The dynamics of neurobehavioural recovery following sleep loss

Rate of recovery of daytime performance and sleepiness following moderate and severe sleep deprivation (SD) was examined when recovery opportunity was either augmented or restricted. Thirty healthy non-smokers, aged 18-33 years, participated in one of three conditions: moderate SD with augmented (9-h) recovery opportunities, moderate SD with restricted (6-h) recovery opportunities, or severe SD with augmented recovery opportunities. Each participant attended the laboratory for 8-9 consecutive nights: an adaptation and baseline night (23:00-08:00 hours), one or two night(s) of wakefulness, and five consecutive recovery sleep opportunities (23:00-08:00 hours or 02:00-08:00 hours). On each experimental day, psychomotor vigilance performance (PVT) and subjective sleepiness (SSS) were assessed at two-hourly intervals, and MSLTs were performed at 1000 h. PSG data was collected for each sleep period. For all groups, PVT performance significantly deteriorated during the period of wakefulness, and sleepiness significantly increased. Significant differences were observed between the groups during the recovery phase. Following moderate SD, response speed, lapses and SSS returned to baseline after one 9-h sleep opportunity, while sleep latencies required two 9-h opportunities. When the recovery opportunity was restricted to six hours, neither PVT performance nor sleepiness recovered, but stabilised at below-baseline levels. Following severe SD, sleepiness recovered after one (SSS) or two (physiological) 9-h sleep opportunities, however PVT performance remained significantly below baseline for the entire recovery period. These results suggest that the mechanisms underlying the recovery process may be more complicated than previously thought, and that we may have underestimated the impact of sleep loss and/or the restorative value of subsequent sleep.     

Modafinil, d-amphetamine and placebo during 64 hours of sustained mental work. II. Effects on two nights of recovery sleep

Polysomnograms were obtained from 37 volunteers, before (baseline) and after (two consecutive recovery nights) a 64-h sleep deprivation, with (d-amphetamine or modafinil) or without (placebo) alerting substances. The drugs were administered at 23.00 hours during the first sleep deprivation night (after 17.5 h of wakefulness), to determine whether decrements in cognitive performance would be prevented; at 05.30 hours during the second night of sleep deprivation (after 47.5 h of wakefulness), to see whether performance would be restored; and at 15.30 hours during the third day of continuous work, to study effects on recovery sleep. The second recovery night served to verify whether drug-induced sleep disturbances on the first recovery night would carry over to a second night of sleep. Recovery sleep for the placebo group was as expected: the debt in slow-wave sleep (SWS) and REM sleep was paid back during the first recovery night, the rebound in SWS occurring mainly during the first half of the night, and that of REM sleep being distributed evenly across REM sleep episodes. Recovery sleep for the amphetamine group was also consistent with previously published work: increased sleep latency and intrasleep wakefulness, decreased total sleep time and sleep efficiency, alterations in stage shifts, Stage 1, Stage 2 and SWS, and decreased REM sleep with a longer REM sleep latency. For this group, REM sleep rebound was observed only during the second recovery night. Results for the modafinil group exhibited decreased time in bed and sleep period time, suggesting a reduced requirement for recovery sleep than for the other two groups. This group showed fewer disturbances during the first recovery night than the amphetamine group. In particular, there was no REM sleep deficit, with longer REM sleep episodes and a shorter REM latency, and the REM sleep rebound was limited to the first REM sleep episode. The difference with the amphetamine group was also marked by less NREM sleep and Stage 2 and more SWS episodes. No REM sleep rebound occurred during the second recovery night, which barely differed from placebo. Hence, modafinil allowed for sleep to occur, displayed sleep patterns close to that of the placebo group, and decreased the need for a long recovery sleep usually taken to compensate for the lost sleep due to total sleep deprivation.     

Trait interindividual differences in the sleep physiology of healthy young adults

Despite decades of sleep research by means of polysomnography (PSG), systematic interindividual differences in PSG-assessed sleep parameters have been scarcely investigated. The present study is the first to quantify interindividual variability in standard PSG-assessed variables of sleep structure in terms of stability and robustness as well as magnitude. Twenty-one carefully screened healthy young adults were studied continuously in a strictly controlled laboratory environment, where their PSGs were recorded for eight nights interspersed with three separate 36 h sleep deprivation periods. All PSG records were scored blind to subject and condition, using conventional criteria, and delta power in the non-REM sleep EEG was computed for four electrode derivations. Interindividual differences in sleep variables were examined for stability and robustness, respectively, by comparing results across equivalent nights (e.g. baseline nights) and across experimentally differentiated nights (baseline nights versus recovery nights following sleep deprivation). Among 18 sleep variables analyzed, all except slow-wave sleep (SWS) latency were found to exhibit significantly stable and robust--i.e. trait-like--interindividual differences. This was quantified by means of intraclass correlation coefficients (ICCs), which ranged from 36% to 89% across physiologic variables, and were highest for SWS (73%) and delta power in the non-REM sleep EEG (78-89%). The magnitude of the trait interindividual differences was considerable, consistently exceeding the magnitude of the group-average effect on sleep structure of 36 h total sleep deprivation. Notably, for non-REM delta power--a putative marker of sleep homeostasis--the interindividual differences were from 9.9 to 12.8 times greater than the group-average increase following sleep deprivation relative to baseline. Physiologic sleep variables did not vary among subjects in a completely independent manner--61.1% of their combined variance clustered in three trait dimensions, which appeared to represent sleep duration, sleep intensity, and sleep discontinuity. Any independent functional significance of these sleep physiologic phenotypes remains to be determined.     

The relationship between frequency of rapid eye movements in REM sleep and SWS rebound

Previous studies have shown a decrease in rapid eye movement (REM) frequency during desynchronized sleep in recovery nights following total or partial sleep deprivation. This effect has been ascribed to an increase in sleep need or sleep depth consequent to sleep length manipulations. The aims of this study were to assess REM frequency variations in the recovery night after two consecutive nights of selective slow-wave sleep (SWS) deprivation, and to evaluate the relationships between REM frequency and SWS amount and auditory arousal thresholds (AAT), as an independent index of sleep depth. Ten normal males slept for six consecutive nights in the laboratory: one adaptation, two baseline, two selective SWS deprivation and one recovery night. SWS deprivation allowed us to set the SWS amount during both deprivation nights close to zero, without any shortening of total sleep time. In the ensuing recovery night a significant SWS rebound was found, accompanied by an increase in AAT. In addition, REM frequency decreased significantly compared with baseline. This effect cannot be attributed to a variation in prior sleep duration, since there was no sleep loss during the selective SWS deprivation nights. Stepwise regression also showed that the decrease in REM frequency is not correlated with the increase in AAT, the traditional index of sleep depth, but is correlated with SWS rebound.     

Sleepiness and REM Sleep Recurrence: The Effects of Stage 2 and REM Sleep Awakenings

Determinants of daytime sleepiness include sleep length, sleep continuity, and circadian factors. Sleep stage composition has not been seen as influencing subsequent daytime functioning; however, earlier studies did not focus explicitly on sleepiness. The present experiment studied the effects of selective sleep-stage restriction on an objective measure of sleep tendency, and explored the relationship between sleepiness and subsequent REM recurrence during REM deprivation. Daytime sleep latency was measured by a modified Multiple Sleep Latency Test prior to and following two nights of awakenings from either REM or Stage 2 sleep in 16 normal young adults. Sleep latency following these awakenings was also measured. REM sleep and Stage 2 awakenings produced comparable levels of sleepiness, both during the Awakening Nights and subsequent daytime Multiple Sleep Latency Testing. Pooling the groups, daytime and nocturnal sleepiness measures were correlated within individuals. In the REM-Awakening Group, Pre-Awakening daytime sleepiness was associated with the tendency for REM sleep to recur following experimental awakenings. Comparable levels of sleepiness may result from nonspecific processes such as sleep curtailment and fragmentation, or alternatively from separate REM and Stage 2 mechanisms. The relationship between REM sleep and sleepiness is discussed in the context of both state and trait models.     

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

Recent studies have shown that periodically disrupted sleep resulted in significant daytime sleepiness and performance loss in normal young adults. One study suggested that the periodicity of disturbance rather than the total number of sleep disturbances was the primary factor in causing degraded function. However, in that study, increased performance levels could have been associated with increased levels of slow wave sleep. The present study was designed to determine whether the amount of SWS rather than the periodic disruption of sleep accounts for decreased performance of Ss with disrupted sleep. Twelve normal young adults spent two 4-night periods in the laboratory. During one 4-night series, Ss were briefly aroused either following each 10 min of sleep or whenever they entered stage 3 sleep (No SWS condition). During the second series of nights, Ss were briefly aroused after each 10 min of sleep (SWS condition). In the second series, additional arousals were performed after 5-min periods (but not when Ss were in SWS) to equalize the total number of arousals in the SWS conditions with those in the No SWS condition. Total experimental arousals were equal in the disruption conditions, and the experimental manipulation was successful in reducing total SWS to infrequent epochs of stage 3 in the No SWS condition while allowing significantly more SWS in the SWS condition. In terms of sleep stages, this difference was balanced by increased stage 2 in the No SWS condition. Despite the differential occurrence of SWS, no performance, mood, or nap latency measure was different in the SWS vs.(ABSTRACT TRUNCATED AT 250 WORDS)     

Slow wave sleep enhancement with gaboxadol reduces daytime sleepiness during sleep restriction

STUDY OBJECTIVES: To evaluate the impact of enhanced slow wave sleep (SWS) on behavioral, psychological, and physiological changes resulting from sleep restriction. DESIGN: A double-blind, parallel group, placebo-controlled design was used to compare gaboxadol (GBX) 15 mg, a SWS-enhancing drug, to placebo during 4 nights of sleep restriction (5 h/night). Behavioral, psychological, and physiological measures of the impact of sleep restriction were assessed in both groups at baseline, during sleep restriction and following recovery sleep. SETTING: Sleep research laboratory. PARTICIPANTS: Forty-one healthy adults; 9 males and 12 females (mean age: 32.0 +/- 9.9 y) in the placebo group and 10 males and 10 females (mean age: 31.9 +/- 10.2 y) in the GBX group. INTERVENTIONS: Both experimental groups underwent 4 nights of sleep restriction. Each group received either GBX 15 mg or placebo on all sleep restriction nights, and both groups received placebo on baseline and recovery nights. MEASUREMENTS AND RESULTS: Polysomnography documented a SWS-enhancing effect of GBX with no group difference in total sleep time during sleep restriction. The placebo group displayed the predicted deficits due to sleep restriction on the multiple sleep latency test (MSLT) and on introspective measures of sleepiness and fatigue. Compared to placebo, the GBX group showed significantly less physiological sleepiness on the MSLT and lower levels of introspective sleepiness and fatigue during sleep restriction. There were no differences between groups on the psychomotor vigilance task (PVT) and a cognitive test battery, but these measures were minimally affected by sleep restriction in this study. The correlation between change from baseline in MSLT on Day 6 and change from baseline in SWS on Night 6 was significant in the GBX group and in both group combined. CONCLUSIONS: The results of this study are consistent with the hypothesis that enhanced SWS, in this study produced by GBX, reduces physiological sleep tendency and introspective sleepiness and fatigue which typically result from sleep restriction.     

Relationship between sleep inertia and sleepiness: cumulative effects of four nights of sleep disruption/restriction on performance following abrupt nocturnal awakenings

Performance deficits are usually evident following both extended wakefulness (sleep deprivation effects) and immediately upon awakening from sleep (sleep inertia effects). In order to determine whether sleep inertia effects are qualitatively different from sleep deprivation effects, performance on addition tests, Stanford Sleepiness Scale (SSS) ratings, and return-to-sleep latencies (RSLs) were assessed during four nights of sleep disruption/restriction. Eight subjects were polygraphically monitored in the sleep laboratory for five consecutive nights, from 2400 to 0700. On the last four nights (after an adaptation night) subjects were awakened at 0040, 0140, 0240, 0340, 0440, and 0540 for a 20-min test session. Sleepiness ratings and performance on 5-min addition tests were measured at 1.5, 7.5, and 13.5 min post-awakening, and RSL was measured at the end of each test session. Analysis of addition test performance across nights revealed that both speed and accuracy of calculations were adversely affected by the sleep disruption/restriction procedure, indicating that increasing sleepiness exacerbates sleep performance deficits upon awakening. Although divergence of SSS ratings and addition test performance across nights was suggestive, there was no conclusive evidence that sleep inertia is qualitatively different from "typical" sleepiness.     

The effects of total sleep deprivation, selective sleep interruption and sleep recovery on pain tolerance thresholds in healthy subjects

The aim of this study was to compare the effects of total sleep deprivation (TSD), rapid eye movement (REM) sleep and slow wave sleep (SWS) interruption and sleep recovery on mechanical and thermal pain sensitivity in healthy adults. Nine healthy male volunteers (age 26--43 years) were randomly assigned in this double blind and crossover study to undergo either REM sleep or SWS interruption. Periods of 6 consecutive laboratory nights separated by at least 2 weeks were designed as follows: N1 Adaptation night; N2 Baseline night; N3 Total sleep deprivation (40 h); N4 and N5 SWS or REM sleep interruption; N6 Recovery. Sleep was recorded and scored using standard methods. Tolerance thresholds to mechanical and thermal pain were assessed using an electronic pressure dolorimeter and a thermode operating on a Peltier principle. Relative to baseline levels, TSD decreased significantly mechanical pain thresholds (-8%). Both REM sleep and SWS interruption tended to decrease mechanical pain thresholds. Recovery sleep, after SWS interruption produced a significant increase in mechanical pain thresholds (+ 15%). Recovery sleep after REM sleep interruption did not significantly increase mechanical pain thresholds. No significant differences in thermal pain thresholds were detected between and within periods. In conclusion this experimental study in healthy adult volunteers has demonstrated an hyperalgesic effect related to 40 h TSD and an analgesic effect related to SWS recovery. The analgesic effect of SWS recovery is apparently greater than the analgesia induced by level I (World Health Organization) analgesic compounds in mechanical pain experiments in healthy volunteers.     

24 hours of sleep deprivation in the rat increases sleepiness and decreases vigilance: introduction of the rat‐psychomotor vigilance task

A novel animal‐analog of the human psychomotor vigilance task (PVT) was validated by subjecting rats to 24 h of sleep deprivation (SD) and examining the effect on performance in the rat‐PVT (rPVT), and a rat multiple sleep latency test (rMSLT). During a three‐phase (separate cohorts) crossover design, vigilance performance in the rPVT was compared with 24 h SD‐induced changes in sleepiness assessed by polysomnographic evaluation and the rMSLT. Twenty‐four hours of SD was produced by brief rotation of activity wheels at regular intervals in which the animals resided throughout the experiment. In the rPVT experiment, exercise controls (EC) experienced the same overall amount of locomotor activity as during SD, but allowed long periods of undisturbed sleep. After 24 h SD response latencies slowed, and lapses increased significantly during rPVT performance when compared with baseline and EC conditions. During the first 3 h of the recovery period following 24 h SD, polysomnographic measures indicated sleepiness. Latency to fall asleep after 24 h SD was assessed six times during the first 3 h after SD. Rats fell asleep significantly faster immediately after SD, than after non‐SD baseline sessions. In conclusion, 24 h of SD in rats increased sleepiness, as indicated by polysomnography and the rMSLT, and impaired vigilance as measured by the rPVT. The rPVT closely resembles the human PVT test widely used in human sleep research and will assist investigation of the neurobiologic mechanisms that produce vigilance impairments after sleep disruption.     

Performance during frequent sleep disruption

Performance on a simple addition task was measured during three schedules of frequent sleep disruption for 2 nights. Five young adults had their sleep briefly disturbed for 2 nights in 3 separate weeks either every 1 min, every 10 min, or at sleep onset after an undisrupted 2.5-h sleep period. Subjects were required to perform a two-number, two-digit addition problem as rapidly as possible on awakening. Main effects were found for sleep disruption condition and time of night, and a significant interaction between the two was also observed. Latency to response was longest for the 10-min condition on night 1, on night 2, however, response latencies were longest in the 1-min condition. Response latencies were fastest in the 2.5-h condition for both nights of disruption. Arousal thresholds were also gathered across both nights. Arousal thresholds were consistently the highest in the 1- and 10-min conditions for both nights of disruption, reaching maximum threshold levels at the end of night 1. Arousal threshold was significantly positively correlated with response latency. Sleep stages (slow-wave sleep (SWS), SWS + REM (SWSR), and total sleep time minus stage 1 sleep) were poor predictors of performance changes across the 2 disruption nights. The data were best explained by sleep continuity theory, which posits that a period of at least 10 min of uninterrupted sleep is required for restoration to take place.     

Inter- and intra-individual variability in performance near the circadian nadir during sleep deprivation

The study purpose was to assess inter- and intra-individual variability in neurobehavioral function near the circadian nadir during sleep deprivation and conduct exploratory factor analyses to assess relationships among alertness and performance measures during sleep deprivation. Twenty-five healthy individuals (16 females) aged 18-25 years participated. Participants were sleep deprived for two nights under controlled laboratory conditions using a modified constant routine procedure. A comprehensive battery of neurobehavioral performance tests, subjective sleepiness (SSS), and objective alertness (MWT) were assessed. Seventeen of the 22 neurobehavioral measures were impaired by sleep deprivation (all P < 0.01). The use of multiple neurobehavioral performance measures revealed impairments for all individuals during sleep deprivation. However, sleep deprivation effects were task dependent within and between individuals. Gender contributed minimally to inter-individual variability in performance. Exploratory factor analysis reduced the 22 measures to seven independent factors. Our findings indicate that no individual was especially vulnerable or resistant to the performance impairing effects of sleep deprivation. Instead, inter- and intra-individual variability in performance during sleep deprivation was task dependent. The finding that subjective sleepiness and objective alertness were not related to any performance measure during sleep deprivation suggests that these measures may assess independent brain functions.     

Comparing the neurocognitive effects of 40 h sustained wakefulness in patients with untreated OSA and healthy controls

We hypothesized that individuals with untreated obstructive sleep apnea (OSA) would exhibit greater vulnerability to sleep deprivation than healthy controls, due to the additional neurobiological 'load' of chronic sleep fragmentation. After baseline sleep with 8 h time in bed, participants remained awake for 40 h. Psychomotor Vigilance Task (PVT, mean slowest 10% 1/RT), AusEd Driving Simulator task (steering and speed deviation), and subjective sleepiness (Karolinska Sleepiness Scale, KSS) were assessed every 2 h. Nonlinear mixed-effects models were used to characterize individual differences in baseline/average performance, the linear effect of increasing hours awake, circadian amplitude and phase. Eight participants with untreated OSA with mean (SD) age 44.6 (8.4), apnea–hypopnea index (AHI) 49.8 (24.7), Epworth Sleepiness Scale (ESS) 11.9 (4.8) and nine healthy controls age 27.8 (3.7), AHI 4.5 (2.7), ESS 7.3 (2.1) completed the protocol. Baseline KSS was significantly higher (1.4 units, P  = 0.03) in the OSA group and there was a trend toward lower baseline speed deviation on the AusEd ( P  = 0.05). After adjusting for the significant effects of accumulated time awake, circadian amplitude and phase (all P  < 0.005), there was no difference in performance decrements between those with and without sleep apnea in PVT, driving simulator performance and subjective sleepiness ( P  > 0.5). Random-effects modeling confirmed the presence of significant inter-individual variability in vulnerability to sleep deprivation. Patients with OSA did not respond differently to sleep deprivation than healthy controls. As expected, total sleep deprivation led to significant worsening in performance and subjective sleepiness in both groups.     

Low levels of alcohol impair driving simulator performance and reduce perception of crash risk in partially sleep deprived subjects

STUDY OBJECTIVES: Partial sleep deprivation and alcohol consumption are a common combination, particularly among young drivers. We hypothesized that while low blood alcohol concentration (<0.05 g/dL) may not significantly increase crash risk, the combination of partial sleep deprivation and low blood alcohol concentration would cause significant performance impairment. DESIGN: Experimental SETTING: Sleep Disorders Unit Laboratory PATIENTS OR PARTICIPANTS: 20 healthy volunteers (mean age 22.8 years; 9 men). INTERVENTIONS: Subjects underwent driving simulator testing at 1 am on 2 nights a week apart. On the night preceding simulator testing, subjects were partially sleep deprived (5 hours in bed). Alcohol consumption (2-3 standard alcohol drinks over 2 hours) was randomized to 1 of the 2 test nights, and blood alcohol concentrations were estimated using a calibrated Breathalyzer. During the driving task subjects were monitored continuously with electroencephalography for sleep episodes and were prompted every 4.5 minutes for answers to 2 perception scales-performance and crash risk. MEASUREMENTS AND RESULTS: Mean blood alcohol concentration on the alcohol night was 0.035 +/- 0.015 g/dL. Compared with conditions during partial sleep deprivation alone, subjects had more microsleeps, impaired driving simulator performance, and poorer ability to predict crash risk in the combined partial sleep deprivation and alcohol condition. Women predicted crash risk more accurately than did men in the partial sleep deprivation condition, but neither men nor women predicted the risk accurately in the sleep deprivation plus alcohol condition. CONCLUSIONS: Alcohol at legal blood alcohol concentrations appears to increase sleepiness and impair performance and the detection of crash risk following partial sleep deprivation. When partially sleep deprived, women appear to be either more perceptive of increased crash risk or more willing to admit to their driving limitations than are men. Alcohol eliminated this behavioral difference.     

Selective slow-wave sleep deprivation and time-of-night effects on cognitive performance upon awakening

We evaluated the effects of selective slow-wave sleep (SWS) deprivation and time-of-night factors on cognitive performance upon awakening. Ten normal men slept for 6 consecutive nights in the laboratory: 1 adaptation, 2 baseline, 2 selective SWS deprivation, and 1 recovery night. Cognitive performance was assessed by means of a Descending Subtraction Task after 2, 5, and 7.5 h of sleep. There was an almost complete selective SWS suppression during both deprivation nights, and a significant SWS rebound during the recovery sleep. Regarding cognitive performance, a progressive linear decrease of sleep inertia upon successive awakenings was found during all experimental nights except for the recovery night. In addition, a significant decrease of sleep inertia was observed upon the morning awakening of the second deprivation night for the measure of performance speed, and a significant increase of sleep inertia upon the morning awakening of the recovery night for the measure of performance accuracy. The results show that cognitive performance upon awakening is adversely affected by sleep depth and that, during the sleep-wake transition, cognitive performance accuracy is more impaired than performance speed.     

The effect of nap frequency on daytime sleep architecture

It is well documented that the quality and quantity of prior sleep influence future sleep. For instance, nocturnal sleep restriction leads to an increase in slow wave sleep (SWS) (i.e. SWS rebound) during a subsequent sleep period. However, few studies have examined how prior napping affects daytime sleep architecture. Because daytime naps are recommended for management of disrupted sleep, understanding the impact of napping on subsequent sleep may be important. We monitored sleep-wake patterns for one week with actigraphy followed by a 75-minute polysomnographically-recorded nap. We found that greater nap frequency was correlated with increased Stage 1 and decreased SWS. We categorized subjects based on nap frequency during the prior week (0 nap, 1 to 2 naps, and 3 to 4 naps) and found differences in Stage 1, Stage 2, and SWS between groups. Subjects who took no naps had the greatest amount of SWS, those who took 1 to 2 naps had the most Stage 2 sleep, and those who took 3 to 4 naps had the most Stage 1. While correlations were not found between nap frequency and nocturnal sleep measures, frequent napping was associated with increased subjective sleepiness. Therefore, frequent napping appears to be associated with lighter daytime sleep and increased sleepiness during the day. Speculatively, low levels of daytime sleepiness and increased SWS in non-nappers may help explain why these individuals choose not to nap.     

Relationships between affect, vigilance, and sleepiness following sleep deprivation

This pilot study examined the relationships between the effects of sleep deprivation on subjective and objective measures of sleepiness and affect, and psychomotor vigilance performance. Following an adaptation night in the laboratory, healthy young adults were randomly assigned to either a night of total sleep deprivation (SD group; n = 15) or to a night of normal sleep (non-SD group; n = 14) under controlled laboratory conditions. The following day, subjective reports of mood and sleepiness, objective sleepiness (Multiple Sleep Latency Test and spontaneous oscillations in pupil diameter, PUI), affective reactivity/regulation (pupil dilation responses to emotional pictures), and psychomotor vigilance performance (PVT) were measured. Sleep deprivation had a significant impact on all three domains (affect, sleepiness, and vigilance), with significant group differences for eight of the nine outcome measures. Exploratory factor analyses performed across the entire sample and within the SD group alone revealed that the outcomes clustered on three orthogonal dimensions reflecting the method of measurement: physiological measures of sleepiness and affective reactivity/regulation, subjective measures of sleepiness and mood, and vigilance performance. Sleepiness and affective responses to sleep deprivation were associated (although separately for objective and subjective measures). PVT performance was also independent of the sleepiness and affect outcomes. These findings suggest that objective and subjective measures represent distinct entities that should not be assumed to be equivalent. By including affective outcomes in experimental sleep deprivation research, the impact of sleep loss on affective function and their relationship to other neurobehavioral domains can be assessed.     

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.     

Sleepiness and Sleep State on a 90-Min Schedule

The effects of REM and slow wave sleep (SWS) on subjective sleepiness were studied in 10 subjects placed on a 90-min sleep-wakefulness schedule for either 5^1/3 or 6 (24-hr) days. Subjects were permitted to sleep for 30-min periods separated by 60 min of enforced wakefulness. Sleep recordings showed that sleep onset REM periods occurred frequently; REM and SWS appeared during the same sleep period only 27 times; and REM sleep tended to occur on sleep periods that alternated with SWS periods. Sleepiness was measured using the Stanford Sleepiness Scale (SSS) given 15 min before (pre-sleep) and 15 min after (post-sleep) each sleep period. Average SSS ratings showed a 24-hr fluctuation in sleepiness. In addition, negative and positive SSS changes tended to alternate with each 90-min period. Significant correlations were found with post-sleep SSS ratings and SWS and with pre-sleep SSS ratings and REM sleep. Differences between pre- and post-sleep SSS scores were also correlated with the sleep states: increased sleepiness was correlated with SWS and decreased sleepiness with REM sleep.     

EEG arousals in normal sleep: variations induced by total and selective slow-wave sleep deprivation

STUDY OBJECTIVES: Aim of the present study was to assess changes in arousal rates after selective slow-wave (SWS) and total sleep deprivations. DESIGN: Two-way mixed design comparing the arousal index (Al), as expressed by the number of EEG arousals divided by sleep duration, in totally or selectively sleep deprived subjects. SETTING: Sleep laboratory. PATIENTS OR PARTICIPANTS: Nineteen normal male subjects [mean age=23.3 years (S.E.M.=0.55)]. INTERVENTIONS: Al was measured in baseline nights and after selective SWS (N=10) and total sleep deprivation (N=9). MEASUREMENTS AND RESULTS: During the baseline nights AI values changed across sleep stages as follows: stage 1 > stage 2 and REM > SWS, but did not present any significant variations as a function of time elapsed from sleep onset. The recovery after deprivation showed a reduction in EEG arousals, more pronounced after total sleep deprivation; this decrease affected NREM but not REM sleep. During the baseline nights Al showed a close-to-significance negative correlation with REM duration, while during the recovery nights a significant positive relation with stage 1 duration was found. CONCLUSIONS: The present results suggest that recuperative processes after sleep deprivation are also associated with a higher sleep continuity as defined by the reduction of EEG arousals.