Beta EEG reflects sensory processing in active wakefulness and homeostatic sleep drive in quiet wakefulness

Markers of sleep drive (<10 Hz; slow‐wave activity and theta) have been identified in the course of slow‐wave sleep and wakefulness. So far, higher frequencies in the waking electroencephalogram have not been examined thoroughly as a function of sleep drive. Here, electroencephalogram dynamics were measured in epochs of active wake (wake characterized by high muscle tone) or quiet wake (wake characterized by low muscle tone). It was hypothesized that the higher beta oscillations (15–35 Hz, measured by local field potential and electroencephalography) represent fundamentally different processes in active wake and quiet wake. In active wake, sensory stimulation elevated beta activity in parallel with gamma (80–90 Hz) activity, indicative of cognitive processing. In quiet wake, beta activity paralleled slow‐wave activity (1–4 Hz) and theta (5–8 Hz) in tracking sleep need. Cerebral lactate concentration, a measure of cerebral glucose utilization, increased during active wake whereas it declined during quiet wake. Mathematical modelling of state‐dependent dynamics of cortical lactate concentration was more precisely predictive when quiet wake and active wake were included as two distinct substates rather than a uniform state of wakefulness. The extent to which lactate concentration declined in quiet wake and increased in active wake was proportionate to the amount of beta activity. These data distinguish quiet wake from active wake. Quiet wake, particularly when characterized by beta activity, is permissive to metabolic and electrophysiological changes that occur in slow‐wave sleep. These data urge further studies on state‐dependent beta oscillations across species.     

The effects of sleep deprivation in humans: topographical electroencephalogram changes in non‐rapid eye movement (NREM) sleep versus REM sleep

Studies on homeostatic aspects of sleep regulation have been focussed upon non‐rapid eye movement (NREM) sleep, and direct comparisons with regional changes in rapid eye movement (REM) sleep are sparse. To this end, evaluation of electroencephalogram (EEG) changes in recovery sleep after extended waking is the classical approach for increasing homeostatic need. Here, we studied a large sample of 40 healthy subjects, considering a full‐scalp EEG topography during baseline (BSL) and recovery sleep following 40 h of wakefulness (REC). In NREM sleep, the statistical maps of REC versus BSL differences revealed significant fronto‐central increases of power from 0.5 to 11 Hz and decreases from 13 to 15 Hz. In REM sleep, REC versus BSL differences pointed to significant fronto‐central increases in the 0.5–7 Hz and decreases in the 8–11 Hz bands. Moreover, the 12–15 Hz band showed a fronto‐parietal increase and that at 22–24 Hz exhibited a fronto‐central decrease. Hence, the 1–7 Hz range showed significant increases in both NREM sleep and REM sleep, with similar topography. The parallel change of NREM sleep and REM sleep EEG power is related, as confirmed by a correlational analysis, indicating that the increase in frequency of 2–7 Hz possibly subtends a state‐aspecific homeostatic response. On the contrary, sleep deprivation has opposite effects on alpha and sigma activity in both states. In particular, this analysis points to the presence of state‐specific homeostatic mechanisms for NREM sleep, limited to <2 Hz frequencies. In conclusion, REM sleep and NREM sleep seem to share some homeostatic mechanisms in response to sleep deprivation, as indicated mainly by the similar direction and topography of changes in low‐frequency activity.     

Sleep tendency during extended wakefulness: insights into adolescent sleep regulation and behavior

Sleep tendency (latency to sleep onset) was examined during extended waking in prepubertal and mature adolescents to determine whether sleep pressure is lower near bedtime in the latter group. Participants were nine prepubertal (pubertal stage Tanner 1, mean age 11.1 years, SD+/-1.3 years, five males) and 11 pubertally mature adolescents (Tanner 5, 13.9+/-1.2 years, three males). They spent 10 nights at home on an identical fixed 10-h sleep schedule followed by a 36-h constant routine with sleep latency tests at 2-h intervals using standard polysomnography. Saliva was collected to assess dim-light melatonin onset (DLMO) phase. DLMO was earlier in the Tanner 1 (mean clock time=20:33 hours, SD=49 min) than Tanner 5 group (21:29 hours+/-42 min). Sleep latency compared at a 'critical period' spanning 12.5 (20:30 hours clock time) to 18.5 h (02:30 hours) after waking did not differ at 20:30 hours, but was shorter for the Tanner 1 group at 22:30 hours (Tanner 1=9.2+/-6.3 min; Tanner 5=15.7+/-5.8 min), 00:30 hours (Tanner 1=3.6+/-1.7 min; Tanner 5=9.0+/-6.4 min), and 02:30 hours (Tanner 1=2.0+/-1.7 min; Tanner 5=4.3+/-3.2 min; trend). These differences were apparent controlling for circadian phase by partial correlation. Sleep tendency after 14.5, 16.5, and 18.5 h awake was lower in mature versus prepubertal adolescents, supporting our hypothesis that a developmental change of intrinsic sleep-wake regulation may provide physiologically mediated 'permission' for later bedtimes in older adolescents.     

The pendulum technique for paradoxical sleep deprivation in rats

A new technique for paradoxical sleep (PS) deprivation in rats is presented. Animals are prevented from entering into PS by allowing them to sleep for only brief periods of time. This is accomplished by an apparatus which moves the animals' cages backwards and forwards like a pendulum. At the extremes of the motion postural imbalance is produced in the animals forcing them to walk downwards to the other side of their cages. A minimal amount of PS and a moderate amount of slow wave sleep (SWS) were detected during a deprivation period of 72 hrs. Following the deprivation treatment the recovery of sleep was monitored for 3 hrs; at the beginning of the light period for one group and at the beginning of the dark period for a second group. The sleep-waking patterns of two baseline groups were established at the time when the recovery sleep was examined in the deprivation groups. The deprivation treatment resulted in a significant increase in the amount of PS and a significant decrease in the amount of SWS. The extent of PS increase was similar in both deprivation groups, in spite of a large difference in the amount of SWS. The decrease of SWS mainly occurred during recovery sleep in the light. It was observed that sleep in the dark differs from sleep in the light in behavioural aspects.     

Sleep and sleep homeostasis in constant darkness in the rat

According to the two-process model of sleep regulation, a homeostatic Process S increases during waking and decreases during sleep. The time course of Process S can be derived on the basis of changes in vigilance states and changes in electroencephalogram slow-wave activity (SWA, activity below 4 Hz) during non-rapid eye movement (NREM) sleep. In most mouse strains, an optimal fit between S and SWA was achieved with one increasing (active during waking and REM sleep) and one decreasing time constant (active during NREM sleep) for Process S. However, in the rat, systematic deviations in the light and dark periods were observed, which were resolved by introducing different decreasing time constants between the light and dark periods. The present study shows that this difference between the rest (light) and active (dark) phases remains, and may even be larger, after animals are adapted to constant dark conditions for at least a week. In addition, the data show that the build-up rate of SWA at the onset of a NREM sleep episode is slow compared with the increase rate under light–dark conditions, and that this build-up rate changes with the circadian phase. The slow build-up rate introduces a systematic error between the simulation of Process S and SWA in NREM sleep. The circadian modulation of the build-up rate may, together with circadian changes in NREM sleep episode duration, be the source of the necessity of introducing a difference in the decreasing time constant between the rest and active phases.     

Topography of homeostatic sleep pressure dissipation across the night in young and middle‐aged men and women

Decline in slow‐wave activity (SWA) across the night is believed to reflect dissipation of the homeostatic sleep drive. This study evaluated the effects of age, sex and topography on SWA dissipation. The sleep electroencephalogram of 48 young [22 women, 26 men; mean = 23.3 years; standard deviation (SD) = 2.4] and 39 middle‐aged (21 women, 18 men; mean = 51.9 years; SD = 4.6) healthy volunteers was analysed. Spectral analysis (0.5–22.0 Hz) was performed per non‐rapid eye movement period for Fp1, F3, C3, P3 and O1. SWA (1.0–5.0 Hz) dissipation was modelled using linear and exponential decay functions applied to each age and sex subgroup data set for each derivation. The relative adequacy of both functions was compared using Akaike’s information criterion. Results suggest that the exponential model provides a better data fit than the linear fit independently of age, gender and brain location. In women, age reduced the span (distance between the y intercept and the asymptote) of SWA decay in Fp1, F3, P3 and O1. In men, however, the effect of age on the span of SWA decay was limited to Fp1 and F3. In all age and sex subgroups, anterior regions showed a higher span than posterior regions. The asymptote was lower in anterior regions in young but not in middle‐aged subjects. These results suggest that the homeostatic process operates on a larger scale in anterior regions. Importantly, ageing reduced the scale of homeostatic dissipation in both sexes, but this effect was more widespread across the brain in women.     

Morningness/eveningness and the need for sleep

The purpose of this study was to determine, in a large sample of adults of all ages (17-80 years), the effect of morningness/eveningness on sleep/wake schedules, sleep needs, sleep hygiene and subjective daytime somnolence. A total of 617 subjects (219 subjects per chronotype group) matched for age, sex and employment status, completed an abridged morningness/eveningness questionnaire, a questionnaire on sleep habits and the quality of sleep, and the Epworth Sleepiness Scale. Eveningness was associated with a greater need for sleep, less time in bed during the week compared to ideal sleep needs, more time in bed at the weekend, a later bedtime and waking-up time especially at the weekend, more irregular sleep/wake habits and greater caffeine consumption. These subjects built up a sleep debt during the week and extended their duration of sleep at the weekend. They did not, however, rate themselves more sleepy than other types, despite the fact that our results showed a clear link between subjectively evaluated daytime somnolence and sleep debt. Why they were less affected by sleep deprivation is not clear. This raises the question of individual susceptibility to the modification of sleep parameters.     

Short-term homeostasis of REM sleep assessed in an intermittent REM sleep deprivation protocol in the rat

An intermittent rapid eye movement (REM) sleep deprivation protocol was applied to determine whether an increase in REM sleep propensity occurs throughout an interval without REM sleep comparable with the spontaneous sleep cycle of the rat. Seven chronically implanted rats under a 12 : 12 light-dark schedule were subjected to an intermittent REM sleep deprivation protocol that started at hour 6 after lights-on and lasted for 3 h. It consisted of six instances of a 10-min REM sleep permission window alternating with a 20-min REM sleep deprivation window. REM sleep increased throughout the protocol, so that total REM sleep in the two REM sleep permission windows of the third hour became comparable with that expected in the corresponding baseline hour. Attempted REM sleep transitions were already increased in the second deprivation window. Attempted transitions to REM sleep were more frequent in the second than in the first half of any 20-min deprivation window. From one deprivation window to the next, transitions to REM sleep changed in correspondence to the amount of REM sleep in the permission window in-between. Our results suggest that: (i) REM sleep pressure increases throughout a time segment similar in duration to a spontaneous interval without REM sleep; (ii) it diminishes during REM sleep occurrence; and (iii) that drop is proportional to the intervening amount of REM sleep. These results are consistent with a homeostatic REM sleep regulatory mechanism that operates in the time scale of spontaneous sleep cycle.     

A selective serotonin reuptake inhibitor reduces REM sleep in the homing pigeon

Avian and mammalian 'rapid eye movement' sleep (REM sleep) resemble each other in several aspects. However, the question of whether REM sleep has a shared evolutionary ancestry in birds and mammals has yet to be thoroughly explored. The brain regions and neurotransmitter systems involved in the generation of mammalian REM sleep are phylogenetically ancient, and are also found in extant birds and reptiles. Several pharmacological experiments in birds indicate that similar neural substrates are involved in the regulation of avian and mammalian sleep. However, because the drugs used in these studies generally resulted in non-specific sleep loss, the neurochemical regulation of avian REM sleep in particular remains uncertain. The selective serotonin reuptake inhibitor (SSRI) zimelidine is known to reduce REM sleep in mammals. If avian REM sleep is similarly regulated by serotonin, it would be expected that an acute dose of a SSRI should also reduce avian REM sleep. To investigate a putative role of serotonin in the regulation of avian REM sleep, changes in sleep electroencephalogram (EEG) and behavior were recorded in five pigeons (Columba livia) after the administration of an acute dose of zimelidine. Our results demonstrate that the effects of zimelidine on avian REM sleep are comparable to those observed in mammals, indicating that serotonin may serve a similar function in the control of avian and mammalian REM sleep.     

Partial sleep restriction modulates secretory activity of thyrotropic axis in healthy men

Sleep and endocrine function are known to be closely related, but studies on the effect of moderate sleep loss on endocrine axes are still sparse. We examined the influence of partial sleep restriction for 2 days on the secretory activity of the thyrotropic axis. Fifteen healthy, normal‐weight men were tested in a balanced, cross‐over study. Serum concentrations of thyrotrophin (TSH), free triiodothyronine (fT3) and free thyroxine (fT4) were monitored at 1‐h intervals during a 15‐h daytime period (08:00–23:00 h) following two nights of restricted sleep (bedtime 02:45–07:00 h) and two nights of regular sleep (bedtime 22:45–07:00 h), respectively. Serum concentrations of fT3 (P < 0.026) and fT4 (P = 0.089) were higher after sleep restriction than regular sleep, with a subsequent blunting of TSH concentrations in the evening hours of the sleep restriction condition (P = 0.008). These results indicate profound alterations in the secretory activity of the thyrotropic axis after 2 days of sleep restriction to ~4 h, suggesting that acute partial sleep loss impacts endocrine homeostasis, with potential consequences for health and wellbeing.     

REM sleep deprivation and food competition in male rats

As a test of the hypothesis that REM deprivation lowers the threshold for “motivational” behaviors, 17 male rats that had been REM deprived were tested against 17 non-deprived male rats in three series of food competition tests, i.e., an immediate, a 3 hr, and a 48 hr series of posttreatment tests. The results provide support for the hypothesis that REM deprivation generally activates “motivational” behaviors, in that the REM deprived animals won more frequently as had been predicted. However, the response gradients of the two groups over the course of the postteatment test series did not conform to prediction. These data are discussed together with the results of other studies which suggest that perhaps the list of behaviors which have been subsumed under the category—“motivational behaviors” is too broad to be of real scientific value.     

Slow oscillations in human non-rapid eye movement sleep electroencephalogram: effects of increased sleep pressure

Slow oscillations (<1 Hz) in the non-rapid eye movement (NREM) sleep electroencephalogram (EEG) result from slow membrane potential fluctuations of cortical neurones, alternating between a depolarized up-state and a hyperpolarized down-state. They are thought to underlie the restorative function of sleep. We investigated the behaviour of slow oscillations in humans under increased sleep pressure to assess their contribution to sleep homeostasis. EEG recordings (C3A2) of baseline and recovery sleep after sleep deprivation (eight healthy males, mean age 23 years; 40 h of prolonged wakefulness) were analysed. Half-waves were defined as positive or negative deflections between consecutive zero crossings in the 0.5–2 Hz range of the band-pass filtered EEG. Increased sleep pressure resulted in a redistribution of half-waves between 0.5 and 2 Hz: the number of half-waves per minute was reduced below 0.9 Hz while it was increased above 1.2 Hz. EEG power was increased above 1 Hz. The increase in frequency was accompanied by increased slope of the half-waves and decreased number of multi-peak waves. In both baseline and recovery sleep, amplitude and slope were correlated highly over a broad frequency range and positive half-waves were characterized by a lower frequency than the negative ones, pointing to a longer duration of up- than down-states. We hypothesize that the higher frequency of slow oscillatory activity after prolonged wakefulness may relate to faster alternations between up- and down-states at the cellular level under increased sleep pressure. This study does not question slow-wave activity as a marker of sleep homeostasis, as the observed changes occurred within the same frequency range.     

Intracranial self-stimulation after paradoxical sleep deprivation induced by the platform method in rats

Lateral hypothalamic intracranial self-stimulation was studied before and after paradoxical sleep deprivation (PSD) induced by the platform method. Rats were assigned to two counterbalanced groups where the sequence order of experimental (small platform) and control (large platform) treatments was permuted. In contrast with previous findings significant changes in the response rates for intracranial self-stimulation were not observed after PSD. Ineffectiveness and nonspecific effects of the treatment are ruled out as the cause for our findings. An hypothesis is suggested that the effect of PSD upon intracranial self-stimulation could be dependent of the brain electrode location.     

Sharp and sleepy: evidence for dissociation between sleep pressure and nocturnal performance

While sleep restriction decreases performance, not all individuals are equal with regard to sensitivity to sleep loss. We tested the hypothesis that performance could be independent of sleep pressure as defined by EEG alpha-theta power. Twenty healthy subjects (10 vulnerable and 10 resistant) underwent sleep deprivation for 25 h. Subjects had to rate their sleepiness (Karolinska Sleepiness Scale) and to perform a 10-min psychomotor vigilance task (PVT) every 2 h (20:00-08:00 hours). Sleep pressure was measured by EEG power spectral analysis (alpha-theta band 6.0-9.0 Hz). Initial performance, EEG spectral power and KSS score were equal in both groups (ANOVA, NS). The performance of vulnerable subjects significantly increased during the night (rANOVA, P < 0.01), whereas resistant subjects globally sustained their performance. Homeostatic pressure and subjective sleepiness significantly increased during the night (rANOVA, P < 0.01) identically in both categories (rANOVA, NS). Resistant subjects sustained their reaction time independently of the increase in homeostatic pressure. The phenotypic determinants of vulnerability to extended wakefulness remain unknown.     

Intense exercise increases adenosine concentrations in rat brain: implications for a homeostatic sleep drive

Intense exercise and sleep deprivation affect the amount of homeostatically regulated slow wave sleep in the subsequent sleep period. Since brain energy metabolism plays a decisive role in the regulation of behavioral states, we determined the concentrations of nucleotides and nucleosides: phosphocreatine, creatine, ATP, ADP, AMP, adenosine, and inosine after moderate and exhaustive treadmill exercise as well as 3 and 5 h of sleep deprivation and sleep in the rat brain using the freeze-clamp technique.

High intensity exercise resulted in a significant increase of the sleep-promoting substance adenosine. In contrast, following sleep, inosine and adenosine levels declined considerably, with an accompanied increase of ADP after 3 h and ATP after 5 h. Following 3 h and 5 h sleep deprivation, ADP and ATP did not differ significantly, whereas inosine increased during the 3 and 5-h period. The concentrations of AMP, creatine and phosphocreatine remained unchanged between experimental conditions.

The present results are in agreement with findings from other authors and suggest that depletion of cerebral energy stores and accumulation of the sleep promoting substance adenosine after high intensity exercise may play a key role in homeostatic sleep regulation, and that sleep may play an essential role in replenishment of high-energy compounds.     

Diurnal changes in electrocorticogram sleep slow‐wave activity during development in rats

According to the homeostatic regulation of sleep, sleep pressure accumulates during wakefulness, further increases during sleep deprivation and dissipates during subsequent sleep. Sleep pressure is electrophysiologically reflected by electroencephalogram slow‐wave activity during non‐rapid eye movement sleep, and is thought to be stable across time. During childhood and adolescence the brain undergoes massive reorganization processes. Slow‐wave activity during these developmental periods has been shown in humans to follow an inverted U‐shaped trajectory, which recently was replicated in rats. The goal of this study was to investigate in rats the diurnal changes of slow‐wave activity during the inverted U‐shaped developmental trajectory of slow‐wave activity. To do so, we performed longitudinal electrocorticogram recordings, and compared the level of slow‐wave activity at the beginning with the slow‐wave activity level at the end of 24‐h baselines in two sets of Sprague–Dawley rats. In younger animals (n = 17) we investigated specific postnatal days when overall slow‐wave activity increases (postnatal day 26), peaks (postnatal day 28) and decreases (>postnatal day 28). The same analysis was performed in older animals (postnatal day 48, n = 6). Our results show a gain of slow‐wave activity across 24 h on postnatal day 26, followed by no net changes on postnatal day 28, which was then followed by a loss of slow‐wave activity during subsequent days (>postnatal day 28). Older animals did not show any net changes in slow‐wave activity across 24 h. These results cannot be explained by differences in vigilance states. Thus, slow‐wave activity during this developmental period may not only reflect the trajectory of sleep pressure but may additionally reflect maturational processes.     

Creatine supplementation reduces increased homocysteine concentration induced by acute exercise in rats

The aim of this study was to evaluate the effect of creatine supplementation on homocysteine (Hcy) metabolism after acute aerobic and anaerobic exercise. A total of 112 Wistar rats were divided into four groups: aerobic exercise (A), aerobic exercise plus creatine supplementation (ACr), anaerobic exercise (An), and anaerobic exercise plus creatine-supplemented (AnCr). Creatine supplementation consisted of the addition of 2% creatine monohydrate to the diet. After 28 days, the rats performed an acute moderate aerobic exercise bout (1 h swimming with 4% of total body weight load) or an acute intense anaerobic exercise bout (6 × 30-s vertical jumps into the water with a 30-s rest between jumps, with 50% of total body weight load). The animals were killed before (pre) and at 0, 2, and 6 h (n = 8) after acute exercise. Plasma Hcy concentration increased significantly (P < 0.05) up to 2 h after anaerobic exercise (An group: pre 8.7 ± 1.2, 0 h 13.2 ± 2.3, 2 h 13.5 ± 4.2, and 6 h 12.1 ± 2.2, μmol/l). The same did not occur in acute aerobic exercised animals. Nevertheless, creatine supplementation significant decreased (P < 0.05) homocysteine concentration independent of exercise intensity (AnCr group: pre 17%, 0 h 80%, 2 h 107%, and 6 h 48%; ACr group: pre 17%, 0 h 19%, 2 h 28%, and 6 h 27%). Increased S-adenosylhomocysteine was also found in the An group. In conclusion, acute intense anaerobic exercise increased plasma Hcy concentration. On the other hand, creatine supplementation decreased plasma Hcy independent of exercise intensity.     

Sleep deprivation suppresses the increase of rapid eye movement density across sleep cycles

We investigated the association between rapid eye movement (REM) density (REMd) and electroencephalogram (EEG) activity during non‐rapid eye movement (NREM) and REM sleep, within the re‐assessment, in a large sample of normal subjects, of the reduction of oculomotor activity in REM sleep after total sleep deprivation (SD). Coherently with the hypothesis of a role of homeostatic sleep pressure in influencing REMd, a negative correlation between changes in REMd and slow‐wave activity (SWA) was expected. A further aim of the study was to evaluate if the decreased REMd after SD affects ultradian changes across sleep periods. Fifty normal subjects (29 male and 21 female; mean age = 24.3 ± 2.2 years) were studied for four consecutive days and nights. Sleep recordings were scheduled in the first (adaptation), second (baseline) and fourth night (recovery). After awakening from baseline sleep, a protocol of 40 h SD started at 10:00 hours. Polysomnographic measures, REMd and quantitative EEG activity during NREM and REM sleep of baseline and recovery nights were compared. We found a clear reduction of REMd in the recovery after SD, due to the lack of REMd changes across cycles. Oculomotor changes positively correlated with a decreased power in a specific range of fast sigma activity (14.75–15.25 Hz) in NREM, but not with SWA. REMd changes were also related to EEG power in the 12.75–13.00 Hz range in REM sleep. The present results confirm the oculomotor depression after SD, clarifying that it is explained by the lack of changes in REMd across sleep cycles. The depression of REMd can not simply be related to homeostatic mechanisms, as REMd changes were associated with EEG power changes in a specific range of spindle frequency activity, but not with SWA.     

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.     

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.