impairment, suggesting that naps longer than those tested may be necessary to cause group differences. However, in participants who napped, more time spent in slow-wave sleep (SWS) was associated with reduced performance deficits on both tasks, effects we interpret in terms of the role of SWS in alleviating sleep pressure and facilitating memory consolidation.

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Body temperature is elevated during the rebound of slow-wave sleep following 40-h of sleep deprivation on a constant routine

Journal of Sleep Research ◽

10.1111/j.1365-2869.1993.tb00073.x ◽

1993 ◽

Vol 2 (3) ◽

pp. 117-120 ◽

Cited By ~ 17

Author(s):

DERK-JAN DIJK ◽

CHARLES A. CZEISLER

Keyword(s):

Body Temperature ◽

Sleep Deprivation ◽

Slow Wave ◽

Slow Wave Sleep

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Effect of Slow Wave Sleep Disruption on Metabolic Parameters in Adolescents

SLEEP ◽

10.5665/sleep.6028 ◽

2016 ◽

Vol 39 (8) ◽

pp. 1591-1599 ◽

Cited By ~ 15

Author(s):

Natalie D. Shaw ◽

Andrew W. McHill ◽

Michele Schiavon ◽

Tairmae Kangarloo ◽

Piotr W. Mankowski ◽

...

Keyword(s):

Slow Wave ◽

Slow Wave Sleep ◽

Metabolic Parameters ◽

Sleep Disruption

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Plasma Catecholamines and Selective Slow Wave Sleep Deprivation

Neuropsychobiology ◽

10.1159/000048681 ◽

2002 ◽

Vol 45 (2) ◽

pp. 81-86 ◽

Cited By ~ 26

Author(s):

Henning Tiemeier ◽

Eva Pelzer ◽

Lothar Jönck ◽

Hans-Jürgen Möller ◽

Marie Luise Rao

Keyword(s):

Sleep Deprivation ◽

Slow Wave ◽

Slow Wave Sleep ◽

Plasma Catecholamines

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Targeted memory reactivation of face-name learning depends on ample and undisturbed slow-wave sleep

npj Science of Learning ◽

10.1038/s41539-021-00119-2 ◽

2022 ◽

Vol 7 (1) ◽

Author(s):

Nathan W. Whitmore ◽

Adrianna M. Bassard ◽

Ken A. Paller

Keyword(s):

Slow Wave ◽

Slow Wave Sleep ◽

Social Contexts ◽

Background Music ◽

Sleep Disruption ◽

Memory Functions ◽

Face Memory ◽

Memory Reactivation ◽

Two Factors ◽

Daytime Nap

AbstractFace memory, including the ability to recall a person’s name, is of major importance in social contexts. Like many other memory functions, it may rely on sleep. We investigated whether targeted memory reactivation during sleep could improve associative and perceptual aspects of face memory. Participants studied 80 face-name pairs, and then a subset of spoken names with associated background music was presented unobtrusively during a daytime nap. This manipulation preferentially improved name recall and face recognition for those reactivated face-name pairs, as modulated by two factors related to sleep quality; memory benefits were positively correlated with the duration of stage N3 sleep (slow-wave sleep) and negatively correlated with measures of sleep disruption. We conclude that (a) reactivation of specific face-name memories during sleep can strengthen these associations and the constituent memories, and that (b) the effectiveness of this reactivation depends on uninterrupted N3 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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