The Effect of Afternoon Body Heating on Body Temperature and Slow Wave Sleep

Recent evidence suggests that body temperature at sleep onset affects the subsequent level of slow wave sleep. According to one hypothesis, the actual temperature is the critical factor determining the relationship. An alternative proposal is that it is the rate of fall of body temperature following sleep onset. These hypotheses were tested by measuring rectal temperature and sleep, following late afternoon passive heating in a warm bath and during a control condition. Passive heating increased rectal temperature, which then returned rapidly toward the control level. However, immediately before lights out rectal temperature was still higher in the passive heating condition, a difference that continued throughout the night. Following passive heating the amount of slow wave sleep was higher in the early part of the night. These results support the hypothesis that body temperature at sleep onset and the amount of slow wave sleep are positively related.     

Age-Related Reduction in Daytime Sleep Propensity and Nocturnal Slow Wave Sleep

Objective:

To investigate whether age-related and experimental reductions in SWS and sleep continuity are associated with increased daytime sleep propensity.

Methods:

Assessment of daytime sleep propensity under baseline conditions and following experimental disruption of SWS. Healthy young (20-30 y, n = 44), middle-aged (40-55 y, n = 35) and older (66-83 y, n = 31) men and women, completed a 2-way parallel group study. After an 8-h baseline sleep episode, subjects were randomized to 2 nights with selective SWS disruption by acoustic stimuli, or without disruption, followed by 1 recovery night. Objective and subjective sleep propensity were assessed using the Multiple Sleep Latency Test (MSLT) and the Karolinska Sleepiness Scale (KSS).

Findings:

During baseline sleep, SWS decreased (P < 0.001) and the number of awakenings increased (P < 0.001) across the 3 age groups. During the baseline day, MSLT values increased across the three age groups (P < 0.0001) with mean values of 8.7min (SD: 4.5), 11.7 (5.1) and 14.2 (4.1) in the young, middle-aged, and older adults, respectively. KSS values were 3.7 (1.0), 3.2 (0.9), and 3.4 (0.6) (age-group: P = 0.031). Two nights of SWS disruption led to a reduction in MSLT and increase in KSS in all 3 age groups (SWS disruption vs. control: P < 0.05 in all cases).

Conclusions:

Healthy aging is associated with a reduction in daytime sleep propensity, sleep continuity, and SWS. In contrast, experimental disruption of SWS leads to an increase in daytime sleep propensity. The age-related decline in SWS and reduction in daytime sleep propensity may reflect a lessening in homeostatic sleep requirement. Healthy older adults without sleep disorders can expect to be less sleepy during the daytime than young adults.

Citation:

Dijk DJ; Groeger JA; Stanley N; Deacon S. Age-related reduction in daytime sleep propensity and nocturnal slow wave sleep. SLEEP 2010;33(2):211-223.     

Evidence for Circadian Influence on Human Slow Wave Sleep During Daytime Sleep Episodes

The occurrence of slow wave sleep within spontaneously initiated daytime sleep episodes was studied to examine hypothesized associations with prior wakefulness and circadian factors. There was a strong relationship between measures of slow wave sleep and the proximity of sleep episodes to the maximum of body core temperature. Those sleep episodes that began within 4 hours of the maximum in body core temperature contained significantly more slow wave sleep than did all other daytime sleep periods, approximating proportions typical of nocturnal sleep. Multiple regression analysis revealed no relationship between measures of slow wave sleep and prior wakefulness. These findings are consistent with an hypothesized approximately-12-hour rhythm in the occurrence of slow wave sleep and they underscore the influence imposed on human sleep by the endogenous circadian timing system.     

Slow Wave Sleep Deficiency Insomnia: A Problem in Thermo-Downregulation at Sleep Onset

The following review article attempts to develop the argument that a regulated, rapid drop in rectal, core-body temperature following sleep onset is a necessary prerequisite to the presence of sustained slow wave sleep (NREM Stage 4). Based upon this premise, a theory1 is presented to suggest that the slow wave sleep deficiency so commonly associated with chronic, primary insomnia (Gaillard, 1976, 1978) is the result of a failure in the thermoregulatory system to show a regulated, rapid decrease in body temperature with sleep onset which persists for the first 1–2 hrs into the sleep period.     

Slow Wave Sleep and REM Sleep Awakenings Do Not Affect Sleep Dependent Memory Consolidation

Study Objectives:

The effects of REM sleep and slow wave sleep (SWS) deprivation on sleep-dependent motor and declarative memory consolidation.

Design:

Randomized, within-subject, cross-over study

Setting:

Weekly (women: monthly) sleep laboratory visits, with retest 60 hours later

Participants:

Twelve healthy subjects (6 men) aged between 20 and 30 years

Interventions:

REM sleep deprivation, SWS deprivation, or undisturbed sleep

Measurements and Results:

We deprived subjects once each of REM sleep and SWS, and once let them sleep undisturbed through the night. After each night, we tested declarative and procedural memory consolidation. We tested memory performance by a verbal paired associate task and a sequential finger-tapping task at 21:00 on the study night and again 60 hours later. Although REM sleep and SWS awakenings led to a significant reduction of the respective sleep stages, memory consolidation remained unaffected. We also found a significant correlation between the declarative task and sleep spindles in the undisturbed condition, especially the sleep spindles in the first third of the night.

Conclusion:

We suggest that word-pair learning relies on stage 2 sleep spindles and requires little SWS. Their sleep dependent consolidation is not affected by SWS deprivation. Simple motor tasks may either be consolidated in stage 2 sleep or depend on only small amounts of REM sleep. Their sleep dependent consolidation is not influenced by REM sleep deprivation.

Citation:

Genzel L; Dresler M; Wehrle R; Grözinger M; Steiger A. Slow wave sleep and REM sleep awakenings do not affect sleep dependent memory consolidation. SLEEP 2009;32(3):302–310.     

褪黑素对睡眠剥夺大鼠记忆的影响

目的探讨褪黑素对睡眠剥夺(SD)大鼠记忆的影响及其机制。方法24只大鼠随机分为对照组(SD 生理盐水)和2个实验组(SD 小、大剂量褪黑素),用小平台水环境法建立大鼠SD模型,SD48h和SD72h后用水迷宫测试大鼠的记忆能力,最后检测大鼠大脑皮层和海马中一氧化氮(NO)和丙二醛(MDA)含量。结果实验组大鼠SD48h和SD72h水迷宫反应时均明显小于对照组(F=11.89、5.44,P=0.00、0.012)。实验组大鼠大脑皮层和海马组织中NO和MDA含量明显低于对照组(F=14.31~27.41,P=0.00)。结论褪黑素对睡眠剥夺大鼠记忆障碍有改善作用,这可能与抑制睡眠剥夺大鼠大脑皮层和海马中NO及MDA的升高作用有关。     

睡眠剥夺对认知功能影响的研究进展

为了充分探究睡眠对认知的作用机制，睡眠剥夺是一个有效的途径。目前有多种手段研究睡眠剥夺如何影响认知功能，包括认知心理学评价、脑成像方法、脑电生理的变化等。所研究的方面覆盖认知科学的多个领域，目前国内外均有学者致力于此研究，并已经取得了初步的成果，但是存在多种影响因素，尚未得到统一的结论。我们从睡眠剥夺引起认知功能下降的机制出发，综述了通过脑成像方法研究神经生理学变化以及脑电生理方法评价认知功能下降的研究进展，并分析研究的影响因素和目前关注的发展方向。     

人参皂甙对睡眠剥夺大鼠记忆保持的影响

目的：探讨人参皂甙（Ginsenosides,GS)对睡眠剥夺（sleep deprivation,SD)大鼠记忆保持的影响。方法：用小平台水环境法（Flower Pot)建立大鼠SD模型,选用Sprague-Dawley大鼠24只,根据SD时间的不同,将大鼠随机分为三组：24SD（24小时SD组）,48SD（48小时SD组）和72SD（72小时SD组）,每组又设实验组和对照组。其中实验组用GS连续灌胃5天,对照组以同样方式给予等量生理盐水,然后给予不同时间的SD。观察各组SD前后在跳台实验中的行为变化。结果：SD后各组大鼠跳台测试第一次触电潜伏期均下降,触电次数和触电时间均增加。SD前实验组和对照组的第一次触电潜伏期,触电次数和触电时间无显著差别（P＞0．05）,72SD大鼠的第一次触电潜伏期实验组显著大于对照组（P＜0．05）,触电次数和触电时间,实验组显著低于对照组（P＜0．05）;24SD,48SD的第一次触电潜伏期,触电次数和触电时间,实验组和对照组无显著差别。结论：连续口服GS对SD造成的大鼠记忆保持能力受损有明显保护作用,在一定睡眠剥夺时间内,这种保护作用随SD时间的延长而增强。     

Effect of Sleep Deprivation on Eye Movement Behavior in Flight Simulation

To examine the effect of sleep deprivation （SD） on eye movement be- havior in flight task, four subjects who were skilled in flight simulator participated in the experiment, which were asked to perform a level flight task in a flight simulator. Eye movement data and flight performance data were measured at the following hours： 11：00, 15：00, 04：00, 11：00, 15：00. The subjects workload and fatigue were assessed with the method of national aeronautics and space administration-task load index （NASA-TLX） and rating of perceived exertion （RPE）. Eye movement indices of average pupil area, av- erage saceade amplitude and average saccade velocity decreased during the 32 h of SD and they all showed significantly change in the final SD while the index of average fixa- tion time increased in the final SD. Flight performance deteriorated during the 32 h of SD, but not significantly. The feeling of fatigue and workload reported by subjects both increased during the 32 h of SD. Daily rhythm effects on the measured indices were also found, there were a obviously change at the hour of 04：00. 32 h of SD has obvious effect on eye movement behaviors which have close relation to fatigue because of SD. The eye movement measurement can be served as a tool to continually monitor fatigue online.     

Enhancing Slow Wave Sleep with Sodium Oxybate Reduces the Behavioral and Physiological Impact of Sleep Loss

Study Objectives:

To investigate whether enhancement of slow wave sleep (SWS) with sodium oxybate reduces the impact of sleep deprivation.

Design:

Double-blind, parallel group, placebo-controlled design

Setting:

Sleep research laboratory

Participants:

Fifty-eight healthy adults (28 placebo, 30 sodium oxybate), ages 18-50 years.

Interventions:

A 5-day protocol included 2 screening/baseline nights and days, 2 sleep deprivation nights, each followed by a 3-h daytime (08:00-11:00) sleep opportunity and a recovery night. Sodium oxybate or placebo was administered prior to each daytime sleep period. Multiple sleep latency test (MSLT), psychomotor vigilance test (PVT), Karolinska Sleepiness Scale (KSS), and Profile of Mood States were administered during waking hours.

Measurements and Results:

During daytime sleep, the sodium oxybate group had more SWS, more EEG spectral power in the 1-9 Hz range, and less REM. Mean MSLT latency was longer for the sodium oxybate group on the night following the first daytime sleep period and on the day following the second day sleep period. Median PVT reaction time was faster in the sodium oxybate group following the second day sleep period. The change from baseline in SWS was positively correlated with the change in MSLT and KSS. During recovery sleep the sodium oxybate group had less TST, SWS, REM, and slow wave activity (SWA) than the placebo group.

Conclusions:

Pharmacological enhancement of SWS with sodium oxybate resulted in a reduced response to sleep loss on measures of alertness and attention. In addition, SWS enhancement during sleep restriction appears to result in a reduced homeostatic response to sleep loss.

Citation:

Walsh JK; Hall-Porter JM; Griffin KS; Dodson ER; Forst EH; Curry DT; Eisenstein RD; Schweitzer PK. Enhancing slow wave sleep with sodium oxybate reduces the behavioral and physiological impact of sleep loss. SLEEP 2010;33(9):1217-1225.     

Mapping Slow Waves by EEG Topography and Source Localization: Effects of Sleep Deprivation

Slow waves are a salient feature of the electroencephalogram (EEG) during non-rapid eye movement (non-REM) sleep. The aim of this study was to assess the topography of EEG power and the activation of brain structures during slow wave sleep under normal conditions and after sleep deprivation. Sleep EEG recordings during baseline and recovery sleep after 40 h of sustained wakefulness were analyzed (eight healthy young men, 27 channel EEG). Power maps were computed for the first non-REM sleep episode (where sleep pressure is highest) in baseline and recovery sleep, at frequencies between 0.5 and 2 Hz. Power maps had a frontal predominance at all frequencies between 0.5 and 2 Hz. An additional occipital focus of activity was observed below 1 Hz. Power maps?≤?1 Hz were not affected by sleep deprivation, whereas an increase in power was observed in the maps?≥?1.25 Hz. Based on the response to sleep deprivation, low-delta (0.5–1 Hz) and mid-delta activity (1.25–2 Hz) were dissociated. Electrical sources within the cortex of low- and mid-delta activity were estimated using eLORETA. Source localization revealed a predominantly frontal distribution of activity for low-delta and mid-delta activity. Sleep deprivation resulted in an increase in source strength only for mid-delta activity, mainly in parietal and frontal regions. Low-delta activity dominated in occipital and temporal regions and mid-delta activity in limbic and frontal regions independent of the level of sleep pressure. Both, power maps and electrical sources exhibited trait-like aspects.     

Effects of Skilled Training on Sleep Slow Wave Activity and Cortical Gene Expression in the Rat

Study Objective:

The best characterized marker of sleep homeostasis is the amount of slow wave activity (SWA, 0.5–4 Hz) during NREM sleep. SWA increases as a function of previous waking time and declines during sleep, but the underlying mechanisms remain unclear. We have suggested that SWA homeostasis is linked to synaptic potentiation associated with learning during wakefulness. Indeed, studies in rodents and humans found that SWA increases after manipulations that presumably enhance synaptic strength, but the evidence remains indirect. Here we trained rats in skilled reaching, a task known to elicit long-term potentiation in the trained motor cortex, and immediately after learning measured SWA and cortical protein levels of c-fos and Arc, 2 activity-dependent genes involved in motor learning.

Design:

Intracortical local field potential recordings and training on reaching task.

Setting:

Basic sleep research laboratory.

Patients or Participants:

Long Evans adult male rats.

Interventions:

N/A

Measurements and Results:

SWA increased post-training in the trained cortex (the frontal cortex contralateral to the limb used to learn the task), with smaller or no increase in other cortical areas. This increase was reversible within 1 hour, specific to NREM sleep, and positively correlated with changes in performance during the prior training session, suggesting that it reflects plasticity and not just motor activity. Fos and Arc levels were higher in the trained relative to untrained motor cortex immediately after training, but this asymmetry was no longer present after 1 hour of sleep.

Conclusion:

Learning to reach specifically affects gene expression in the trained motor cortex and, in the same area, increases sleep need as measured by a local change in SWA.

Citation:

Hanlon EC; Faraguna U; Vyazovskiy VV; Tononi G; Cirelli C. Effects of skilled training on sleep slow wave activity and cortical gene expression in the rat. SLEEP 2009;32(6):719-729.     

32小时完全睡眠剥夺对个体心理旋转能力的影响

目的:探讨32小时完全睡眠剥夺对个体心理旋转能力的影响。方法:8名健康男性青年在32小时睡眠剥夺条件下,分别在8个时间点(0800;2000;2400;0200;0400;0600;1000;1400)进行计算机呈现的多边形图形心理旋转测试和POMS测验。采用拉丁方实验设计。结果:随睡眠剥夺时间的延长,多边形图形心理旋转测验绩效下降,以剥夺后24小时最低,之后略有恢复,具有统计学显著意义(p<0.05);同时POMS情绪负性因子T、D、F、C各要素自评得分增加,情绪正性因子V得分减低。结论:32小时睡眠剥夺在一定程度上影响着心理旋转作业绩效,随着睡眠剥夺时间的延长,作业绩效呈下降趋势,在睡眠剥夺24小时时作业绩效下降最明显。此外,个体的情绪亦受累及。     

Recovery of Performance During Sleep Following Sleep Deprivation

Very few studies have systematically examined recovery of performance after sleep deprivation. In the present study, 12 young adult males were sleep deprived for periods of 40 and 64 hrs. Each period was preceded by baseline nights of sleep and followed by two recovery nights of sleep. Immediate recall and reaction time were tested at 2300, 0145, 0400, 0615, and 0830 during baseline, deprivation, and recovery nights. Performance efficiency showed a progressive decline after 2 hrs of recovery sleep following both periods of deprivation. Return to baseline was apparent after 4 hrs of steep following 40 hrs awake and after 8 hrs of sleep following 64 hrs awake. These results suggested that, in terms of behavioral efficiency, an equal amount of sleep is not required to compensate for sleep lost.     

睡眠剥夺对内隐记忆的影响

目的:探讨不同时间睡眠剥夺(sleep deprivation,SD)对内隐记忆的影响。方法:将32名青年男性随机分为4组:对照组、SD21、SD45和SD69组,每组8名。采用补笔测验和组词测验对4组被试进行测试。结果:SD 后无论知觉启动还是语义启动,启动量降低,并随SD 时间延长而减少。同一组内,两种测验进行比较,除对照组外,其他SD 组两两比较,语义启动的启动量大于知觉启动(P<0.05)。知觉启动中,SD45同SD69 相比无显著差异(P=0.245),其他两两比较差异均有统计学意义(P<0.01);语义启动中,SD21同对照组相比差异无统计学意义(P=0.316),其他两两比较差异均有统计学意义(P<0.01)。结论:SD 后内隐记忆受损,并同SD 时间有关;SD 后语义启动和知觉启动出现分离,知觉启动更受SD 影响。     

睡眠剥夺对值班医生情绪的影响

目的：研究一夜睡眠缺失及恢复睡眠后对外科值班医生情绪的影响。方法：采用简明心境量表、状态焦虑问卷及斯坦福困倦量表，对23名外科医生进行值班前后及恢复一夜睡眠后情绪变化的研究。结果：外科医生在值班后，负性情绪增加，正性情绪减少，其中以愤怒-敌意、疲惫-惰性、困惑-迷茫、有力-好动为显著；焦虑和困倦程度增加；恢复1d后，负性情绪有所减少，但同值班前相比，有所增加，以疲惫-惰性为显著。结论：医生在值夜班后负性情绪增加，正性情绪减少。恢复睡眠后有所恢复。     

Sleep Deprivation Therapy in Depression Syndromes

Sleep deprivation may significantly help some endogenously depressed patients who do not respond well to chemotherapy. Although no severe physical side-effects have resulted from sleep deprivation, existing symptoms of depression have been known to become worse in some patients. Sleep deprivation does not appear to interfere with the action of antidepressant drugs and may actually augment and sustain their effect.     

Local Mechanisms Underling the Regulatory Effect of Kropanol on Hemopoiesis during Paradoxical Sleep Deprivation

We studied the effect of Kropanol on local regulatory mechanisms of hemopoiesis during paradoxical sleep deprivation. The regulatory effect of Kropanol on granulomonocytopoiesis was determined by increased binding capacity of stromal cells in relation to granulocyte-macrophage precursors and increased formation of mixed hemopoietic islets leading to accelerated maturation of granulocyte-macrophage precursors and hyperplasia of the granulomonocytic hemopoietic stem. Stimulation of erythropoiesis with Kropanol was associated with increased formation of erythroid hemopoietic islets, accelerated differentiation of erythroid precursors, and high content of erythroid cells in the bone marrow. Kropanol increased proliferative activity of erythroid precursors. Stimulation of these processes depended on enhanced production of short-distance humoral regulators of erythro- and granulomonocytopoiesis.