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PubMed2000

The effects of exercise as a countermeasure for fatigue in sleep-deprived aviators.

This study examined the effectiveness of exercise for sustaining performance despite moderate amounts of sleep. Twelve volunteers engaged in 10-min bouts of exercise during one 40-hr period of sleep deprivation and rested for an equivalent amount of time during a 2nd period. Participants were more alert immediately following exercise, as evidenced by longer sleep latencies, than after the resting, control condition. However, electroencephalogram data collected 50 min following exercise or rest showed that exercise facilitated increases in slow-wave activity, signs of decreased alertness. Cognitive deficits and slowed reaction times associated with sleep loss were equivalent in both conditions. The results from this study suggest that short bouts of exercise may ameliorate some of the increases in sleepiness and fatigue associated with sleep loss for a short period of time but are not likely to prevent performance decrements. In addition, less than 1 hr following exercise, significant increases in fatigue and sleepiness may occur.

Adult↗
PubMed1995

Interest of modafinil, a new psychostimulant, during a sixty-hour sleep deprivation experiment.

Modafinil, a new psychostimulant, was evaluated in eight healthy volunteers subjected to 60 hours of sleep deprivation. During continued wakefulness, vigilance was evaluated by self-assessment questionnaires, analogue visual scales, multiple sleep latency tests (MSLT), sleep logs, and continuous ambulatory electroencephalographic recordings (EEG). Modafinil (200 mg) or a placebo was given every 8 hours for three days; the sessions were separated by a 15 day wash out period. Results indicated a satisfactory level of vigilance, both subjective and objective, after the administration of modafinil, characterised by the quasi total absence of microsleep episodes which gradually occurred under placebo conditions. The confirmed wakening potency of modafinil makes this substance suitable for therapeutic use in patients with sleep disorders such as Gelineau's syndrome and hypersomnia.

Adult↗
PubMed2006

Functional imaging of working memory following normal sleep and after 24 and 35 h of sleep deprivation: Correlations of fronto-parietal activation with performance.

Working memory was evaluated after normal sleep, and at 24 and 35 h of sleep deprivation (SD) in 26 healthy young adults to examine the neural correlates of inter-individual differences in performance. The extent of performance decline was not significantly different between the two SD test periods although there was greater variability in performance at SD35. In both SD sessions, there was reduced task-related activation (relative to normal sleep) in both superior parietal regions and the left thalamus. Activation of the left parietal and left frontal regions after normal sleep was negatively correlated with performance accuracy decline from normal sleep to SD24 thus differentiating persons who maintained working memory performance following SD from those who were vulnerable to its effects.

Adult↗
PubMed1996

Time course of reaction time and EEG while performing a vigilance task during total sleep deprivation.

Nine young adult male (23-30 years old) paid volunteers were subjected to total sleep deprivation (TSD), after two consecutive nights in the laboratory, for 40 hours (from 0800 hours on the first day to 2400 hours on the following day). Oral temperature (OT), reaction time (RT) in a visual vigilance task, and electroencephalogram (EEG; C3, C4, T3, and T4) while performing the task were recorded every 2 hours during TSD and after recovery sleep. One second of EEG, before target and non-target stimuli for every subject and condition was visually inspected, and artifact-free epochs were Fourier transformed. Absolute power (AP) was calculated for 4-20 Hz (full band) and for theta, alpha 1, alpha 2, and beta 1. Analyses of variance (ANOVAs), with TSD and time-of-day as factors, showed the following significant results. TSD induced an increase in RT and AP of the full band at C3 and C4, of all bands at C3, of theta at T3, and of beta 1 at T4 (p < 0.009 for all comparisons). No time-of-day effects nor interactions were found. OT was not affected by TSD. All variables returned to baseline values after recovery sleep. RT and EEG power showed a linear increase with accumulating hours of wakefulness. The increment in RT also correlated with the increase in EEG power. The results demonstrate that the increment in RT is associated with the increase in AP, particularly in the left central cortex; that the EEG may be used to identify sleepiness; and that EEG during task performance is more sensitive to TSD than during relaxed wakefulness.

Adult↗
PubMed2002

Interhemispheric sleep EEG asymmetry in the rat is enhanced by sleep deprivation.

Vigilance state-related topographic variations of electroencephalographic (EEG) activity have been reported in humans and animals. To investigate their possible functional significance, the cortical EEG of the rat was recorded from frontal and parietal derivations in both hemispheres. Records were obtained for a 24-h baseline day, 6-h sleep deprivation (SD), and subsequent 18-h recovery. During the baseline 12-h light period, the main sleep period of the rat, low-frequency (<7.0 Hz) power in the non-rapid eye-movement (NREM) sleep EEG declined progressively. Left-hemispheric predominance of low-frequency power at the parietal derivations was observed at the beginning of the light period when sleep pressure is high due to preceding spontaneous waking. The left-hemispheric dominance changed to a right-hemispheric dominance in the course of the 12-h rest-phase when sleep pressure dissipated. During recovery from SD, both low-frequency power and parietal left-hemispheric predominance were enhanced. The increase in low-frequency power in NREM sleep observed after SD at the frontal site was larger than at the parietal site. However, frontally no interhemispheric differences were present. In REM sleep, power in the theta band (5.25-8.0 Hz) exhibited a right-hemispheric predominance. In contrast to NREM sleep, the hemispheric asymmetry showed no trend during baseline and was not affected by SD. Use-dependent local changes may underlie the regional differences in the low-frequency NREM sleep EEG within and between hemispheres. The different interhemispheric asymmetries in NREM and REM sleep suggest that the two sleep states may subserve different functions in the brain.

Animals↗
PubMed1986

REM sleep deprivation induces a decrease in norepinephrine-stimulated 3H-cyclic AMP accumulation in slices from rat brain.

Beta adrenergic sites in rat brain are reduced after repeated treatment with antidepressant drugs, with REM sleep deprivation (REMSd) having the same effect. This paper reports the effects of REMSd in the production of 3H-cyclic AMP in frontal cortical slices by NE challenge. Data presented in this paper report a marked decrease in 3H-cyclic AMP synthesis after REMSd, which is in accordance with previous results showing adrenergic receptor down-regulation following REMSd. Results are discussed in view of possible interaction with dopaminergic systems and depression management.

Adenylyl Cyclases↗
PubMed1993

Total sleep deprivation in the rat transiently abolishes the delta amplitude response to darkness: implications for the mechanism of the "negative delta rebound".

1. The homeostatic model of delta sleep has provided a useful framework for basic sleep research. This model is based on the relation of delta EEG to the duration of prior waking in man, a relation highlighted by the marked increase (rebound) in the delta EEG of nonrapid eye movement (NREM) sleep that follows total sleep deprivation (TSD). The generality of this model is severely challenged by the response to TSD in the rat. In the 12-h light period (LP) that immediately follows TSD, the rat shows a massive increase in REM sleep but only a modest increase in NREM delta EEG. Although this initial delta increase does not nearly compensate for the delta lost during deprivation, the rat then exhibits a depressed rate of delta production (the "negative delta rebound"). This robust and reproducible reaction worsens the delta deficit. 2. Using rats with chronic electrode implantations, we deprived them of all sleep for 24 h by handling them gently when they became inactive. We found that the negative delta rebound entails a transient, near-total failure of delta amplitude to increase normally in response to the onset of darkness. This loss of the rat's EEG response to darkness suggests a disruption of basic sleep physiology and raises the possibility that the negative rebound is also a pathological response. 3. We hypothesize that the negative rebound is maladaptive, and is caused by the massive increase in REM sleep that precedes it; this hypothesis can be tested experimentally.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Does REM sleep deprivation induce subsensitivity of presynaptic dopamine or postsynaptic acetylcholine receptors in the rat brain?

Yawning behavior was used to evaluate the sensitivity of presynaptic dopamine receptors and postsynaptic acetylcholine receptors of normal and REM sleep-deprived (REMSD) rats. The results show a lowering of the dose-response curve obtained with apomorphine and pilocarpine, as well as a shift to the right in the curve obtained with physostigmine. These results suggest that REMSD induces subsensitization of presynaptic dopamine receptors and/or postsynaptic acetylcholine receptors with different characteristics related to the mechanism of action of the cholinomimetic agent employed.

Animals↗
PubMed1977

[Repeated sessions of sleep deprivation in the treatment of depression].

30 depressed patients were submitted to repeated sessions of sleep deprivation. The results obtained in a previous study were confirmed: after 36 hours of wakefulness there is an important overall improvement, albeit followed by a partial or total relapse the second day after. There are no counter-indications, even for elderly subjects with psycho-organic symptoms.

Adult↗
PubMed1997

Sleepiness, performance, and neuroendocrine function during sleep deprivation: effects of exposure to bright light or exercise.

The temporal profiles of subjective fatigue (as assessed by the Stanford Sleepiness Scale), of cognitive performance (on a digit symbol substitution test and a symbol copying task), of body temperature, and of the peripheral concentrations of melatonin, thyroid-stimulating hormone (TSH), and cortisol were obtained simultaneously at frequent intervals in 17 normal young subjects submitted to a 43-h period of constant routine conditions involving continuous wakefulness at bed rest in dim indoor light. The subjects had knowledge of time of day. Caloric intake was exclusively in the form of an intravenous glucose infusion, and plasma glucose levels were monitored continuously in 8 of the 17 subjects. Under these conditions, fluctuations in plasma glucose reflect primarily changes in glucose use because endogenous glucose production is suppressed by the exogenous infusion. Following the completion of a baseline constant routine study, the volunteers participated in two subsequent studies using the same protocol to determine the immediate psychophysiological effects of exposure to a 3-h pulse of bright light or to a 3-h pulse of physical exercise. Sleepiness and performance varied in a mirror image, with significant negative correlations. Sleepiness scores were minimal around noon and then increased at a modest rate throughout the rest of the normal waking period. Staying awake during usual bedtime hours was associated with an acceleration in the rate of increase in sleepiness, which coincided with decreasing body temperature, rapidly rising cortisol concentrations, and maximal levels of melatonin and TSH. When body temperature reached its nadir, a further major increase in sleepiness occurred in parallel with a pronounced decrease in plasma glucose (reflecting increased glucose use). Recovery from maximal sleepiness started when blood glucose levels stopped falling and when significant decreases in cortisol and melatonin concentrations were initiated. Lower levels of subjective sleepiness resumed when glucose concentrations and body temperature had returned to levels similar to those observed prior to sleep deprivation and when melatonin and TSH concentrations had returned to daytime levels. The synchrony of behavioral, neuroendocrine, and metabolic changes suggests that circulating hormonal levels could exert modulatory influences on sleepiness and that metabolic alterations may underlie the sudden increase in fatigue consistently occurring at the end of a night of sleep deprivation. Effects of bright light or exercise exposure on subjective sleepiness appeared to be critically dependent on the timing of exposure.

Adult↗
PubMed1993

Sleep deprivation in the rat: XVII. Effect of aspirin on elevated body temperature.

Previous studies of total sleep deprivation (TSD) in the rat have shown an elevation of waking body temperature (Tb) early in the deprivation period. TSD rats defend this rise behaviorally by selecting warm ambient temperatures and autonomically by increasing heat production, thus indicating an elevation of thermoregulatory setpoint. Prostaglandins (PGs) can elevate setpoint and Tb. To investigate whether the TSD-induced rise in setpoint and Tb was mediated by PGs, aspirin, which blocks the synthesis of PGs, was administered 100 mg/kg s.q. to 11 TSD and 13 control (TSC) rats in baseline and deprivation. During baseline, aspirin produced a nonsignificant (0.16 degrees C) rise across all rats in waking Tb. For the sampled time period, waking Tb during deprivation day 3 was significantly elevated in TSD rats (0.64 degrees C, p < 0.01) but not in TSC rats (0.27 degrees C). Aspirin was administered on deprivation day 4. It produced a fall in waking Tb in TSD rats from its deprivation-induced elevation. The difference between the response to aspirin during baseline and during deprivation was significant (-0.25 degrees C, p < 0.05) for TSD rats but not TSC rats (-0.17 degrees C). Time awake after aspirin increased significantly (16.2%, p < 0.05) during baseline and declined nonsignificantly (1.1%) during deprivation. These data imply that at least part of the rise in Tb that is characteristic of TSD is mediated by PGs. To the extent that PGD2 promotes lower Tb and sleep in rats but PGE2 has opposite effects, the results are consistent with a shift from PGD2 predominance in baseline toward PGE2 predominance during TSD.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2004

Local mechanisms underlying the regulatory effect of Kropanol on hemopoiesis during paradoxical sleep deprivation.

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

Animals↗
PubMed1999

Effects of sleep deprivation: the phosphorus metabolism in the human brain measured by 31P-magnetic resonance spectroscopy.

Sleep deprivation (SD) has an antidepressant effect in some, but not all, patients with depression, although its biological mechanisms have not yet been characterized. We previously reported altered brain phosphorus metabolism measured by phosphorus-31 magnetic resonance spectroscopy (31P-MRS) in patients with bipolar depression. We preliminarily examined effects of SD on phosphorus metabolism in the frontal lobes of 15 normal subjects using 31P-MRS. No significant differences of membrane phospholipid metabolism, high-energy phosphate metabolism and intracellular pH were found between before and after SD in these subjects. Further studies will be necessary to elucidate the physiological mechanism of SD for depressive patients.

Adolescent↗
PubMedDate not supplied

Delta sleep ratio as a predictor of sleep deprivation response in major depression.

The fast but short-lasting improvement of depressive symptoms by sleep deprivation (SD) in about 60% of patients with a major depressive disorder is well established, but the mechanisms of action are still not clear. Recent studies suggest that changes in non rapid eye movement (NREM) sleep, especially in slow wave activity (SWA), could be associated with the therapeutic outcome of SD. In the current study, spectral analysis of NREM sleep EEG directly prior to SD was performed to determine if automatically derived sleep parameters predict SD response. Sixteen pair matched and drug free patients with a major depressive disorder, 8 SD responders and 8 non-responders (response criterion: 50% reduction on the 6-item HAMD score), were included. Average EEG spectral power was calculated for the whole night before SD and for single NREM episodes. While whole-night averages of spectral power did not differ significantly between subgroups, SD responders showed a steady decrease of SWA across successive NREM episodes, whereas in non-responders an increase from the first to the second episode was observed. The different distribution of SWA was significantly expressed in the delta sleep ratio (quotient of SWA in the first to the second NREM episode). In conclusion, a high delta sleep ratio is a positive predictor for SD response. Referred to psycho- and pharmacotherapeutic results it is hypothesized that low and high values of the delta sleep ratio characterize subgroups of depressed patients with different neurobiological alterations, which could be relevant for further scientific and therapeutic approaches.

Adult↗
PubMed2006

Caffeine challenge in insomniac patients after total sleep deprivation.

BACKGROUND AND PURPOSE: This study compared the effects of caffeine in patients with primary insomnia and normal volunteers. The main goal was to determine the differences in sensitivity to caffeine between the groups. We investigated the effects on daytime sleep of placebo or caffeine after a night of total sleep deprivation (SD). We hypothesized that insomniacs would be more affected by caffeine, which would suggest a change in adenosine receptor (number or sensitivity) in primary insomniacs. PATIENTS AND METHODS: Six primary insomnia patients (Diagnostic and Statistical Manual of Mental Disorders (DSM-IV)) and six normal volunteers with no sleep complaints participated in a double-blind study with caffeine or placebo administered under a cross-over design with each subject serving as his or her own control. The participants did not have a history of drinking coffee or caffeinated beverages. Data from all-night polysomnography and multiple sleep latency test (MSLT) were collected in the sleep research laboratory of National Institute of Medical Sciences and Nutrition Salvador Zubirán. RESULTS: During the baseline night, patients with insomnia had significantly less delta sleep and less total sleep time than the normal volunteers. Mean sleep latency under basal MSLT did not differ between the groups. However, insomnia patients had significantly less total sleep during each nap compared to normal volunteers. After one night of total SD and under caffeine administration, the insomniacs had significantly longer sleep latency and less total sleep time in MSLT compared to normal volunteers. After SD, healthy volunteers reduced sleep latencies in MSLT with or without caffeine. CONCLUSIONS: Patients with insomnia had a higher sensitivity to the diurnal awakening effect of caffeine even after one night of SD. This suggests that changes in the adenosine receptors could, in part, be responsible for the hyperarousal state that has been reported in primary insomnia.

Adult↗
PubMed2000

Temporal order of sleepiness, performance and physiological indices during 19-h sleep deprivation.

Nineteen-hour variation of subjective sleepiness, performance and physiological indices were assessed during sleep deprivation. Longitudinal data of each index had its characteristic curve through which the values changed from day level to night level. A comparison of the time when each curve crossed its mid-range (50% value of its range) showed that those of subjective sleepiness and heart rate were significantly earlier than those of tracking error and coefficient of variation of R-R interval (CV(R-R)), P<0.01. That of rectal temperature was located at between 1:00 and 4:00 am. These temporal relationships were reproducible under two lighting conditions. These results will be useful in considering the occurrence of human errors by night-time workers in the early morning.

Adult↗
PubMed2001

Effect of noradrenergic denervation of medial prefrontal cortex and dentate gyrus on recovery after sleep deprivation in the rat.

The noradrenergic-locus coeruleus (LC) system has a regulatory influence on forebrain neuronal networks. We have previously shown that the amygdala is strongly implicated in the mechanism of rebound seen after a 10 h sleep deprivation (SD). In the present study, our objective was to determine whether the medial prefrontal cortex and dentate gyrus (DG) which receive an important innervation from the LC, play a role in the rebound mechanisms. We found that microinjection of the specific noradrenergic neurotoxin, N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine, into these regions had no effect on the increase in paradoxical sleep duration seen after SD, suggesting that noradrenergic (NA) innervation of the prefrontal cortex and DG are not involved in sleep rebound regulation.

Adrenergic Agents↗
PubMed2003

Facilitation of ejaculation after methamphetamine administration in paradoxical sleep deprived rats.

This study investigated the effects of methamphetamine (MA) on genital reflexes in paradoxical sleep deprived (PSD) rats. Different doses of MA (0, 4, 16 and 64 mg/kg) were acutely given after PSD or the equivalent time to control animals. We observed enhancement of spontaneous ejaculation in PSD rats with larger doses of MA, the highest of which induced ejaculation in 100% of the PSD rats. This was significantly higher than the 30% in the control. Although testosterone exerts motivational effects on male sexual behavior, our data shows that testosterone levels were lower after the PSD period in saline and in the 64 mg/kg MA groups, which present ejaculation at different rates (20% and 100%, respectively). Progesterone levels were significantly higher in PSD-saline in relation to control group and in the 16 and 64 mg/kg of MA groups compared to the other doses. Since PSD induces dopaminergic alterations and dopamine (DA) has a key role in male sexual behavior, plasma DA was also measured. The DA concentration was enhanced in all PSD groups compared with their control group. The mechanism that activates steroid hormones may represent an important physiological effect through which neurotransmitters can affect behavioral events. These data show that MA facilitates ejaculation in PSD rats, however, further studies need to be carried out in order to clarify the hormonal-neurochemical mechanisms involved.

Analysis of Variance↗