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PubMed1989

Maximal aerobic exercise following prolonged sleep deprivation.

The effect of 60 h without sleep upon maximal oxygen intake was examined in 12 young women, using a cycle ergometer protocol. The arousal of the subjects was maintained by requiring the performance of a sequence of cognitive tasks throughout the experimental period. Well-defined oxygen intake plateaus were obtained both before and after sleep deprivation, and no change of maximal oxygen intake was observed immediately following sleep deprivation. The endurance time for exhausting exercise also remained unchanged, as did such markers of aerobic performance as peak exercise ventilation, peak heart rate, peak respiratory gas exchange ratio, and peak blood lactate. However, as in an earlier study of sleep deprivation with male subjects (in which a decrease of treadmill maximal oxygen intake was observed), the formula of Dill and Costill (4) indicated the development of a substantial (11.6%) increase of estimated plasma volume percentage with corresponding decreases in hematocrit and red cell count. Possible factors sustaining maximal oxygen intake under the conditions of the present experiment include (1) maintained arousal of the subjects with no decrease in peak exercise ventilation or the related respiratory work and (2) use of a cycle ergometer rather than a treadmill test with possible concurrent differences in the impact of hematocrit levels and plasma volume expansion upon peak cardiac output and thus oxygen delivery to the working muscles.

Adult↗
PubMed2000

The usefulness of sleep and sleep deprivation as activating methods in electroencephalographic recording: contribution to a long-standing discussion.

Sedated sleep and sleep deprivation are commonly used methods to increase the diagnostic yield of the electroencephalogram (EEG), especially in the evaluation of people with epilepsy, but the rate of activation achieved by them is controversial, as is the issue of whether it is sleep itself, or sleep deprivation which is responsible for their alleged efficacy. We retrospectively studied the EEGs of epileptic patients, examined in our laboratory, who, after having undergone an inconclusive initial routine recording, had then been examined with a second recording. This was after either: (1) sleep deprivation with evidence of drowsiness in the recordings, (2) sleep deprivation without drowsiness (indicative of the effect which sleep deprivation per se has in eliciting abnormal patterns), or (3) drug-induced sedation. The activation rates found were (1) 22.5%, (2) 24% (22.6% for sleep deprivation collectively, regardless of the presence or not of subsequent drowsiness) and (3) 27% respectively. Only the sleep deprivation rate was statistically different from the 9.6% increased rate of abnormal patterns elicited by the simple repeating of a second routine recording, while the rate of drug-induced sleep was not. Although, sleep deprivation appeared to be more effective as an activating method of EEG compared with sedated sleep, no conclusions could be drawn about which stage of sleep, wakefulness or drowsiness, is primarily responsible for the method's efficacy.

Adolescent↗
PubMed2000

Effects of sleep deprivation on free-operant avoidance.

Two studies examined effects of sleep deprivation on free-operant avoidance by rats. In Experiment 1, a 5-s shock-shock (SS) interval and 20-s response-shock (RS) interval produced baseline performances, which were reestablished after each experimental manipulation. Once baselines were established, animals were exposed to 24, 48, or 96 hr of sleep deprivation and equivalent periods of home cage and food restriction as a control condition. Compared to baseline, sleep deprivation increased response rates by increasing the proportion of brief interresponse times (IRTs); response rates changed little in the control conditions. Percentage of shocks avoided did not systematically change across conditions. In Experiment 2, the RS interval was manipulated (10, 20, and 40 s), while the SS interval (5 s) and level of sleep deprivation (48 hr) were held constant. Across RS intervals, sleep deprivation increased response rates via a shift toward brief IRTs. In addition, sleep deprivation increased the percentage of shocks avoided as an inverse function of RS intervals.

Animals↗
PubMed1996

Effects of sleep deprivation on performance: a meta-analysis.

To quantitatively describe the effects of sleep loss, we used meta-analysis, a technique relatively new to the sleep research field, to mathematically summarize data from 19 original research studies. Results of our analysis of 143 study coefficients and a total sample size of 1.932 suggest that overall sleep deprivation strongly impairs human functioning. Moreover, we found that mood is more affected by sleep deprivation than either cognitive or motor performance and that partial sleep deprivation has a more profound effect on functioning than either long-term or short-term sleep deprivation. In general, these results indicate that the effects of sleep deprivation may be underestimated in some narrative reviews, particularly those concerning the effects of partial sleep deprivation.

Affect↗
PubMed1986

Electrophysiological evaluation of three paradoxical sleep deprivation techniques in rats.

Three different techniques were used to study the effects of 72 hr deprivation of paradoxical sleep on percentages total sleep, light slow wave sleep, deep slow wave sleep and paradoxical sleep during deprivation and recovery periods in rats. The paradoxical sleep deprivation methods used were the classical platform, the pendulum and the multiple platform techniques. The different groups were continuously recorded over a base-line day, three deprivation days and four recovery days. All three groups showed clear suppression of paradoxical sleep throughout the deprivation period, although small differences between the pendulum and the multiple platform technique emerged. The distribution of sleep across the day and the amount of deep slow wave sleep were affected differently. Besides an exception immediately after deprivation, no important differences were detected on the recovery days. The recovery is characterized by an immediate rebound of paradoxical sleep, completed within two days, as well as rapid re-normalization of sleep percentages. A small rebound of deep slow wave sleep was recorded at the end of the dark period during the first three recovery days. Various sleep and non-sleep related variables of the PS deprivation techniques are discussed. It is improbable that the platform-pendulum controversy is due to differences in the amount of PS deprivation or the other sleep parameters measured here. Rather it looks as though non-specific platform effects override the effects of PS deprivation.

Animals↗
PubMed1998

Sleep deprivation activates epileptiform discharges independent of the activating effects of sleep.

An electroencephalogram (EEG) recorded after sleep deprivation (SDEEG) in epilepsy patients often discloses epileptiform discharges (ED) when routine EEG (REEG) does not, but since sleep alone activates ED, activation during SDEEG may result merely from the induction of sleep. We retrospectively investigated whether SDEEG is useful when REEG containing wakefulness and sleep fails to show ED. Subjects were patients with definite or highly probable epilepsy whose REEG lacked ED and who later underwent SDEEG. All had wakefulness and at least stage II sleep during both REEG and SDEEG. Patients with ED on REEG were specifically excluded to avoid including patients with activation due merely to the occurrence of sleep. Patient and EEG characteristics were studied, including duration of wakefulness and each sleep stage and timing and characteristics of ED. Fifteen of 29 patients (52%) had activation on SDEEG; exclusively during wakefulness in 1, exclusively during sleep in 6 and in both wakefulness and sleep in 8. Activation rates were not significantly different between wakefulness (9, 60%), stage I (11, 74%) and stage II (11, 74%). EEG characteristics were similar for REEG and SDEEG, except that total EEG duration and stage II sleep were longer in SDEEG than in REEG, which did not influence activation by a logistic regression model (p > 0.05). We conclude that sleep deprivation activates ED independent of the activating effects of sleep and therefore is useful in evaluation of suspected epilepsy even when REEG contains sleep.

Adolescent↗
PubMed1983

Sleep deprivation decreases ventilatory response to CO2 but not load compensation.

Because sleep is known to reduce ventilatory drive, and sleep deprivation is a common accompaniment to ventilatory failure, we tested ventilatory response to carbon dioxide (delta V1/delta PCO2) and response to an inspiratory flow resistive load (change in delta P100/delta PCO2 with load) after both a normal night of sleep and after 24 hours of sleep deprivation in 13 healthy volunteers. Sleep deprivation was associated with a significant decrease in delta V1/delta PCO2 from 2.51 +/- .36 to 2.09 +/- .34 L/min/mm Hg (p less than 0.02). However, load compensation was preserved during sleep deprivation. Since many acutely-ill patients are sleep deprived, an associated reduction of ventilatory drive may play a role in progressive respiratory insufficiency.

Adult↗
PubMed1992

Is sleep deprivation useful in the treatment of depression?

OBJECTIVE: The authors critically reviewed the literature on clinical applications of sleep deprivation in the treatment of depression. DATA COLLECTION: They included all studies using sleep deprivation for clinical purposes, with the exception of treatment studies that did not provide follow-up beyond a night of recovery sleep. They focused on six uses of sleep deprivation: 1) to potentiate response to antidepressant medication (13 studies), 2) to hasten the onset of action of antidepressant medication or lithium (five studies), 3) to prevent recurrent mood cycles (four studies), 4) as an alternative to antidepressant medication (five studies), 5) as a diagnostic probe (two studies), and 6) to predict response to antidepressant medication (nine studies). FINDINGS: Although the literature appears to demonstrate the efficacy of sleep deprivation as a potentiation strategy, these treatment studies have substantial methodological shortcomings. Well-designed pilot studies indicate that sleep deprivation may hasten the onset of action of thymoleptic medications. Sleep deprivation may prevent premenstrual mood swings, and response to sleep deprivation may differentiate depressive pseudodementia from primary degenerative dementia with depression. Studies attempting to use sleep deprivation to predict response to antidepressant medication have yielded inconsistent results. CONCLUSIONS: Given the noninvasive nature of sleep deprivation, it would be useful to determine if even a small subset of refractory patients respond to it. The authors suggest future research directions to determine the usefulness of this potential treatment.

Depressive Disorder↗
PubMed1982

Changes in the circadian rhythm of serum iron induced by a 5-day sleep deprivation.

The effect of 5 days of sleep deprivation on the circadian rhythm of serum iron was studied in a group of six healthy male volunteers. The results were compared with a control group of five individuals, whose normal sleep cycle was preserved, but whose daily regimen was otherwise identical with the sleep deprivation group. Their biorhythm was processed mathematically using cosinor analysis. Sleep deprivation markedly reduced the mean level of iron, diminished the absolute and relative amplitude of oscillations, disturbed the shape of the daily course of serum iron and gradually decreased the computative acrophase, i.e., shortened the period of rhythm. Forty-eight hours of recovery resulted only in a partial normalization of all the observed changes. The potential mechanisms of the observed changes are discussed.

Adult↗
PubMed1992

Sleep deprivation and house staff performance. Update 1984-1991.

All English language studies since 1984 of sleep deprivation and house staff performance are reviewed. Manual and computer surveys identified 14 such studies. Our goal is to examine whether the current literature supports the hypothesis that sleep deprivation significantly impairs house staff performance. Our review finds that the current data remain inconclusive. The causes for this uncertainty include different methodologies in assessing performance, the arbitrary definitions of sleep deprived and rested states, and lack of separation of the effects of acute and chronic sleep deprivation. Our review notes striking difference in reported effects of sleep deprivation depending on medical specialty. Surgical studies most frequently show little effect of sleep deprivation. All studies since 1990 support the hypothesis that sleep deprivation significantly impairs performance. Most studies support the impairment of physician mood with increasing sleep deprivation.

Clinical Competence↗
PubMed1994

Sleep deprivation in the rat: XVIII. Regional brain levels of monoamines and their metabolites.

Several theories have linked sleep with change in monoamine activity. However, the use of sleep deprivation to show that changes in sleep generate changes in monoamines (directly or through feedback) has produced inconsistent results. To explore whether longer sleep deprivation, better documented sleep loss, more complete controls or regional brain analyses would produce clear sleep loss-induced change, eight rats were subjected to total sleep deprivation (TSD) by the disk-over-water method for 11-20 days and were guillotined along with yoked control (TSC) and home-cage control (HCC) rats. Brains were removed and dissected to obtain the caudate, frontal cortex, hippocampus, hypothalamus, midbrain and hindbrain (pons-medulla). Tissue sections were analyzed for concentrations of serotonin (5HT), its metabolite 5-hydroxyindoleacetic acid (5HIAA), dopamine (DA), its metabolite 3,4-dihydroxyphenylacetic acid (DOPAC), and either norepinephrine or, in the caudate section, the DA metabolite homovanillic acid. The ratios DOPAC/DA and 5HIAA/5HT, which under some conditions are indicators of turnover, were also calculated. Because sleep deprivation time varied across sets of TSD, TSC and HCC rats and not all eight sets were analyzed simultaneously, a repeated-measures ANOVA was performed within sets with HCC, TSC and TSD considered as successive levels of sleep deprivation treatment. In no case did TSD rats have significantly higher or lower values of amines, metabolites or ratios than both HCC and TSC rats. The most common outlying values were for TSC rats. Thus, these results failed to demonstrate sleep loss-induced regional changes in levels of major brain monoamines or their metabolites.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dihydroxyphenylacetic Acid↗
PubMed1991

Effects of sleep deprivation on sleepiness and increased REM sleep in rats selectively bred for cholinergic hyperactivity.

In this study we employed a modification of the multiple sleep latency test (MSLT) to determine whether rats of a strain with increased cholinergic activity were sleepier compared to randomly bred control rats. Seven rats each from the Flinders sensitive line (FSL, hypercholinergic) and Flinders resistant line (FRL, age-matched controls) were kept awake for 20 min and then allowed to sleep ad libitum for 20 min. The regimen of 20 min of wakefulness followed by 20 min of sleep was repeated 12 times during the day. There were no differences in latency to sleep or to rapid eye movement (REM) sleep or in percent total sleep time, drowsy, or slow-wave sleep between FSL rats and FRL rats. However, FSL rats showed a significant increase in REM sleep compared to FRL rats. This selective increase in REM sleep may be coupled to an increase in brain muscarinic receptors in the FSL rats.

Animals↗
PubMed2004

Inter- and intra-individual variability in performance near the circadian nadir during sleep deprivation.

The study purpose was to assess inter- and intra-individual variability in neurobehavioral function near the circadian nadir during sleep deprivation and conduct exploratory factor analyses to assess relationships among alertness and performance measures during sleep deprivation. Twenty-five healthy individuals (16 females) aged 18-25 years participated. Participants were sleep deprived for two nights under controlled laboratory conditions using a modified constant routine procedure. A comprehensive battery of neurobehavioral performance tests, subjective sleepiness (SSS), and objective alertness (MWT) were assessed. Seventeen of the 22 neurobehavioral measures were impaired by sleep deprivation (all P < 0.01). The use of multiple neurobehavioral performance measures revealed impairments for all individuals during sleep deprivation. However, sleep deprivation effects were task dependent within and between individuals. Gender contributed minimally to inter-individual variability in performance. Exploratory factor analysis reduced the 22 measures to seven independent factors. Our findings indicate that no individual was especially vulnerable or resistant to the performance impairing effects of sleep deprivation. Instead, inter- and intra-individual variability in performance during sleep deprivation was task dependent. The finding that subjective sleepiness and objective alertness were not related to any performance measure during sleep deprivation suggests that these measures may assess independent brain functions.

Adolescent↗
PubMed2000

Can critically timed sleep deprivation be useful in pregnancy and postpartum depressions?

BACKGROUND: The aim of this study was to test the efficacy of critically timed sleep deprivation in major mood disorders (MMD) occurring during pregnancy and postpartum. METHODS: Nine women who met DSM-IV criteria for a MMD with onset during pregnancy or within 1 year postpartum underwent a trial of either early-night sleep deprivation (ESD), in which they were sleep deprived in the early part of one night and slept from 03:00-07:00 h, or late-night sleep deprivation (LSD), in which they were deprived of sleep in the latter part of one night and slept from 21:00-01:00 h. Mood was assessed before the night of sleep deprivation, after the night of sleep deprivation, and after a night of recovery sleep (sleep 22:30-06:30 h) by trained clinicians, blind to treatment condition, using standardized scales. RESULTS: More patients responded to LSD (nine of 11 trials: 82%) compared with ESD (two of six trials: 33%) and they responded more after a night of recovery sleep (nine of 11 nights: 82%) than after a night of sleep deprivation (six of 11 nights: 55%). Pregnant women were the only responders to ESD and the only nonresponders to LSD. LIMITATIONS: The small and heterogeneous sample size prevents us from making more definitive conclusions based on statistical analyses. CONCLUSIONS: Although the findings are preliminary, the results suggest that with further study, critically timed sleep deprivation interventions may benefit women with pregnancy or postpartum major mood disorders and potentially provide a viable alternative treatment modality for those women who are not candidates for pharmacologic or psychotherapeutic interventions. Such interventions are needed to help prevent the devastating effects of depression during pregnancy and the postpartum period on the mother, infant, her family and society.

Adult↗
PubMed1980

EEG findings and sleep deprivation.

EEG findings after sleep deprivation in 452 cases are reported. Effectiveness and specificity of this activating method in the field of epilepsy both in adult and in younger people are emphasized.

Adolescent↗
PubMed1976

Recovery sleep following different visual conditions during total sleep deprivation in man.

The findings of visual impairment during total sleep deprivation were used as a basis for a possible link between vision and sleep. It was proposed that the level of visual load imposed during sleep deprivation was an important variable, and would have a substantial effect upon recovery sleep. Six young male subjects underwent two conditions of 64 h of sleep deprivation on separate occasions. One condition incorporated a high visual load, and the other a low load. Exercise and sound were balanced. All night sleep EEGs were taken for two baseline nights, and also for two recovery nights following each condition. There was a significant increase of stage 4 on all recovery nights and a REM rebound on the second recovery night. SWS, particularly stage 4, TST and REM density, were significantly greater following the high load. Implications of these findings for sleep theories and for sleep deprivation research are discussed.

Adult↗