The relationship of interleukin-1 and immune functions to sleep in humans

Serial sampling of peripheral blood from six healthy adult male volunteers was performed during daytime waking and nighttime sleeping. In addition, sleep physiology was assessed in all subjects (Ss) and sleep stages scored blind by standard criteria. Samples of plasma were analyzed for cortisol (Co) levels, functional interleukin-1 (IL-1), and interleukin-2 (IL-2) activity. Peripheral blood monocytes (PBM) were assayed to evaluate natural killer (NK) activity and mitogen responsiveness. Dramatic increase in IL-1 activity along with changes in other immune functions occurred during sleep and were related to onset of slow wave sleep.     

Effects of sleep on endotoxin-induced host responses in healthy men

OBJECTIVE: To examine whether increased sleep during viral or bacterial infections supports host defense mechanisms. METHODS: To test this assumption in humans, healthy male subjects were assigned either to sleep from 2300 to 0700 hours (n = 10) or to stay awake through the night (n = 10). In the sleeping subjects Salmonella abortus equi endotoxin (0.4 ng/kg) or placebo were intravenously injected in balanced order during the first SWS episode. The age-matched, sleep-deprived subjects were injected at the same time point. RESULTS: As expected, endotoxin significantly increased rectal temperature, the plasma levels of cortisol, tumor necrosis factor-alpha (TNF-alpha), the soluble TNF receptors p55 and p75, Interleukin (IL)-6, the IL-1 receptor antagonist (RA), leukocyte, and granulocyte counts in both sleeping and sleep-deprived subjects, whereas lymphocyte and monocyte counts were transiently reduced. Time courses of endotoxin-induced host responses did not differ between the sleep and sleep deprivation groups. Endotoxin did not affect the amount of nocturnal wakefulness, nonrapid-eye-movement (NREM) sleep, or rapid-eye-movement (REM) sleep across the total night compared with placebo, but significantly increased electroencephalogram-arousals (EEG-arousals) in stage 2 and decreased arousals in SWS. In addition, the amount of SWS, spectral EEG-delta and -theta power was increased at the beginning and at the end of the sleep period, respectively, when the degree of immune activation was relatively low. CONCLUSION: The present results support the notion that short-term sleep deprivation is unlikely to harm the immune system as far as unspecific acute responses are concerned. The effects of endotoxin on sleep in this case support prior observations that in humans, enhanced SWS and intensified NREM sleep occur when host defense activation is subtle.     

Effects of different sleep duration on delta sleep in recovery nights

The study assessed the effects of different amounts of sleep restriction on slow wave sleep (SWS) in the ensuing recovery nights. After one adaptation night and an 8-hr baseline night, six healthy men were individually studied during and following five nights in which sleep was reduced to 5, 4, 3, 2, and 1 hr with a 1-week interval between conditions. Bach sleep reduction was followed by an 8-hr recovery night. Finally, a second 8-hr baseline night was recorded. A trend analysis revealed that SWS amount in recovery nights increases with decreasing previous sleep duration. Regression analyses showed that, within each participant, the rebound of SWS after a sleep reduction is predicted better by the total duration of sleep than by the specific amount of SWS lost.     

Kindling stimuli delivered at different times in the sleep-wake cycle

STUDY OBJECTIVES: Clinical and experimental observations argue that sleep disturbances are common and coexist in patients with epilepsy. Our previous observations have suggested that neural-immune interactions between corticotropin-releasing hormone (CRH) and interleukin-1 (IL-1) are involved in the regulation of physiological sleep-wake behavior. In the present study, we determined the involvement of CRH and IL-1 in the alteration of sleep-wake activities in rats when amygdala kindling was given either at the beginning of the light period (light-onset kindling) or at the beginning of the dark period (dark-onset kindling). DESIGN: The analysis of sleep-wake activities was performed before and after full-blown kindling, and the actions of CRH and IL-1 were tested by pharmacological blockade. SETTING: Neuroscience Laboratory at China Medical University Hospital. PARTICIPANT AND INTERVENTIONS: Male Sprague-Dawley rats were implanted with electroencephalogram (EEG) electrodes and an intracerebroventricular (ICV) guide cannula. Kindling stimuli delivered via a bipolar electrode placing in the right central nucleus of the amygdala. MEASUREMENT AND RESULTS: Amygdala kindling induced diverse effects on sleep. Slow-wave sleep (SWS) and rapid eye movement (REM) sleep decreased during the first 12-hour light period when rats were kindled at light onset. When dark-onset kindling was given, SWS increased but REM sleep was not altered during the first 12-hour dark period. After light-onset kindling, the circulating corticosterone concentrations increased and were blocked by ICV administration of the CRH receptor antagonist, astressin or alpha-hCRH. The ICV administration of the CRH antagonist blocked the light-onset kindling-induced decrease of SWS in a dose-dependent manner. After dark-onset kindling, IL-1 mRNA expression in the hippocampus and cortex increased. The dark-onset kindling-induced SWS was blocked in a dose-dependent manner by ICV administration of IL-1 receptor antagonist (IL-1 ra). The slow-wave activity during SWS was enhanced regardless of when kindling occurred, but both CRH antagonists and IL-1 ra had little effect on the alteration of slow-wave activity. CONCLUSION: These observations argue that amygdala-kindling-induced sleep-wake alterations are modulated by central increases in CRH or IL-1.     

Activation of human natural killer cells by lipopolysaccharide and generation of interleukin-1 alpha, beta, tumour necrosis factor and interleukin-6. Effect of IL-1 receptor antagonist.

The presence in the body of an antigen species or a bacterial lipopolysaccharide (LPS) has a pleiotropic effect on the immune system activating macrophages, lymphocytes and natural killer (NK) cells. Recently it has been reported that human macrophages not only secrete interleukin-1 (IL-1) but also its inhibitor, called IL-1 receptor antagonist (IL-1ra), structurally similar to IL-1 beta, but with no IL-1-like activity and which binds to the IL-1 receptor. In this study we show that LPS stimulates NK cell activity and IL-1ra potentiates the stimulatory effect of human recombinant interleukin-2 (hrIL-2) on NK cell activity. In addition, we found that hrIL-1ra inhibits DNA synthesis in lymphocyte culture stimulated with phytohaemagglutinin (PHA) (20 micrograms/ml), presumably via IL-1 inhibition. We also found that LPS is a potent stimulator of monokines: IL-6, tumour necrosis factor-alpha (TNF-alpha), and IL-1 beta, as determined by radioimmunoassay method, and interferon-gamma (IFN-gamma), IL-2, TNF-alpha and IL-1 alpha, as determined by ELISA method, in peripheral blood mononuclear cells (PBMC). We used PBMC as effector cells since LPS requires the presence of accessory cells to activate lymphocytes and bind to the HLA-DR molecule on accessory cells. The effect of LPS on PBMC cytotoxicity has been compared with an endotoxin-free extract of Escherichia coli, OM-8990, which did not provoke cytokine production nor did it cause enhancement of NK cell activity. We found that human recombinant IL-1ra potentiates the stimulatory effect of IL-2 on NK cell activity, similar to hrIL-1 beta. The potentiation of IL-2 in stimulating NK cell activity by IL-1ra is not yet understood. Since IL-1ra is a part of the IL-1 family, it may work in a similar fashion to IL-1, which also potentiates IL-2 to enhance NK cell activity but has been shown not to be directly important in tumour cell killing. In addition, hrIL-1ra can amplify the effect of IL-2 on NK activity, possibly by inhibiting the cyclo-oxygenase products, which are immunosuppressive and are generated in antigen-stimulated PBMC cultures. The generation of IFN-gamma by PBMC after treatment with LPS strongly suggests that the enhancement of NK cell activity may be indirectly due to IFN production.     

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.     

On the immune reaction to autologous human lymphoblasts: evidence for the stimulation by activating factors rather than induction by autoantigens

This report questions the nature of stimulation in the lymphoblast-induced autologous mixed leukocyte reaction (AMLR). Using immobilized phytohemagglutinin (PHA) and pokeweed mitogen (PWM), we show that the AMLR generated with PHA lymphoblasts (PHA X AMLR) was not significantly different from the AMLR generated with untreated stimulators. The PWM lymphoblasts of 15 out of 33 apparently normal blood donors generated an AMLR (PWM X AMLR) greater than their respective normal AMLR. The positive PWM X AMLR was not related to the expression of HLA-DR or surface IgM, since expression of both was increased by both PHA and PWM, yet only PWM blasts stimulated in the AMLR. Fixation of PWM-stimulated cells prior to the AMLR completely abolished stimulatory capacity, indicating further against new or increased antigen expression. Inactivation by uv irradiation of surface HLA-D on the stimulators had no effect upon the PWM X AMLR, while intact protein synthesis was required in order to stimulate. The ability of cells to stimulate was associated with the release of soluble helper factors capable of stimulating autologous cells independently. These factors were neither contaminating PWM nor secreted IL-1 or IL-2, although IL-1-like activity was released by all cells regardless of their ability to stimulate. The individual variation in the PWM X AMLR response and secretion of helper factors is discussed in relation to B-cell hyperproliferation and altered immunoglobulin production in autoimmune manifestations.     

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 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.     

The effect of experimental haemocarbofiltration upon activity of mononuclear cells from normal and autoimmune patients

We examined the functional activity of peripheral blood mononuclears (PBM) of 18 healthy subjects, 18 patients with pemphigus vulgaris, 12 with bullous pemphigoid and nine with discoid lupus erythematosus, after haemofiltration on carbon haemo-adsorbents of 'SKN' type. Proliferation in the response to PHA and Con A, for IL-1 and IL-2 production, and exogenous IL-2 absorption were assayed. The presence of IL-1 and IL-2 inhibitors in haemocarbo-adsorbent eluants was shown. We also investigated the natural killer (NK) and antibody-dependent cellular cytotoxic (ADCC) activities. We found significant increases of both lectin-dependent proliferation and of interleukin production by PBM of autoimmune patients after two to four perfusions. The ability of PBM to absorb IL-2 displayed a steady growth after each perfusion, whereas increase of NK and ADCC activities was observed after not less than six passes. The enhancement of PBM functional activity in autoimmune patients was accompanied by accumulation of IL-1 and IL-2 inhibitors in the sorbent. It was concluded that therapeutic effects of haemofiltration in autoimmune diseases involve improvement of immunocompetent cell function due to their deligandization by activated charcoal.     

Regulation of immune functions by human surfactant

Human peripheral blood mononuclear cells (MNC) were incubated in vitro with highly purified human surfactant to examine its effect on various T cell functions. Surfactant inhibited DNA synthesis by lymphocytes in response to concanavalin A (Con A), phytohemagglutinin (PHA), and in the autologous mixed lymphocyte reaction (AMLR). In contrast, surfactant had no effect on pokeweed-mitogen (PWM, T cell-dependent B lymphocyte mitogen)-induced DNA synthesis or on interleukin-2 (IL-2) receptor expression on T cells activated with PHA, Con A or PWM. Furthermore, surfactant had either no effect or enhanced (depending upon the concentration of IL-2 used) the response of exogenous recombinant IL-2 on IL-2-dependent T cell line, In vitro addition of recombinant IL-2 corrected the suppressive effect of surfactant on the AMLR. These data show immunosuppressive effect of surfactant on T lymphocyte functions.     

Increased EEG spectral power density during sleep following short-term sleep deprivation in pigeons (Columba livia): evidence for avian sleep homeostasis

Birds provide a unique opportunity to evaluate current theories for the function of sleep. Like mammalian sleep, avian sleep is composed of two states, slow-wave sleep (SWS) and rapid eye-movement (REM) sleep that apparently evolved independently in mammals and birds. Despite this resemblance, however, it has been unclear whether avian SWS shows a compensatory response to sleep loss (i.e., homeostatic regulation), a fundamental aspect of mammalian sleep potentially linked to the function of SWS. Here, we prevented pigeons (Columba livia) from taking their normal naps during the last 8 h of the day. Although time spent in SWS did not change significantly following short-term sleep deprivation, electroencephalogram (EEG) slow-wave activity (SWA; i.e., 0.78-2.34 Hz power density) during SWS increased significantly during the first 3 h of the recovery night when compared with the undisturbed night, and progressively declined thereafter in a manner comparable to that observed in similarly sleep-deprived mammals. SWA was also elevated during REM sleep on the recovery night, a response that might reflect increased SWS pressure and the concomitant 'spill-over' of SWS-related EEG activity into short episodes of REM sleep. As in rodents, power density during SWS also increased in higher frequencies (9-25 Hz) in response to short-term sleep deprivation. Finally, time spent in REM sleep increased following sleep deprivation. The mammalian-like increase in EEG spectral power density across both low and high frequencies, and the increase in time spent in REM sleep following sleep deprivation suggest that some aspects of avian and mammalian sleep are regulated in a similar manner.     

Cell-mediated immunity in patients with invasive carcinoma of the cervix

Multiple in vitro immune parameters were investigated in thirty-four untreated patients with invasive carcinoma of the cervix and in twenty-five controls. The parameters measured were percentages and absolute counts of T and B cells, percentage of T cell subsets, lymphocyte response to phytohemagglutinin (PHA) and concanavalin A (Con A), natural killer (NK) activity, antibody-dependent cellular cytotoxicity (ADCC), and interleukin 2 (IL-2) activity. Patients with invasive cervical carcinoma, as compared with controls, showed a decrease in the percentage and count of T cells, a decrease in the percentage of helper-inducer (CD4+) T cells, decreased CD4+/CD8+ ratio, depressed lymphocyte response to PHA and Con A, and depressed NK and ADCC activities. There were no significant differences in these immune parameters between early and advanced tumor stages. The levels of total lymphocytes, monocytes, suppressor-effector (CD8+) T cells, and B cells were similar to those of the controls. IL-2 productivity in patients was lower than that in controls. In patients with invasive cervical carcinoma, a decrease in the percentage of CD4+ cells was associated with depressed PHA response and decreased IL-2 productivity was correlated with the reduced percentage of CD4+ cells and decreased NK activity. This study shows a significant defect in an important immune surveillance mechanism in patients with invasive carcinoma of the cervix and suggests that impaired IL-2 activity production may be related to quantitative and qualitative alterations in lymphocyte subpopulations which play a major role in immune surveillance against cervical cancer.     

Sleep,neuroimmune and neuroendocrine functions in fibromyalgia and chronic fatigue syndrome

The justification for disordered chronobiology for fibromyalgia and chronic fatigue syndrome (CFS) is based on the following evidence: The studies on disordered sleep physiology and the symptoms of fibromyalgia and CFS; the experimental studies that draw a link between interleukin-1 (IL-1), immune-neuroendocrine-thermal systems and the sleep-wake cycle; studies and preliminary data of the inter-relationships of sleep-wakefulness, IL-1, and aspects of peripheral immune and neuroendocrine functions in healthy men and in women during differing phases of the menstrual cycle; and the observations of alterations in the immune-neuroendocrine functions of patients with fibromyalgia and CFS (Moldofsky, 1993b, d). Time series analyses of measures of the circadian pattern of the sleep-wake behavioural system, immune, neuroendocrine and temperature functions in patients with fibromyalgia and CFS should determine whether alterations of aspects of the neuro-immune-endocrine systems that accompany disordered sleep physiology result in nonrestorative sleep, pain, fatigue, cognitive and mood symptoms in patients with fibromyalgia and CFS.     

Immunological Changes in Human Immunodeficiency Virus (HIV)-Infected Individuals During HIV-Specific Protease Inhibitor Treatment

The present study examines the influence of effective anti-retroviral treatment on immune function, evaluated by a broad array of immunological tests. We followed 12 individuals infected with human immunodeficiency virus (HIV) for 6 months after initiation of combination anti-retroviral treatment including a protease inhibitor. Unstimulated and pokeweed mitogen (PWM)-, interleukin (IL)-2- and phytohaemagglutinin (PHA)-stimulated lymphocyte proliferative responses increased during follow-up reaching average levels from 1.3-fold (PHA) to 3.7-fold (PWM) above baseline values. The total CD4+ lymphocyte count increased mainly due to increases in numbers of CD4+ CD28+ and CD4+ CD45RO+ cells, whereas increases in numbers of CD4+ CD45RA+ cells contributed little to the increase in CD4+ cell count. The total cytotoxic T-cell (CTL) killing of autologous B cells infected with HIV-encoding recombinant Vaccinia virus was increased after 3-6 months, whereas the specific HIV-directed CTL activity and the concentration and lytic activity of natural killer (NK) cells were unchanged during follow-up. These results demonstrate that the initiation of a treatment including an HIV protease inhibitor is followed by an increase in lymphocyte proliferation and lymphocyte-mediated cytotoxicity. However, unchanged levels of specific HIV CTL and NK cell activity warn us that not all measures of immune function may respond simultaneously to anti-retroviral treatment.     

Effects of Exhaustive Exercise on the Sleep of Men and Women

The effects of exhaustive exercise on sleep were examined in 5 women and 4 men who performed an acute bout of submaximal exercise (50–70% Vo_2max) to the point of volitional exhaustion. Significant changes were observed in the quantity and temporal distribution of slow-wave sleep (SWS) on the exercise night. The duration of SWS prior to rapid eye movement (REM) sleep onset increased markedly, along with a moderate increase in stage 4 and total SWS. REM sleep variables were affected in the early portion of the night, with an increased latency to first REM onset and a decrease in the duration of the first REM period. Initial REM cycle length (from first to second REM period onset) decreased as well. The magnitude of the SWS increase prior to REM onset was sex-related, averaging 24 min for women and 5.7 min for men. A correlation of .85 was observed between this increase and total caloric expenditure during exercise for the women. Cardiovascular measures indicated significant elevations of heart rate and cardiac output during sleep on the exercise night. Analysis of urine samples revealed a significant drop in nocturnal cortisol excretion rates after exercise. The results suggest that exhaustive exercise affects sleep primarily in the early portion of the night, inducing an increase in SWS pressure at the expense of REM sleep.     

The influence of two behavioral regimens on the distribution of sleep and wakefulness in narcoleptic patients

Thirty-two hours (night-day-night) of polygraphic recordings were performed on 14 patients with a diagnosis of narcolepsy-cataplexy. Half of the patients stayed in bed during the day, whereas the other half were seated at a table. Patients were free to nap whenever they wanted to. Patients under continuous bedrest slept 2-3 times more during the day than patients who were sitting at the table. Rapid-eye-movement (REM) sleep and slow-wave sleep (SWS, stages 3 and 4) were nearly absent during daytime sleep in the table group, but not in the bed group. The differential behavioral regimes during the day resulted in different amounts of SWS in the consecutive night sleep. Although SWS increased from the first to the second night in the table group, it decreased in the bed group. This result suggests that the presumably homeostatic regulation of SWS is intact in narcoleptic patients.     

Oral administration of lactoferrin increases NK cell activity in mice via increased production of IL-18 and type I IFN in the small intestine.

Evidence that lactoferrin (LF) influences various immune functions is now accumulating. Recent reports have shown that bovine LF (BoLF) enhances antimicrobial, antiviral, and antitumor immune activities when orally administered. Here, we report that orally administered BoLF increases natural killer (NK) cell populations in peripheral blood and spleen in a dose-dependent manner and enhances interferon-gamma (IFN-gamma) production by NK cells. Using intraperitoneal (i.p.) injection of poly(I:C) to induce NK cell trafficking into the peritoneum, oral BoLF increased NK cell migration. Oral BoLF also produced an immediate increase in the levels of interleukin-18 (IL-18) in the portal circulation. In IL-18 knockout (KO) mice, BoLF did not increase the numbers of NK cells, although NK cell cytotoxic activity and poly(I:C)-induced trafficking activity were both enhanced by oral BoLF, even in IL-18 KO mice. Furthermore, oral BoLF increased the expression of IFN-alpha and IFN-beta in Peyer's patches (PP) and mesenteric lymph nodes (MLN). Oral administration of 2- chloroadenosine selectively depleted the PP cells and blocked the ability of oral BoLF to increase NK cell accumulation in the peritoneum following poly(I:C) i.p. injection. Collectively, these results demonstrate that orally administered BoLF stimulates intestine-associated immune functions, including the production of IL- 18 and type I IFNs and increased NK cell activity.     

Sleep restriction and SWS-suppression: effects on daytime alertness and night-time recovery

SUMMARY  This study evaluated the effects of sleep curtailment and SWS-suppression, respectively, on daytime alertness and subsequent night sleep. Seven subjects participated in four conditions: an undisturbed 8-h sleep (8U; 23.00–07.00 hours), an undisturbed 4-h sleep (4U; 03.00–07.00 hours), a 4-h sleep (4D; 03.00–07.00 hours) that was acoustically disturbed when delta waves appeared, and a condition with no sleep (0). Subjective sleepiness, sleep latency, and simple reaction time (RT) were measured. In addition, sleep quality was rated. 4D contained 50% of the SWS (as well as spectral slow-wave energy; SWE) compared to 8U, whereas the curtailment to 4-h did not significantly decrease SWS. 4D had lower subjective quality than the other two sleeps. The main difference in daytime sleep latency was between the 8U and the 0 conditions. Rated alertness was highest after the 8U sleep. The two 4-h sleeps did not differ significantly with respect to rated sleepiness or sleep latency. However, the effects of the 4U sleep were closer to those of the 8U sleep and the effects of the 4D sleep were closer to those of the no sleep condition. RT performance was significantly better during the 8U condition. Recovery sleep after 4D sleep contained significantly more SWS than recovery after 4U and 8U. The effects on SWE during recovery were less clear. It was concluded that sleep duration might be more important for daytime alertness than SWS content and that loss of SWS during one night is recovered during the following night.     

Sleep deprivation and phasic activity of REM sleep: independence of middle-ear muscle activity from rapid eye movements

In the recovery nights after total and partial sleep deprivation there is a reduction of rapid eye movements during REM sleep as compared to baseline nights; recent evidence provided by a selective SWS deprivation study also shows that the highest percentage of variance of this reduction is explained by SWS rebound. The present study assesses whether the reduction of rapid eye movements (REMs) during the recovery night after total sleep deprivation is paralleled by a decrease of middle-ear muscle activity (MEMA), another phasic muscle activity of REM sleep. Standard polysomnography, MEMA and REMs of nine subjects were recorded for three nights (one adaptation, one baseline, one recovery); baseline and recovery night were separated by a period of 40 hours of continuous wake. Results show that, in the recovery night, sleep deprivation was effective in determining an increase of SWS amount and of the sleep efficiency index, and a decrease of stage 1, stage 2, intra-sleep wake, and NREM latencies, without affecting REM duration and latency. However, MEMA frequency during REM sleep did not diminish during these nights as compared to baseline ones, while there was a clear effect of REM frequency reduction. Results indicate an independence of phasic events of REM sleep, suggesting that the inverse relation between recovery sleep after sleep deprivation and REM frequency is not paralleled by a concomitant variation in MEMA frequency.