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PubMed2001

Sleep deprivation blunts the night time increase in aldosterone release in humans.

The aim of this study was to determine the effect of sleep deprivation on the 24-h profile of aldosterone and its consequences on renal function. Aldosterone and its main hormonal regulatory factors, ACTH (evaluated by cortisol measurement) and the renin-angiotensin system [RAS, evaluated by plasma renin activity (PRA) measurement] were determined every 10 min for 24 h in eight healthy subjects in the supine position, once with nocturnal sleep and once during total 24-h sleep deprivation. Plasma Na(+) and K(+) were measured every 10 min in four of these subjects. In an additional group of 13 subjects under enteral nutrition, diuresis, natriuresis and kaliuresis were measured once during the sleep period (23.00--07.00 h) and once during a 23.00--07.00 hours sleep deprivation period. During sleep deprivation, aldosterone displayed lower plasma levels and pulse amplitude in the 23.00--07.00-hour period than during sleep. Similarly, PRA showed reduced levels and lower pulse frequency and amplitude. Plasma cortisol levels were slightly enhanced during sleep deprivation. Overnight profiles of plasma K(+) and Na(+) were not affected. Diuresis and kaliuresis were not influenced by sleep deprivation. In contrast, natriuresis significantly increased during sleep deprivation. This study demonstrates that sleep deprivation modifies the 24-h aldosterone profile by preventing the nocturnal increase in aldosterone release and leads to altered overnight hydromineral balance.

Adrenocorticotropic Hormone↗

PubMed2005

Impairment of error monitoring following sleep deprivation.

STUDY OBJECTIVES: To verify if error monitoring, involving detection and remedial actions, is affected by sleep deprivation. DESIGN: Event-related brain potentials (ERPs) and electroencephalogram spectrum during performance of Flanker task were obtained in a within-subject, counter-balanced, repeated-measures design. SETTING: Sleep deprivation and data collection were conducted in a laboratory setting. PARTICIPANTS: Sixteen young healthy adults (7 women, 18-23 years old) INTERVENTIONS: Performance and electroencephalogram data were collected after normal sleep and sleep deprivation. MEASUREMENTS AND RESULTS: Compared to normal sleep, 1 night of sleep deprivation resulted in slower and more varied reaction times, more response errors and omissions, and impaired posterror adjustments to response accuracy. Concomitantly, 2 error-related ERPs, error-related negativity and Pe, showed reduced amplitude measurements after sleep deprivation. Conversely, conflict monitoring as expressed behaviorally and by the N2 component of the ERP was not attenuated by sleep deprivation. Ten of the sixteen participants maintained similar accuracy levels under both sleep conditions, although they still showed reduced error-related negativity and error positivity amplitude measurements and impaired error remedial actions for accuracy. Electroencephalogram spectral activity at beta and theta frequency bands was related to response correctness on subsequent trials but not related to that of preceding trials under both sleep conditions. CONCLUSIONS: One night of sleep deprivation impaired both the error detection and error remedial actions and highlighted the inability to avoid making errors again after erroneous responses were already made. The results showed that a vicious cycle occurred between performance deterioration and impairment of error-remedial mechanisms that inevitably led to making more successive errors.

Adolescent↗

PubMed1993

Effects of sleep deprivation and exercise on glucose tolerance.

Previous studies suggest that sleep deprivation (SD) decreases glucose tolerance in humans. The present study examined the ability of 10 males to process a glucose load during two conditions separated by at least 10 d. Condition I consisted of sedentary daily activity and sleep deprivation (SDS). Condition II consisted of daily physical activity and sleep deprivation (SDX). In both the SDS and SDX conditions, subjects were sleep deprived for 60 h followed by 7 h of normal sleep. An oral glucose tolerance test (OGTT) was administered at 10 and 60 h of SD, and after a night of recovery sleep in each condition, and plasma glucose and insulin concentrations were measured. No differences in the total plasma glucose response to the OGTT were observed over the total experimental period during Conditions I and II. However, the insulin response to the OGTT was elevated in the two conditions after 60 h of SD. Furthermore, the sedentary Condition I (SDS) resulted in higher insulin responses at all times compared to exercise Condition II (SDX). It is suggested that SD contributes to the development of an insulin resistance that can be partially reversed by physical activity. The results support the suggestion that SD results in decreased insulin sensitivity at peripheral receptor sites which can eventually lead to insulin exhaustion at pancreatic sites after longer periods of SD.

Activities of Daily Living↗

PubMed2003

Detection of juvenile sleep deprivation by stochastic optimization of pupillographic records.

OBJECTIVE: To address the challenging problem of measuring juvenile sleep deprivation, we test the hypothesis that a pupillographic method found successful for adult narcoleptics might also discriminate between sleep deprived juveniles acting as their own controls. METHODS: A linear, nonstationary model relating pupillary diameter and a random photic stimulus are estimated by recursive regressions from pupillographic records of 8 juveniles of median age 7 years acting as their own rested controls. The estimated pupillary impulse response noise functions are stochastically optimized using the Kullback divergence measure to maximally separate the sleep deprived records from the control records. RESULTS: Both the average and covariance statistics of the estimated pupillary noise functions exhibit statistically significant differences between sleep deprived and rested subjects. The main result is that sleep deprivation decreases pupillary noise variance; a finding consistent with a previous study of adult narcoleptics. Further, it was found that virtually the same stochastic parameters were optimal for the juvenile sleep deprived data and for the previous adult narcoleptic study. CONCLUSIONS: Although our results are preliminary, the consistent reduction of pupillary noise appears to justify a comprehensive clinical trial across a broad range of age classes. In addition, the finding that the same parameters stochastically optimize both juvenile and adult recordings suggests the procedure holds promise as a clinical test which could produce sleep deprivation measures simultaneous with data collection.

Algorithms↗

PubMed1994

Stress-related behavior and central norepinephrine concentrations in the REM sleep-deprived rat.

Rapid eye movement sleep deprivation (REMd) is a potent stressor in the rat. Behavioral abnormalities are among the earliest overt symptoms of REMd, the mechanisms for which remain largely unknown. The phenomena of hyperphagia and weight loss that are associated with REMd may contribute to its later morbidity; however, little is known about the onset of these phenomena or the neurotransmitter mechanisms that are involved. The aim of this study was to determine whether the earliest effects of REMd on consumatory behavior in the rat and its performance in the swimming cylinder of Porsolt are related to changes in norepinephrine (NE) concentrations in the cerebral cortex and selected areas of the hypothalamus. Sprague-Dawley rats were divided into three groups (n = 6): the REMd group resided in a water tank on 6.5-cm diameter pedestals for 96 h; the tank control (TC) group resided in the water tank on 15-cm pedestals for 96 h; the cage controls (CC) remained in their home cages for the duration of the study. In the first series of experiments, body weights and caloric intake were recorded daily, along with the performance of all animals in the swimming cylinder of Porsolt. In the second series of experiments, body weights and caloric intake were recorded, but the Porsolt test was not employed and the brains were dissected after 96 h for NE analysis by HPLC. It was observed that the REMd group had lower immobility times (p < 0.05) in the Porsolt test after only 24 h, compared to groups TC and CC.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

The influence of alcohol and sleep deprivation on stimulus evaluation.

The effects of alcohol and sleep deprivation on choice reaction time (RT) as a function of stimulus intensity, stimulus quality, and response compatibility were investigated. Fifty-four male subjects were assigned to one of three levels of alcohol (0.00, 0.07, or 0.10 BAC), and one of two levels of sleep deprivation (0 or 24 h). Stimulus intensity, stimulus quality, and response compatibility were varied (high or low), with RTs identified according to time on task. Significant main effects of each of the stimulus variables were present in baseline analysis, with low-level conditions producing longer RTs. Alcohol produced an overall slowing of RT. The combination of both treatments led to larger increases in RT for low stimulus quality. Sleep deprivation increased RT for high stimulus intensity. Alcohol increased RT for low stimulus intensity, but only when subjects were not sleep deprived. These results imply higher risk with degraded stimulus conditions, e.g., driving in settings of low visibility or at night.

Adult↗

PubMed1992

Long-term sleep deprivation as a game. The wear and tear of wakefulness.

We report here the first sleep deprivation study done on a group of 5 healthy students (1 female, 4 males, 23-24 years of age) while playing a game (Triviant). In 2 persons an EEG was recorded for 6 consecutive 24 h periods with an ambulatory monitor from the baseline night until 72 h after deprivation. The baseline night showed normal hypnograms. The students were deprived of sleep for 65 h following the baseline night. Sleep deprivation was complete and resulted in bradyphrenia, loss of memory and contact with reality, ataxia, decrease in body temperature and loss of body weight. The main sign of recuperation was a strongly increased slow-wave sleep synchronization during the first recuperation period (day-time sleep) only. There were no signs of REM rebound.

Adult↗

PubMed1989

Effect of sleep deprivation on EEG slow wave activity within non-REM sleep episodes in the rat.

Recordings of 10 rats were obtained during the first 8 h of the light period under control conditions and after 24 h of sleep deprivation (SD). Non-rapid eye movement sleep (non-REMS) and EEG spectra in the range of 0.5-4.0 Hz were analyzed for 4 sec epochs. The time course of EEG slow wave activity within non-REMS episodes was closely approximated by a saturating exponential function. The time constant of approx. 50 sec varied little over consecutive 2 h periods and was not significantly changed by SD. The maximal level of EEG slow wave activity attained within non-REMS episodes (corresponding to the asymptote level of the fitted function) decreased over consecutive 2 h periods and was massively enhanced after SD. The study documents both the invariant and the homeostatically regulated aspect of the intraepisodic build-up of EEG slow wave activity.

Animals↗

PubMed2002

Sleep deprivation potentiates the onset and duration of loss of righting reflex induced by propofol and isoflurane.

BACKGROUND: Sleep and anesthesia differ physiologically but produce a similar loss of responsiveness to environmental stimuli. Recent data suggest that neuronal networks active in naturally occurring sleep also play a role in the anesthetized state. Changes in the propensity to sleep may then modify the response to anesthetic agents. The authors tested the hypothesis that sleep-deprived rats would require less anesthetic than rested rats to achieve a similar loss of responsiveness. METHODS: Rats were subjected to a 24-h period of either sleep deprivation or ad libitum activity. Sleep deprivation was produced by placing rats on a disk that rotated when sleep was detected by electroencephalographic and electromyographic (EEG, EMG) monitoring. A fixed dose of anesthetic agent was then administered, and the time required to induce loss of righting reflex was measured. Anesthetic administration was then stopped, and the time to recovery measured. All rats received both treatments separated by 7 days. RESULTS: Sleep deprivation reduced the time to loss of righting reflex by 40% for propofol (P < 0.025) and 55% for isoflurane (P < 0.025) and prolonged the time to recovery. In a separate control experiment, exposure to the deprivation environment but with disk rotation modified to allow adequate sleep did not affect the response to anesthetic administration. CONCLUSIONS: Sleep deprivation significantly potentiated the ability of inhaled and intravenous anesthetic agents to induce a loss of righting reflex. These results support the hypothesis that neuronal networks active in sleep are also involved in the anesthetized state and suggest that sleep deprivation may partly explain the variability in patient response to anesthesia.

Administration, Inhalation↗

PubMed2004

The effects of dopaminergic agonists on genital reflexes in paradoxical sleep-deprived male rats.

Dopamine (DA) agonists provide evidence that different receptor subtypes in the central nervous system (CNS) have influence in sexual behavior. Sleep deprivation induces supersensibility of DA receptors and previous work has shown that the DA agonist apomorphine enhances spontaneous genital reflexes (penile erection-PE and ejaculation-EJ) in rats deprived of paradoxical sleep. The present study sought to extend the latter finding by assessing the effects of other DA agonists in paradoxical sleep-deprived (PSD) male rats. The DA drugs (bromocriptine and piribedil) were acutely administered to rats that had been deprived of sleep for 4 days and to normal controls. Sleep deprivation alone induced PE and this effect was potentiated by piribedil, with maximal effects occurring with the 8 mg/kg dose, whereas only one dose of bromocriptine (8 mg/kg) induced more PE in PSD rats than in non-deprived treated controls. EJs were increased in piribedil PSD groups but this response was absent after bromocriptine treatment in the dose range tested. Our data show the genital reflexes that occurred in PSD rats are potentialized by piribedil and not by bromocriptine. These DA agonists showed distinct effects in sexual response suggesting that these effects are probably due to PSD-induced DA receptor supersensitivity even though different mechanisms are involved.

Analysis of Variance↗

PubMed1989

The effects of d-amphetamine on arousal, cognition, and mood after prolonged total sleep deprivation.

Thirty-six normal male subjects underwent total sleep deprivation for 48 hours, were then administered either placebo, 5, 10, or 20 mg of d-amphetamine, and sleep deprived for an additional 12 hours. Sleep deprivation produced a significant reduction in sleep latency, as well as marked decrements in cognitive performance and self-ratings reflecting vigor and fatigue. Amphetamine reversed these effects in a dose-related way but the pattern and persistence of the reversal varied across measures. After 20 mg, sleep latency normalized for several hours, but then declined. Behavioral effects tended to follow the pattern of sleep latency. On cognitive tasks, 20 mg produced a sustained return to normal performance in an attentional arithmetic task and a gradual improvement in a verbal reasoning task. The partial temporal dissociation among sleep latency, behavioral, and cognitive effects suggests that varying doses of amphetamine may have time-related differential neurochemical effects or that various dimensions of arousal and alertness may be differentially sensitive to amphetamine.

Adult↗

PubMed2000

Sleep deprivation stimulates serotonin release in the suprachiasmatic nucleus.

Recent literature suggests that sleep deprivation has a general stimulatory effect on the central serotonergic system. Herein we report that in hamsters, sleep deprivation induced by gentle handling for 3 h under dim red light at midday stimulates serotonin release in the suprachiasmatic nuclei by as much as 171%. Basal levels of 5-HT release are re-established within 1 h after cessation of treatment. Sleep deprivation also evokes phase advances of the circadian activity rhythm averaging 2 h. When sleep deprivation is undertaken in bright light, serotonin release is stimulated, but phase-shifting is greatly inhibited. It is therefore proposed that if the phase-resetting response to sleep deprivation is mediated by increased serotonin release, light inhibits the phase-resetting effect by blocking the postsynaptic or other downstream actions of serotonin.

Animals↗

PubMed2005

Differential effects of sleep deprivation on saccadic eye movements.

STUDY OBJECTIVES: This study was designed to show the influence of sleep deprivation on different types of saccadic eye movements. DESIGN: Performance of saccadic eye movements was compared after normal sleep and sleep deprivation in a randomized, within-subjects paradigm. Parameters of voluntary and reflexive saccades were measured before and after experimental nights and after a night of recovery sleep. Additionally, subjects spent 1 adaptation night in the laboratory before the experiments. SETTING: Experiments took place under controlled laboratory conditions. PARTICIPANTS: Fifteen healthy male volunteers (aged 19-30 years). INTERVENTIONS: Each subject participated in 1 night of sleep deprivation followed by a night of recovery sleep and, on another occasion, in 2 successive nights of undisturbed sleep. MEASUREMENTS AND RESULTS: Horizontal prosaccades, antisaccades, and memory-guided saccades were recorded by means of electrooculography. They were analysed semiautomatically with respect to accuracy, peak velocity, and latency. Peak velocity was significantly reduced in all saccade tasks after 1 night of sleep deprivation but recovered after another night of sleep. Latency was prolonged after sleep deprivation only for memory-guided saccades; accuracy showed a decrease after 1 night without sleep only for prosaccades. CONCLUSIONS: Sleep deprivation has a general impairing effect on the peak velocity of saccades, reflecting possible dysfunction at the level of the brainstem reticular formation. Deficits of accuracy and latency point to dysfunction of specific brain sites such as the supplementary eye field and cerebellum, whereas the cardinal functions of the frontal and parietal eye fields were not affected. These results suggest the possibility of measuring fatigue by means of saccadic parameters, especially saccadic peak velocity.

Adult↗

PubMed1996

Effect of extended sleep deprivation on tumor growth in rats.

To assess the effect of chronic sleep deprivation on host defense, we observed growth and regression of a subdermal allogenic carcinoma (Walker 256 rat tumor) in rats undergoing 10 days of total sleep deprivation (TSD rats), yoked stimulus control (TSC) rats that were partially sleep deprived, and home cage control (HCC) rats. Tumor size was measured daily. Integrated tumor size was smaller in TSD rats than in both TSC (P = 0.04) and HCC rats (P = 0.0003). Thus host defense against these tumors (as defined by reduction in tumor size) was improved by sleep deprivation. This improvement could be a nonspecific effect, e.g., tumor growth can be inhibited by a catabolic state (dietary restriction). TSD and TSC rats lost body weight, indicating a catabolic state. However, tumor size was not predicted by body weight change, but was predicted by change in sleep time (P = 0.02). Host defense enhancement could alternatively result from enhanced immune response. Early tumor size (5 days) was similar in the three groups, but peaked sooner in TSD rats than in both TSC (P = 0.05) and HCC rats (P = 0.01), leading to large differences in size later. Immune-suppressed rats also showed little difference from HCC rats in early growth but large differences later. Thus host defense in an in vivo model that manifests a systemic immune response can be enhanced by sleep deprivation with timing, which is consistent with an enhancement of the immune response.

Animals↗

PubMedDate not supplied

Sleep deprivation selectively impairs memory consolidation for contextual fear conditioning.

Many behavioral and electrophysiological studies in animals and humans have suggested that sleep and circadian rhythms influence memory consolidation. In rodents, hippocampus-dependent memory may be particularly sensitive to sleep deprivation after training, as spatial memory in the Morris water maze is impaired by rapid eye movement sleep deprivation following training. Spatial learning in the Morris water maze, however, requires multiple training trials and performance, as measured by time to reach the hidden platform is influenced by not only spatial learning but also procedural learning. To determine if sleep is important for the consolidation of a single-trial, hippocampus-dependent task, we sleep deprived animals for 0-5 and 5-10 h after training for contextual and cued fear conditioning. We found that sleep deprivation from 0-5 h after training for this task impaired memory consolidation for contextual fear conditioning whereas sleep deprivation from 5-10 h after training had no effect. Sleep deprivation at either time point had no effect on cued fear conditioning, a hippocampus-independent task. Previous studies have determined that memory consolidation for fear conditioning is impaired when protein kinase A and protein synthesis inhibitors are administered at the same time as when sleep deprivation is effective, suggesting that sleep deprivation may act by modifying these molecular mechanisms of memory storage.

Analysis of Variance↗

PubMed2003

Deficits in avoidance responding after paradoxical sleep deprivation are not associated with altered [3H]pirenzepine binding to M1 muscarinic receptors in rat brain.

Previous work had indicated that animals that were sleep-deprived and then trained on a passive avoidance task show poor retention of the task 24 h later after being allowed to sleep freely again. Cholinergic involvement is suggested by the fact that this effect is prevented by treatment with the muscarinic agonist pilocarpine during sleep deprivation. The observation that similar deficits are observed in non-deprived rats after treatment with M1-selective antagonist compounds such as dicyclomine or pirenzepine cause similar impairments, and gave rise to the hypothesis that sleep deprivation might induce significant reductions in M1 binding in brain areas involved in learning and memory processes. Rats were deprived of sleep for 96 h and then either immediately killed, or allowed to recover sleep for 24 h before being killed. [3H]pirenzepine binding to M1 sites was examined by quantitative autoradiography in 39 different brain areas in cage controls, sleep-deprived and sleep-recovered animals (N=8 per group). No significant differences among groups were found in any brain region. A separate group of animals was subjected to the sleep deprivation procedure and then trained in a simple avoidance task. Animals were then allowed to sleep and retested 24 h later. This group showed a significant impairment in the avoidance task compared to cage controls, in agreement with previous observations. These data suggest that proactive learning/memory deficits induced by sleep deprivation cannot be attributed to altered M1 binding either immediately after deprivation (when avoidance training occurs) or after sleep has recovered (when acquisition/retention are tested). The possibility remains that alterations in M1 function occur at post-membrane second messenger systems.

Analysis of Variance↗

PubMed1990

Maintenance of antidepressant effect of sleep deprivation with the help of lithium.

The antidepressant effect of sleep deprivation is often not longer than 1 or 2 days. Therefore we investigated systematically the combination of lithium and sleep deprivation on 26 depressive patients (ICD/DSM 296). We measured the depression scores with the Hamilton Depression Scale and the Brief Depression Rating Scale on 4 days. A comparison between sleep deprivation with and without lithium showed a highly significant difference on the 2nd and 3rd days after sleep deprivation. The positive antidepressant effect remained with those who received lithium.

Adult↗

PubMed1995

Sleep deprivation: effects on work capacity, self-paced walking, contractile properties and perceived exertion.

The primary purpose of this study was to examine the effect of a 48-hour period of sleep deprivation on the performance of selected physical work tasks [30-45% of maximum oxygen consumption (VO2max)]. In addition, this study assessed the effect of continual performance of physical work during sleep deprivation on standardized physiological and psychological test scores. Nineteen male subjects performed six different physical tasks, designed to involve all major muscle groups, during a 48-hour period of sleep deprivation. Fourteen subjects served as sleep-deprivation controls. Performance on all physical work tasks decreased significantly. Neither sleep deprivation (SD) or sleep deprivation in conjunction with continuous physical work (SDW) had any effect on muscle contractile properties, anaerobic power measures or resting blood glucose and lactate concentrations. Only SD subjects demonstrated a decline in cardiorespiratory function. Self-selected walking pace decreased and perceived exertion increased significantly in the SDW group. Positive and negative mood scores were adversely affected in both groups, the total change being greatest in SD subjects. The results indicate that performance of physical work tasks requiring 30-45% VO2max declines significantly over a 48-hour period of sleep deprivation. However, maximal physiological function is not unduly compromised by either the work tasks in conjunction with sleep deprivation or by sleep deprivation alone.

Adult↗