SEARCH · PubMed Health

Results for “SLEEP DEPRIVATION”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources

PubMed1996

Natural hypothermia and sleep deprivation: common effects on recovery sleep in the Djungarian hamster.

Sleep, daily torpor, and hibernation have been considered to be homologous processes. However, in the Djungarian hamster, daily torpor is followed by an increase in slow-wave activity (SWA; electroencephalogram power density 0.75-4.0 Hz) that is similar to the increase observed after sleep deprivation. A positive correlation was found between torpor episode length and the subsequent increase in SWA, which was highest when SWA was assumed to increase with a saturating exponential function. Thus the increase in SWA propensity during daily torpor followed similar kinetics as during waking, supporting the hypothesis that when the animal is in torpor it is incurring a sleep debt. An alternative hypothesis, proposing that the mode of arousal causes the subsequent SWA increase, was tested by warming the animals during emergence from daily torpor. Irrespective of mode of arousal, more non-rapid eye movement (NREM) sleep and a similar SWA increase was found after torpor. The data are compatible with a putative neuronal restorative function for sleep associated with the expression of SWA in NREM sleep. During torpor, when brain temperature is low, this function is inhibited, whereas the need for restoration accumulates. Recovery takes place only after return to euthermia.

Animals↗

PubMed2000

Uncompetitive stimulation of rat brain Na-K ATPase activity by rapid eye movement sleep deprivation.

Rapid eye movement sleep deprivation is associated with an increase in Na-K ATPase activity. In order to understand the possible biochemical mechanism of this increase, the kinetics of Na-K ATPase was studied. Although the enzyme activity increased after the deprivation, the catalytic efficiency of the enzyme remained unaltered. The rapid eye movement sleep deprivation increased both the Vmax and the Km suggesting an uncompetitive stimulation of the enzyme. While increase in norepinephrine resulted in an increased Vmax, that of calcium increased the Km. Since an increase in norepinephrine has been suggested after deprivation, the increased Vmax is attributed to increased norepinephrine level following deprivation. However, since rapid eye movement sleep deprivation is reported to be associated with a decrease in calcium levels, the increase in Km following deprivation may be attributed to changes in factor(s) other than calcium.

Adenosine Triphosphate↗

PubMed2000

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.

Adult↗

PubMed1995

Pituitary and peripheral thyroid hormone responses to thyrotropin-releasing hormone during sustained sleep deprivation in freely moving rats.

Sleep deprivation is associated with poor cognitive ability and impaired physical health, but the ways in which the brain and body become compromised are not understood. In sleep-deprived rats, plasma total T4 and T3 concentrations decline progressively to 78% and 47% below baseline values, respectively, brown adipose tissue 5'-deiodinase type II activity increases 100-fold, and serum TSH values are unknown. The progressive decline in plasma thyroid hormones is associated with a deep negative energy balance despite normal or increased food intake and malnutrition-like symptoms that eventuate in hypothermia and lethal systemic infections. The purpose of the present experiment was to evaluate the probable causes of the low plasma total T4 during sleep deprivation by measuring the free hormone concentration to minimize binding irregularities and by challenging the pituitary-thyroid axis with iv TRH to determine both 1) the pituitary release of TSH and 2) the thyroidal response of free T4 (FT4) and free T3 (FT3) release to the TSH increment. Sleep-deprived rats were awake 91% of the total time compared with 63% of the total time in yoked control rats and 50% of the total time during the baseline period. Cage control comparison rats were permitted to sleep normally. Sustained sleep deprivation resulted in a decline from baseline in plasma FT4 of 73 +/- 6% and FT3 of 45 +/- 12%, which were similar to the declines in total hormone concentrations observed previously; nonstimulated TSH was unchanged. In the yoked and cage control groups, FT4 also declined, but much less than that of the sleep-deprived group. The relative changes in free compared with total hormone concentrations over the study were also less parallel than those in the sleep-deprived group. The plasma TSH response to TRH was similar in all groups across experimental days. The plasma FT4 and FT3 concentrations in sleep-deprived rats increased after TRH-stimulated TSH release to an extent comparable to control values. Taken together, low basal FT4 and FT3 hormone concentrations and unchanged TSH and thyroidal responses to TRH suggest a pituitary or hypothalamic contribution to the hypothyroxinemia during sleep deprivation.

Adipose Tissue, Brown↗

PubMed1994

Administration of auditory stimulation during recovery after REM sleep deprivation.

Rapid eye movement (REM) sleep deprivation and auditory stimulation (ADS), separately, increase REM sleep in rats, cats and humans. The main goal of the present study was to test whether administration of ADS during REM sleep rebound has a synergistic effect on REM sleep elicitation. Male Wistar rats were implanted with standard sleep recording electrodes. Following the recovery period, animals were randomly assigned to the following conditions: undeprived (i.e. control) and 24, 48, 96 and 120 hours of REM sleep deprivation by the platform method. Undeprived and REM sleep-deprived animals were divided into two groups, with and without ADS. ADS was a "beep" of 80 dB and 2,000 Hz, lasting 20 msec every 10 seconds. This stimulus was applied for the first 4 hours of sleep recordings after deprivation. After that, animals were recorded for another 4 hours. In the undeprived situation, the group that received ADS increased REM sleep approximately 70% above the group that did not receive ADS, as has been reported previously (REM sleep without ADS: 38.1 +/- 13.84 vs. with ADS: 64.6 +/- 11.8, p < 0.005). No synergistic effect was observed between REM sleep deprivation and ADS for any REM sleep-deprivation schedule. This result may be explained as an increase in the excitability pattern of pontine neurons and/or changes in the cholinergic system due to REM sleep deprivation that could not be further increased by ADS.

Acetylcholine↗

PubMed1994

Effects of sleep deprivation on naval seamen: II. Short recovery sleep on performance.

Twenty male naval volunteers, aged 18 to 20 years, with 12 to 14 years of education, underwent a total sleep deprivation experiment on board a Republic of Singapore Navy landing ship in the South China Sea for a period of 42-102 hours. The sleep group comprised eight volunteers who dropped out at the 44th-46th h of the experiment and were randomly assigned to a 2 or 4 h sleep regime. The rest served as sleep-deprived controls. Neurobehavioural performance tests, profile of mood state and the Stanford Sleepiness Scale were applied 6 hourly starting from 6.00 am on the first experimental day. No thresholds were observed in the performance of tests related to manual tasks and subjective feeling, including naval tasks, mood and sleepiness scale during the sleep deprivation experiment. However, thresholds were observed in the performance of tests requiring cognitive and perceptive skills, including the grooved peg board, trail making, sea-shore rhythm, addition, digit span, digit symbol, flicker fusion and dynamometer tests. Performances in these tests were observed to deteriorate only after approximately 30 h of sleep deprivation. The Z score for the non-threshold tests (Z-N) deteriorated from -0.01 at the start of the experiment to 1.25 at the 42nd h of the experiment just before the imposed sleep and improved to 0.81 at the 48th h of the experiment just after the imposed sleep; and the Z score for the threshold tests (Z-T) varied from -0.07 at the start to 0.49 just before sleep (at the 42nd h) and to continuously deteriorate to 0.83 just after sleep (at the 48th h).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1989

Sleep deprivation and the effect on exercise performance.

Sleep deprivation or partial sleep loss are common in work conditions as rotating shifts and prolonged work hours, in sustained military operations and in athletes competing in events after crossing several time zones or engaged in ultramarathon or triathlon events. Although it is well established that sleep loss has negative effects on mental performance, its effects on physical performance are equivocal. This review examines the latter question in light of recent studies published on this problem. Sleep deprivation of 30 to 72 hours does not affect cardiovascular and respiratory responses to exercise of varying intensity, or the aerobic and anaerobic performance capability of individuals. Muscle strength and electromechanical responses are also not affected. Time to exhaustion, however, is decreased by sleep deprivation. Although ratings of perceived exertion always increased during exercise in sleep-deprived (30 to 60 hours) subjects compared with normal sleep, this is not a reliable assessment of a subject's ability to perform physical work as the ratings of perceived exertion are dissociated from any cardiovascular changes in sleep deprivation. Examination of the various hormonal and metabolic parameters which have been measured in the studies reviewed reveals that the major metabolic perturbations accompanying sleep deprivation in humans are an increase in insulin resistance and a decrease in glucose tolerance. This may explain the reduction in observed time to exhaustion in sleep-deprived subjects. The role of growth hormone in mediating altered carbohydrate metabolism may be of particular relevance as to how sleep deprivation alters the supply of energy substrate to the muscle.

Exercise↗

PubMed1993

Repeated partial sleep deprivation progressively changes in EEG during sleep and wakefulness.

The effect of repeated partial sleep deprivation on sleep stages and electroencephalogram (EEG) power spectra during sleep and wakefulness was investigated in nine healthy young subjects. Three baseline nights of 8 hours (2300-0700 hours) were followed by four nights with 4 hours of sleep (2300-0300 hours) and three recovery nights of 8 hours (2300-0700 hours). Sleep restriction curtailed sleep stages 1 and 2 as well as rapid eye movement (REM) sleep, but left slow wave sleep largely unaffected. In the first two recovery nights, total sleep time and REM sleep were enhanced, and sleep latency was shortened. Slow wave sleep was increased only in the first recovery night. In accordance with the prediction of the two-process model of sleep regulation, slow wave activity (SWA; spectral power density in the 0.75-4.5-Hz range) in nonrapid eye movement (NREM) sleep increased by approximately 20% in the first night following sleep restriction, remained at this level in the subsequent 3 nights and decreased immediately after the first recovery night. In contrast to these immediate changes, progressive and more persistent changes were seen in the EEG activity of higher frequencies. Thus, activity in the upper delta band tended to gradually increase from night to night during the sleep restriction period, whereas after an initial increase, activity in the theta-alpha band changed in the opposite direction. The progressive changes were also present in the EEG spectra of REM sleep and wakefulness. Because the time course of these changes paralleled the cumulative deficit in REM sleep, they may represent a correlate of REM sleep pressure.

Adult↗

PubMed1998

Selective REM sleep deprivation in humans: effects on sleep and sleep EEG.

To investigate rapid eye movement (REM) sleep regulation, eight healthy young men were deprived of REM sleep for three consecutive nights. In a three-night control sleep deprivation (CD) session 2 wk later, the subjects were repeatedly awakened from non-REM sleep in an attempt to match the awakenings during the REM sleep deprivation (RD) nights. During the RD nights the number of sleep interruptions required to prevent REM sleep increased within and across consecutive nights. REM sleep was reduced to 9.2% of baseline (CD nights: 80.7%) and rose to 140.1% in the first recovery night. RD gave rise to changes in the EEG power spectra of REM sleep. Power in the 8.25- to 11-Hz range was reduced in the first recovery night, an effect that gradually subsided but was still present in the third recovery night. The rising REM sleep propensity, as reflected by the increase of interventions within and across RD nights, and the moderate REM sleep rebound during recovery can be accounted for by a compensatory response that serves REM sleep homeostasis. The changes in the electroencephalogram power spectra, which were observed during enhanced REM sleep propensity, may be a sign of an altered quality of REM sleep.

Adult↗

PubMed1986

Sleep deprivation and kindled seizures.

Total sleep deprivation in a treadmill, and REM sleep and partial slow-wave sleep deprivation by the platform technique led to reduced seizure threshold in kindled rats. After treadmill deprivation there was also a reduction in seizure duration. Arousing aspects of the sleep deprivation procedures counteracted the sleep deprivation effect. In the treadmill experiment this led to an increase in seizure threshold in the control group. In the platform experiment the reduction in seizure threshold was delayed for 24 h after the deprivation because of these short-acting processes. Seizure thresholds remained low for at least 72 h.

Animals↗

PubMed1985

Sleep function, with particular reference to sleep deprivation.

Human total sleep deprivation (TSD) findings up to the present show that the organ most affected is the brain, which displays psychological and some neurological decriments. The rest of the body seems to cope surprisingly well, indicating little sign of stress or malfunction. Central nervous system (CNS) effects also include some impairment to homeostatic control, particularly thermoregulation, which in humans seem to be minor, but for small mammals the outcome may be more serious. In humans, only a specific part of the lost sleep is made up, suggesting that a certain portion of a night's sleep ("obligatory" sleep) is essential to the brain, and that the remainder ("facultative" sleep) is more dispensable. Contrasting with the nominal TSD effects on the body (excluding the CNS), there are claims that sleep is necessary for general tissue growth and repair. The underlying evidence is examined, but is shown to have alternative interpretations. Anabolism may not rely so much on sleep, but on food intake and rest.

Behavior↗

PubMed1991

Effects of selective adrenoceptor agonists and antagonists on aggressive behavior elicited by apomorphine, DL-dopa and fusaric acid in REM-sleep-deprived rats.

REM sleep deprivation (REMSD) results in behavioral changes such as the appearance of affective aggression induced by apomorphine (APO) and other dopaminergic agents. REMSD modifies dopamine-mediated behavior as well as the adrenergic receptor sensitivity. This paper evaluates the interaction between these two neurotransmission systems through changes in APO-, DL-DOPA- and fusaric acid (FA)-induced aggressive behavior in REMSD rats pretreated with phentolamine, propranolol, metaraminol, prazosin, clonidine, yohimbine, isoproterenol, butoxamine and maprotiline. Only isoproterenol reduced FA-induced aggressiveness. No specific changes in aggressiveness were noticed with other treatments and not even inhibitors of norepinephrine transmission induced aggressive behavior. It is concluded that norepinephrine had a slight inhibitory action on aggressiveness elicited by dopaminomimetic agents in REMSD rats. Beta-adrenoceptors could be responsible for this effect since only beta-selective drugs reduced aggression. As REMSD reduces beta-adrenoceptor sensitivity, only minor changes in aggressiveness could be observed. It was noted that the three drugs used to induce aggressive behavior elicited different patterns of aggression.

Aggression↗

PubMed1997

Sleep latency measures of caffeine effects during sleep deprivation.

Studies of stimulants during sleep deprivation have used performance assessment batteries (PABs) and occasionally the multiple sleep latency test (MSLT) as measures. Another type of sleep latency test, the maintenance of wakefulness test (MWT), assesses ability to remain awake without assistance, rather than ability to go to sleep. The MWT previously has not been used in studies of stimulants during sleep deprivation. This study of caffeine during 64 h without sleep included a PAB, the MSLT, and a single MWT trial per day. The PAB and the MSLT were sensitive to caffeine effects during the first 24 h without sleep. The MWT demonstrated that caffeine improved ability to remain awake even after 2 nights of sleep deprivation. Ability to go to sleep and ability to stay awake during sleep deprivation appear to be affected differently by caffeine. PAB testing may fail to detect this stimulant effect because technicians prevent subjects from nodding off during PAB testing, an external support not available to subjects during the MWT and also not available in many real-world work environments. The MWT was more sensitive to stimulant amelioration of sleep-deprivation effects. The findings need to be validated with MWTs at other times of day and with other stimulants.

Adult↗

PubMed2001

Sleep deprivation as a model experimental antidepressant treatment: findings from functional brain imaging.

This paper reviews the functional brain imaging studies in depressed patients treated with sleep deprivation. Sleep deprivation is an excellent experimental model of antidepressant treatments which offer new opportunities to understand the basic neural mechanisms. Its antidepressant effects are efficacious and rapid; sleep deprivation is easy to administer, inexpensive, and relatively safe; it can be studied in patients, normal controls, and animals; and it may lead to new treatments and new paradigms for antidepressant therapies. Seven published papers, coming from five different research centers, using either positron emission tomography (PET) with 18fluorodeoxyglucose (FDG) or single photon emission computerized tomography (SPECT) with Technetium-99-bexamethyl propyleneamine oxime (HMPAO) have relatively consistent findings. First, before sleep deprivation, responders have significantly elevated metabolism compared with non-responders, and usually the normal controls, in the orbital medial prefrontal cortex, and especially in the ventral portions of the anterior cingulate cortex. Secondly, after sleep deprivation, these hyperactive areas normalize in the responders. The magnitude of the clinical improvement was significantly correlated with decreased local glucose metabolic rate or cerebral blood flow in three studies. The results are consistent with some but not all functional brain imaging studies of antidepressant medications in depressed patients. Finally, a SPECT study using a radioactively labeled D2 receptor antagonist suggests that the antidepressant benefits of sleep deprivation are correlated with endogenous release of dopamine.

Brain↗

PubMed1988

Sleep deprivation increases thalamocortical excitability in the somatomotor pathway, especially during seizure-prone sleep or awakening states in feline seizure models.

Pathological somatomotor system excitability and generalized seizures occur throughout the sleep-awake cycle but peak at different times in the amygdala kindling and systemic penicillin epilepsy models. Sleep loss increases seizure activity in both models during all waking and sleep states but does not alter the timing of seizure susceptibility in the sleep-wake cycle. Although the mechanism for sleep-deprivation seizures is unknown, we propose that sleep loss magnifies somatomotor system hyperexcitability patterns in all states, thereby increasing seizure vulnerability at all times but preferentially during seizure-prone intervals. To evaluate this hypothesis, the timing of ventral lateral thalamic and motor cortex excitability, indexed by amplitudes of primary evoked responses, was studied throughout the sleep-wake cycle in eight cats before and after nearly total sleep deprivation. Sleep loss was induced by 24-h exposure to a modified "flower pot" procedure; the control procedure consisted of 24-h exposure to a larger pedestal which did not affect sleep time. Findings confirmed the hypothesis, as follows: (i) Sleep deprivation increased ventral lateral thalamic and motor cortical excitability nonspecifically. (ii) Motor cortex hyperexcitability correlated best with penicillin seizure activity; both were elevated in slow-wave sleep and drowsiness after awakening from slow-wave sleep before sleep loss and were further increased by sleep loss. (iii) Ventral lateral thalamic hyperexcitability patterns correlated best with the timing of kindled seizure susceptibility; both peaked during transitions from slow-wave to REM sleep before and after sleep loss but were maximal after sleep loss. (iv) Sleep loss increased thalamocortical excitability and seizure susceptibility during stable REM sleep in both models, but values were lower than in other states. These results suggest a chronic neuropathology at different levels of the neuraxis for dissimilar epilepsy models and upon which the sleep-waking state modulation of seizures is superimposed. Sleep deprivation may aggravate seizures in both models by nonspecific enhancement of thalamic and cortical excitability.

Animals↗

PubMed1998

Subdiaphragmatic vagotomy does not block sleep deprivation-induced sleep in rats.

Cytokines, such as interleukin-1beta (IL-1beta), are involved in physiological sleep regulation and in the sleep responses to sleep deprivation. Sleep deprivation increases systemic cytokine levels and recent evidence suggests that cytokine-to-brain communication occurs via the vagus nerve. Furthermore, the vagus nerve plays a role in sleep responses elicited by feeding and vagal activity affects electroencephalographic (EEG) activity. Thus, this study examined sleep-wake activity and brain temperature (Tbr) responses to sleep deprivation in subdiaphragmatically vagotomized and sham-operated rats. In control rats, 6 h of total sleep deprivation significantly increased nonrapid eye movement sleep (NREMS), rapid eye movement sleep (REMS), and electroencephalographic slow-wave activity during nonrapid eye movement sleep. Brain temperature was significantly increased during the 6 h of sleep deprivation and decreased following sleep deprivation. Vagotomy had no significant effects on any of these variables. These results indicate that the subdiaphragmatic vagus nerve is not critical in the sleep and thermoregulatory responses after 6 h of sleep deprivation. Together with other data, the current results suggest that central pools of interleukin-1 are important in moderate sleep deprivation-induced sleep responses and that vagotomy does not disrupt the ability to increase sleep using a well-known sleep-inducing stimulus likely mediated by brain cytokines.

Animals↗

PubMed2005

Manipulating REM sleep in older adults by selective REM sleep deprivation and physiological as well as pharmacological REM sleep augmentation methods.

Experimental approaches to manipulate REM sleep within the cognitive neuroscience of sleep are usually based on sleep deprivation paradigms and focus on younger adults. In the present study, a traditional selective REM sleep deprivation paradigm as well as two alternative manipulation paradigms targeting REM sleep augmentation were investigated in healthy older adults. The study sample consisted of 107 participants, male and female, between the ages of 60 and 82 years, who had been randomly assigned to five experimental groups. During the study night, a first group was deprived of REM sleep by selective REM sleep awakenings, while a second group was woken during stage 2 NREM sleep in matched frequency. Physiological REM sleep augmentation was realized by REM sleep rebound after selective REM sleep deprivation, pharmacological REM sleep augmentation by administering an acetylcholinesterase inhibitor in a double-blind, placebo-controlled design. Deprivation and augmentation paradigms manipulated REM sleep significantly, the former affecting more global measures such as REM sleep minutes and percentage, the latter more organizational aspects such as stage shifts to REM sleep, REM latency, REM density (only pharmacological augmentation) and phasic REM sleep duration. According to our findings, selective REM sleep deprivation seems to be an efficient method of REM sleep manipulation in healthy older adults. While physiological rebound-based and pharmacological cholinergic REM sleep augmentation methods both failed to affect global measures of REM sleep, their efficiency in manipulating organizational aspects of REM sleep extends the traditional scope of REM sleep manipulation methods within the cognitive neuroscience of sleep.

Aged↗

PubMed1975

Total sleep deprivation on endogenous depression.

Ten endogenous depressive patients were deprived of sleep for two whole nights according to the following schedule: sleep/sleep deprivation/sleep/sleep deprivation/sleep. No drugs were administered. Experimental conditions were as neutral as possible. Blind and nonblind ratings were taken. The patients were generally rated as improved after sleep deprivation, but a substantial effect, though temporary with rapid relapse, occurred in only two cases. After subsequent sleep, relapse followed as a rule. The net antidepressive effect of the total procedure was slightly more than nil.

Adult↗