Effects of rapid versus slow accumulation of eight hours of sleep loss

The present study assessed alertness, memory, and performance following three schedules of approximately 8 hr of sleep loss (slow, intermediate, and rapid accumulation) in comparison to an 8-hr time in bed (TIB) sleep schedule. Twelve healthy individuals aged 21-35 completed each of four conditions according to a Latin Square design: no sleep loss (8-hr TIB for 4 nights; 2300-0700), slow (6-hr TIB for 4 nights; 0100-0700), intermediate (4-hr TIB for 2 nights; 0300-0700), and rapid (0-hr TIB for 1 night) sleep loss. On each day, participants completed a multiple sleep latency test (MSLT), a probed-recall memory task, a psychomotor vigilance task, a divided attention task, and the Profile of Mood States. "Rapid" sleep loss produced significantly more impairment on tests of alertness, memory, and performance compared to the "slow" accumulation of a comparable amount of sleep loss. The impairing effects of sleep loss vary as a function of rate, suggesting the presence of a compensatory adaptive mechanism operating in conjunction with the accumulation of a sleep debt.     

Neurobehavioral Dynamics Following Chronic Sleep Restriction: Dose-Response Effects of One Night for Recovery

Objective:

Establish the dose-response relationship between increasing sleep durations in a single night and recovery of neurobehavioral functions following chronic sleep restriction.

Design:

Intent-to-treat design in which subjects were randomized to 1 of 6 recovery sleep doses (0, 2, 4, 6, 8, or 10 h TIB) for 1 night following 5 nights of sleep restriction to 4 h TIB.

Setting:

Twelve consecutive days in a controlled laboratory environment.

Participants:

N = 159 healthy adults (aged 22-45 y), median = 29 y).

Interventions:

Following a week of home monitoring with actigraphy and 2 baseline nights of 10 h TIB, subjects were randomized to either sleep restriction to 4 h TIB per night for 5 nights followed by randomization to 1 of 6 nocturnal acute recovery sleep conditions (N = 142), or to a control condition involving 10 h TIB on all nights (N = 17).

Measurements and Results:

Primary neurobehavioral outcomes included lapses on the Psychomotor Vigilance Test (PVT), subjective sleepiness from the Karolinska Sleepiness Scale (KSS), and physiological sleepiness from a modified Maintenance of Wakefulness Test (MWT). Secondary outcomes included psychomotor and cognitive speed as measured by PVT fastest RTs and number correct on the Digit Symbol Substitution Task (DSST), respectively, and subjective fatigue from the Profile of Mood States (POMS). The dynamics of neurobehavioral outcomes following acute recovery sleep were statistically modeled across the 0 h-10 h recovery sleep doses. While TST, stage 2, REM sleep and NREM slow wave energy (SWE) increased linearly across recovery sleep doses, best-fitting neurobehavioral recovery functions were exponential across recovery sleep doses for PVT and KSS outcomes, and linear for the MWT. Analyses based on return to baseline and on estimated intersection with control condition means revealed recovery was incomplete at the 10 h TIB (8.96 h TST) for PVT performance, KSS sleepiness, and POMS fatigue. Both TST and SWE were elevated above baseline at the maximum recovery dose of 10 h TIB.

Conclusions:

Neurobehavioral deficits induced by 5 nights of sleep restricted to 4 h improved monotonically as acute recovery sleep dose increased, but some deficits remained after 10 h TIB for recovery. Complete recovery from such sleep restriction may require a longer sleep period during 1 night, and/or multiple nights of recovery sleep. It appears that acute recovery from chronic sleep restriction occurs as a result of elevated sleep pressure evident in both increased SWE and TST.

Citation:

Banks S; Van Dongen HPA; Maislin G; Dinges DF. Neurobehavioral dynamics following chronic sleep restriction: dose-response effects of one night for recovery. SLEEP 2010;33(8):1013–1026.     

No effect of 8-week time in bed restriction on glucose tolerance in older long sleepers

The aim of this study was to investigate the effects of 8 weeks of moderate restriction of time in bed (TIB) on glucose tolerance and insulin sensitivity in healthy older self-reported long sleepers. Forty-two older adults (ages 50-70 years) who reported average sleep durations of >or=8.5 h per night were assessed. Following a 2-week baseline, participants were randomly assigned to two 8-week treatments: either (i) TIB restriction (n = 22), which involved following a fixed sleep schedule in which time in bed was reduced by 90 min compared with baseline; (ii) a control (n = 18), which involved following a fixed sleep schedule but no imposed change of TIB. Sleep was monitored continuously via wrist actigraphy recordings, supplemented with a daily diary. Glucose tolerance and insulin sensitivity were assessed before and following the treatments. Compared with the control treatment, TIB restriction resulted in a significantly greater reduction of nocturnal TIB (1.39 +/- 0.40 h versus 0.14 +/- 0.26 h), nocturnal total sleep time (TST) (1.03 +/- 0.53 h versus 0.40 +/- 0.42 h), and 24-h TST (1.03 +/- 0.53 h versus 0.33 +/- 0.43 h) from baseline values. However, no significant effect of TIB restriction was found for glucose tolerance or insulin sensitivity. These results suggest that healthy older long sleepers can tolerate 8 weeks of moderate TIB restriction without impairments in glucose tolerance or insulin sensitivity.     

Emotional working memory during sustained wakefulness

In the present study we investigated whether one night of sleep deprivation can affect working memory (WM) performance with emotional stimuli. Twenty‐five subjects were tested after one night of sleep deprivation and after one night of undisturbed sleep at home. As a second aim of the study, to evaluate the cumulative effects of sleep loss and of time‐of‐day changes on emotional WM ability, the subjects were tested every 4 h, from 22:00 to 10:00 hours, in four testing sessions during the sleep deprivation period (deprivation sessions: D1, D2, D3 and D4). Subjects performed the following test battery: Psychomotor Vigilance Task, 0‐back task, 2‐back task and an ‘emotional 2‐back task’ with neutral, positive and negative emotional pictures selected from the International Affective Picture System. Results showed lower accuracy in the emotional WM task when the participants were sleep‐deprived relative to when they had slept, suggesting the crucial role of sleep for preserving WM ability. In addition, the accuracy for the negative pictures remains stable during the sessions performed from 22:00 to 06:00 hours (D1, D2 and D3), while it drops at the D4 session, when the participants had accumulated the longest sleep debt. It is suggested that, during sleep loss, attentional and WM mechanisms may be sustained by the higher arousing characteristics of the emotional (negative) stimuli.     

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.     

The spectrum of the non‐rapid eye movement sleep electroencephalogram following total sleep deprivation is trait‐like

The sleep electroencephalogram (EEG) spectrum is unique to an individual and stable across multiple baseline recordings. The aim of this study was to examine whether the sleep EEG spectrum exhibits the same stable characteristics after acute total sleep deprivation. Polysomnography (PSG) was recorded in 20 healthy adults across consecutive sleep periods. Three nights of baseline sleep [12 h time in bed (TIB)] following 12 h of wakefulness were interleaved with three nights of recovery sleep (12 h TIB) following 36 h of sustained wakefulness. Spectral analysis of the non‐rapid eye movement (NREM) sleep EEG (C3LM derivation) was used to calculate power in 0.25 Hz frequency bins between 0.75 and 16.0 Hz. Intraclass correlation coefficients (ICCs) were calculated to assess stable individual differences for baseline and recovery night spectra separately and combined. ICCs were high across all frequencies for baseline and recovery and for baseline and recovery combined. These results show that the spectrum of the NREM sleep EEG is substantially different among individuals, highly stable within individuals and robust to an experimental challenge (i.e. sleep deprivation) known to have considerable impact on the NREM sleep EEG. These findings indicate that the NREM sleep EEG represents a trait.     

Recovery sleep and performance following sleep deprivation with dextroamphetamine

Twelve subjects were studied to determine the after-effects of using three 10-mg doses of dextroamphetamine to sustain alertness during sleep deprivation. Sleep architecture during recovery sleep was evaluated by comparing post-deprivation sleep beginning 15 h after the last dextroamphetamine dose to post-deprivation sleep after placebo. Performance and mood recovery were assessed by comparing volunteers who received dextroamphetamine first (during sleep deprivation) to those who received placebo first. Stages 1 and 2 sleep, movement time, REM latency, and sleep latency increased on the night after sleep deprivation with dextroamphetamine vs. placebo. Stage 4 was unaffected. Comparisons to baseline revealed more stage 1 during baseline than during either post-deprivation sleep period and more stage 2 during baseline than during sleep following placebo. Stage 4 sleep was lower during baseline than it was after either dose, and REM sleep was lower during baseline and after dextroamphetamine than after placebo. Sleep onset was slowest on the baseline night. Next-day performance and mood were not different as a function of whether subjects received dextroamphetamine or placebo during deprivation. These data suggest dextroamphetamine alters post-deprivation sleep architecture when used to sustain alertness during acute sleep loss, but next-day performance and subjective mood ratings are not substantially affected. A recovery sleep period of only 8 h appears to be adequate to regain baseline performance levels after short-term sleep deprivation.     

Relation between ambulatory actigraphy and laboratory polysomnography in insomnia practice and research

Actigraphy is increasingly used in practice and research studies because of its relative low cost and decreased subject burden. How multiple nights of at‐home actigraphy compare to one independent night of in‐laboratory polysomnography (PSG) has not been examined in people with insomnia. Using event markers (MARK) to set time in bed (TIB) compared to automatic program analysis (AUTO) has not been systematically evaluated. Subjects (n = 30) meeting DSM‐5 criteria for insomnia and in‐laboratory PSG sleep efficiency (SE) of <85% were studied. Subjects were free of psychiatric, sleep or circadian disorders, other chronic conditions and medications that effect sleep. Subjects had an in‐laboratory PSG, then were sent home for 7 nights with Philips Actiwatch Spectrum Plus. Data were analysed using Philips Actiware version 6. Using the mean of seven nights, TIB, total sleep time (TST), SE, sleep‐onset latency (SOL) and wake after sleep onset (WASO) were examined. Compared to PSG, AUTO showed longer TIB and TST and less WASO. MARK only differed from PSG with decreased WASO. Differences between the PSG night and the following night at home were found, with better sleep on the first night home. Actigraphy in people with insomnia over seven nights is a valid indicator of sleep compared to an independent in‐laboratory PSG. Event markers increased the validity of actigraphy, showing no difference in TIB, TST, SE and SOL. AUTO was representative of SE and SOL. Increased SE and TST without increased TIB suggests possible compensatory sleep the first at night home after in‐laboratory PSG.     

Symptoms of sleep disturbance in persons with Alzheimer's disease and normal elderly

We retrospectively analyzed sleep time and sleep disturbance symptoms in 399 healthy, non-demented elderly (NDE) and 263 persons with a diagnosis of possible (n = 53) or probable (n = 210) Alzheimer's disease (AD). Our primary objective was to determine differences in subjective sleep disturbance between these samples. Secondary objectives were to determine if subjects with time in bed (TIB) < or =6 h per night reported more sleep disturbance and whether sleep complaints were associated with more severe cognitive and/or functional impairment. The prevalence of 'sleep problems' (a single item) was significantly lower in NDE (18.3%) than AD (27.6%), and the proportions of each cohort reporting TIB < or =6 h per night were very low (NDE: 6.0%; AD: 3.5%) and not significantly different. Less TIB was correlated with better cognitive function for AD (P < 0.01), and cognition and function were significantly worse for AD subjects with estimates of >6 h of TIB compared with those with estimates of < or =6 h (P < 0.05). Greater sleep disturbance was correlated with greater functional impairment in both cohorts; but only in AD did greater estimated TIB also correlate with greater functional impairment (all P < 0.05). In general, estimated TIB was not associated with mood in either cohort; however, in both cohorts depression was significantly associated with sleep disturbance symptoms and was significantly worse in those who reported having 'sleep problems'. There was no association between subjective perception of 'sleep problems', the number and frequency of sleep disturbance symptoms, and estimated TIB in either group.     

Effects of sleep restriction on the sleep electroencephalogram of adolescents

Study ObjectivesThis report describes findings from an ongoing longitudinal study of the effects of varied sleep durations on wake and sleep electroencephalogram (EEG) and daytime function in adolescents. Here, we focus on the effects of age and time in bed (TIB) on total sleep time (TST) and nonrapid eye movement (NREM) and rapid eye movement (REM) EEG.MethodsWe studied 77 participants (41 male) ranging in age from 9.9 to 16.2 years over the 3 years of this study. Each year, participants adhered to each of three different sleep schedules: four consecutive nights of 7, 8.5, or 10 h TIB.ResultsAltering TIB successfully modified TST, which averaged 406, 472 and 530 min on the fourth night of 7, 8.5, and 10 h TIB, respectively. As predicted by homeostatic models, shorter sleep durations produced higher delta power in both NREM and REM although these effects were small. Restricted sleep more substantially reduced alpha power in both NREM and REM sleep. In NREM but not REM sleep, sleep restriction strongly reduced both the all-night accumulation of sigma EEG activity (11–15 Hz energy) and the rate of sigma production (11–15 Hz power).ConclusionsThe EEG changes in response to TIB reduction are evidence of insufficient sleep recovery. The decrease in sigma activity presumably reflects depressed sleep spindle activity and suggests a manner by which sleep restriction reduces waking cognitive function in adolescents. Our results thus far demonstrate that relatively modest TIB manipulations provide a useful tool for investigating adolescent sleep biology.     

The cumulative cost of additional wakefulness: dose-response effects on neurobehavioral functions and sleep physiology from chronic sleep restriction and total sleep deprivation

OBJECTIVES: To inform the debate over whether human sleep can be chronically reduced without consequences, we conducted a dose-response chronic sleep restriction experiment in which waking neurobehavioral and sleep physiological functions were monitored and compared to those for total sleep deprivation. DESIGN: The chronic sleep restriction experiment involved randomization to one of three sleep doses (4 h, 6 h, or 8 h time in bed per night), which were maintained for 14 consecutive days. The total sleep deprivation experiment involved 3 nights without sleep (0 h time in bed). Each study also involved 3 baseline (pre-deprivation) days and 3 recovery days. SETTING: Both experiments were conducted under standardized laboratory conditions with continuous behavioral, physiological and medical monitoring. PARTICIPANTS: A total of n = 48 healthy adults (ages 21-38) participated in the experiments. INTERVENTIONS: Noctumal sleep periods were restricted to 8 h, 6 h or 4 h per day for 14 days, or to 0 h for 3 days. All other sleep was prohibited. RESULTS: Chronic restriction of sleep periods to 4 h or 6 h per night over 14 consecutive days resulted in significant cumulative, dose-dependent deficits in cognitive performance on all tasks. Subjective sleepiness ratings showed an acute response to sleep restriction but only small further increases on subsequent days, and did not significantly differentiate the 6 h and 4 h conditions. Polysomnographic variables and delta power in the non-REM sleep EEG-a putative marker of sleep homeostasis--displayed an acute response to sleep restriction with negligible further changes across the 14 restricted nights. Comparison of chronic sleep restriction to total sleep deprivation showed that the latter resulted in disproportionately large waking neurobehavioral and sleep delta power responses relative to how much sleep was lost. A statistical model revealed that, regardless of the mode of sleep deprivation, lapses in behavioral alertness were near-linearly related to the cumulative duration of wakefulness in excess of 15.84 h (s.e. 0.73 h). CONCLUSIONS: Since chronic restriction of sleep to 6 h or less per night produced cognitive performance deficits equivalent to up to 2 nights of total sleep deprivation, it appears that even relatively moderate sleep restriction can seriously impair waking neurobehavioral functions in healthy adults. Sleepiness ratings suggest that subjects were largely unaware of these increasing cognitive deficits, which may explain why the impact of chronic sleep restriction on waking cognitive functions is often assumed to be benign. Physiological sleep responses to chronic restriction did not mirror waking neurobehavioral responses, but cumulative wakefulness in excess of a 15.84 h predicted performance lapses across all four experimental conditions. This suggests that sleep debt is perhaps best understood as resulting in additional wakefulness that has a neurobiological "cost" which accumulates over time.     

Banking Sleep: Realization of Benefits During Subsequent Sleep Restriction and Recovery

Objective:

Determine whether sleep extension (a) improves alertness and performance during subsequent sleep restriction and (b) impacts the rate at which alertness and performance are restored by post-restriction recovery sleep.

Design:

Participants were randomly assigned to an Extended (10 h time in bed [TIB]) or Habitual TIB [mean (SD) hours = 7.09 (0.7)] sleep group for one week, followed by 1 Baseline (10 hours or habitual TIB), 7 Sleep Restriction (3 h TIB), and 5 Recovery Sleep nights (8 h TIB). Performance and alertness tests were administered hourly between 08:00–18:00 during all in-laboratory phases of the study.

Setting:

Residential sleep/performance testing facility.

Participants:

Twenty-four healthy adults (ages 18–39) participated in the study.

Interventions:

Extended vs. habitual sleep durations prior to sleep restriction.

Results:

Psychomotor vigilance task (PVT) lapses were more frequent and modified maintenance of wakefulness (MWT) sleep latency was shorter in the Habitual group than in the Extended group across the sleep restriction phase. During the Recovery phase, PVT speed rebounded faster (and PVT lapsing recovered significantly after the first night of recovery sleep) in the Extended group. No group differences in subjective sleepiness were evident during any phase of the study.

Conclusion:

The extent to which sleep restriction impairs objectively measured alertness and performance, and the rate at which these impairments are subsequently reversed by recovery sleep, varies as a function of the amount of nightly sleep obtained prior to the sleep restriction period. This suggests that the physiological mechanism(s) underlying chronic sleep debt undergo long-term (days/weeks) accommodative/adaptive changes.

Citation:

Rupp TL; Wesensten NJ; Bliese PD; Balkin TJ. Banking sleep: realization of benefits during subsequent sleep restriction and recovery. SLEEP 2009;32(3):311–321.     

The effect of varying prophylactic naps on performance, alertness and mood throughout a 52-hour continuous operation

The current study reports the effect of 0-8-hr naps placed prior to two consecutive nights of total sleep deprivation. A total of 104 young adult male subjects were randomly assigned to one of four prophylactic nap conditions (0, 2, 4 or 8 hr). After a normal baseline night of sleep and a morning of baseline test performance, subjects returned to bed at 1200, 1600 or 1800 hr or not at all prior to a continuous operation that extended until each subject's normal bedtime on the third following night. All subjects who napped arose at 2000 hr, and all subjects maintained the same schedule of computer-administered performance tests throughout the sleep-loss period. Results indicated that performance and alertness in all nap conditions were improved in a dose-response fashion compared to a no-nap control throughout the first 24 hr of sleep loss. However, significant improvement in nap conditions compared to the no-nap condition was not seen in many variables during the second night of sleep loss. Whereas an 8-hr nap prior to an operation maintained performance at a high level for 24-30 hr, significant improvement in alertness and performance as compared to the no-nap control was also documented by shorter naps. No nap could reverse the profound loss of alertness seen during the second night of sleep loss.     

The impact of music upon sleep tendency as measured by the multiple sleep latency test and maintenance of wakefulness test

Previous work has shown that background noise or music has a small positive impact on performance during sleep deprivation. The current study examined the effect of background music on the ability to fall asleep or remain awake. Twelve normal-sleeping young adults took multiple sleep latency tests (MSLT) and maintenance of wakefulness tests (MWT) after baseline sleep and one night of total sleep deprivation either with background music or under standard (quiet) conditions. It was hypothesized that the music would help maintain wakefulness both under baseline and sleep deprivation conditions. The results of the study showed that sleep latencies were increased in both MSLT and MWT when music was presented, but that this effect occurred primarily before subjects were sleep-deprived (a significant Music by Sleep Deprivation interaction). Sleep latencies were 15 and 11 min on the MSLT (33 and 26 min on the MWT) with Music as compared to Quiet after baseline sleep. Heart rate, used as a measure of physiological arousal, was significantly elevated in MWT and MSLT trials where music was presented. These data support previous work showing that level of arousal has an impact on measured sleep tendency which is independent of that of the sleep system. On a practical level, these data indicate that music may play a small beneficial role in helping to maintain arousal.     

Interaction of chronic sleep restriction and circadian system in humans

Nocturnal sleep restriction and compensation with daytime naps is common in today’s society. In a between‐participants design, we examined the effects of chronic (10 nights) sleep restriction on 24 h plasma melatonin profiles in humans. Following a baseline period with 8.2 h time in bed (TIB) for sleep, participants were randomized to a control (8.2 h TIB) or sleep‐restriction condition (4.2 h TIB), with and without diurnal naps. Sleep restriction was achieved via delaying bedtime and advancing wake time by 2 h each relative to the baseline sleep period. Participants were maintained in a controlled, time isolated laboratory environment throughout the protocol, with light levels below 40 lx at all times. Twenty‐four hour plasma melatonin profiles were assessed at baseline and at the end of the sleep‐restriction period, with subjects maintained in a constant posture protocol. Compared with the baseline assessment and the 8.2 h TIB control group, a significant phase delay in melatonin onset (1.2 ± 0.9 h) occurred in all sleep‐restriction (4.2 h TIB) groups (P < 0.05). There was no evidence of a phase advance or shortening of the period of melatonin secretion associated with the advanced waking time. These results suggest that nocturnal light and dark exposure may be more potent in effecting circadian phase shifts than exposure to morning light, at least in conditions of controlled, dim lighting in the laboratory.     

Residual,differential neurobehavioral deficits linger after multiple recovery nights following chronic sleep restriction or acute total sleep deprivation

Study ObjectivesThe amount of recovery sleep needed to fully restore well-established neurobehavioral deficits from sleep loss remains unknown, as does whether the recovery pattern differs across measures after total sleep deprivation (TSD) and chronic sleep restriction (SR).MethodsIn total, 83 adults received two baseline nights (10–12-hour time in bed [TIB]) followed by five 4-hour TIB SR nights or 36-hour TSD and four recovery nights (R1–R4; 12-hour TIB). Neurobehavioral tests were completed every 2 hours during wakefulness and a Maintenance of Wakefulness Test measured physiological sleepiness. Polysomnography was collected on B2, R1, and R4 nights.ResultsTSD and SR produced significant deficits in cognitive performance, increases in self-reported sleepiness and fatigue, decreases in vigor, and increases in physiological sleepiness. Neurobehavioral recovery from SR occurred after R1 and was maintained for all measures except Psychomotor Vigilance Test (PVT) lapses and response speed, which failed to completely recover. Neurobehavioral recovery from TSD occurred after R1 and was maintained for all cognitive and self-reported measures, except for vigor. After TSD and SR, R1 recovery sleep was longer and of higher efficiency and better quality than R4 recovery sleep.ConclusionsPVT impairments from SR failed to reverse completely; by contrast, vigor did not recover after TSD; all other deficits were reversed after sleep loss. These results suggest that TSD and SR induce sustained, differential biological, physiological, and/or neural changes, which remarkably are not reversed with chronic, long-duration recovery sleep. Our findings have critical implications for the population at large and for military and health professionals.     

Leptin and hunger levels in young healthy adults after one night of sleep loss

Short‐term sleep curtailment associated with activation of the stress system in healthy, young adults has been shown to be associated with decreased leptin levels, impaired insulin sensitivity, and increased hunger and appetite. To assess the effects of one night of sleep loss in a less stressful environment on hunger, leptin, adiponectin, cortisol and blood pressure/heart rate, and whether a 2‐h mid‐afternoon nap reverses the changes associated with sleep loss, 21 young healthy individuals (10 men, 11 women) participated in a 7‐day sleep deprivation experiment (four consecutive nights followed by one night of sleep loss and two recovery nights). Half of the subjects were randomly assigned to take a mid‐afternoon nap (14:00–16:00 hours) the day following the night of total sleep loss. Serial 24‐h blood sampling and hunger scales were completed on the fourth (predeprivation) and sixth day (postdeprivation). Leptin levels were significantly increased after one night of total sleep loss, whereas adiponectin, cortisol levels, blood pressure/heart rate, and hunger were not affected. Daytime napping did not influence the effects of sleep loss on leptin, adiponectin, or hunger. Acute sleep loss, in a less stressful environment, influences leptin levels in an opposite manner from that of short‐term sleep curtailment associated with activation of the stress system. It appears that sleep loss associated with activation of the stress system but not sleep loss per se may lead to increased hunger and appetite and hormonal changes, which ultimately may lead to increased consumption of ‘comfort’ food and obesity.     

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.     

Effects of prolonged wakefulness on cyclic alternating pattern (CAP) during sleep recovery at different circadian phases

Two separate groups of healthy subjects aged between 20 and 30 years underwent a random sequence of two non-consecutive polysomnographic recordings under standard conditions (night basal sleep) and after continuous sleep deprivation (recovery sleep). In the first group of 6 subjects (3 males and 3 females) recovery sleep occurred in the morning (after 24 h of prior waking); in the second group of 6 subjects (3 males and 3 females) recovery sleep occurred in the night (after 36 h of prior waking). In all cases the recording time was restricted to 500 minutes. Scoring was accomplished on conventional sleep variables and on Cyclic Alternating Pattern (CAP) parameters, while statistical analysis was based on a 2 x 2 ANOVA test. Compared to the night basal conditions, total sleep time and total NREM sleep were significantly longer in night recovery sleep and shorter in morning recovery sleep, respectively. No significant differences were found for sleep latency, intra-sleep awakenings, stage 2, REM sleep, NREM stages and slow-wave sleep. Total CAP time, CAP time in slow-wave sleep and all CAP rates were significantly higher in morning recovery sleep and lower in night recovery sleep. The enhanced amounts of CAP time and CAP rates during morning recovery sleep may be the outcome of two opposite forces, i.e. high sleep pressure versus maximum wake propensity. In contrast, the lower values of CAP during night recovery sleep suggest an in-phase associations between strong sleep pressure and the circadian clock.     

Development of sleep patterns in early adolescence

This study examines the developmental changes of sleep patterns as a function of gender and puberty and assesses the prevalence of sleep habits and sleep disturbances in early adolescence. It also investigates the relationship between sleep patterns, sleep habits and difficulty falling asleep and nocturnal awakenings. The present analyses are based on results available for 588 boys and 558 girls for whom mothers completed questions concerning demographics and sleep at annual intervals when their child was aged 10--13 years. The results indicated that nocturnal sleep times decreased, bedtimes were delayed and differences between weekend and school day sleep schedules progressively increased with age. Gender and puberty were both associated with the timing of sleep on weekends. Girls presented longer weekend time in bed (TIB) and later weekend wake time than boys. Similarly, subjects with higher pubertal status showed longer weekend TIB and later weekend wake time than subjects with lower pubertal status. Difficulty falling asleep was associated with later weekend wake time and with sleeping with a night light. In conclusion, the gender differences commonly reported in adolescents' sleep patterns are most likely explained by girls' higher pubertal status. This study emphasizes the link between puberty and a putative physiological need for more sleep, in presence of a general reduction of sleep times during adolescence. From age 10--13 years, the delay and lengthening of the sleep period on weekends in comparison to schooldays is associated with difficulty falling asleep.