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At least 19 recordsLinked to original sources
PubMed2000

Caffeine during sleep deprivation: sleep tendency and dynamics of recovery sleep in rats.

The adenosine antagonist caffeine disrupts sleep, but whether caffeine promotes wakefulness by interfering with the expression of sleep or by attenuating sleepiness is unknown. The ability of caffeine to reduce sleep tendency in rats was directly tested by quantifying the number of stimuli needed to maintain wakefulness during sleep deprivation for 6 h after systemic caffeine treatment. In addition, the influence of caffeine on the dynamics between nonrapid-eye-movement (NREM) and rapid-eye-movement (REM) sleep was investigated by comparing the magnitude and time course of the compensatory sleep responses for 42 h postsleep deprivation. Caffeine significantly reduced the attempts to sleep during sleep deprivation, F(1,9) 8.83, p = 0.0157; 44.9% of vehicle), but did not change compensatory slow-wave activity during recovery sleep. During the initial recovery phase, caffeine suppressed compensatory REM sleep and reduced, but did not block, compensatory NREM sleep duration and continuity. By 42 h postsleep deprivation, the amount of NREM recovered (70.0% of deficit) did not differ from vehicle. In contrast, the REM sleep deficit recovered after caffeine (100%) was more than after vehicle (43.9%). Thus, caffeine slowed the rate of compensatory sleep after sleep deprivation, as indexed by the duration of sleep states and sleep continuity.

Animals↗
PubMed1987

Sleep EEG with or without sleep deprivation? Does sleep deprivation activate more epileptic activity in patients suffering from different types of epilepsy?

A sleep EEG of 190 patients without sleep deprivation was recorded, followed by a sleep EEG after 24 h of sleep deprivation on the next day. The patients suffered from various types of epilepsy, in their routine EEGs no epileptic discharges were seen. Both sleep EEGs were recorded under the same antiepileptic drugs. A waking EEG was recorded immediately before each sleep EEG. The activation rates of epileptic activity in 52.6% (without sleep deprivation) and 53.2% (with sleep deprivation) of the patients showed no significant differences. Also on classifying the epileptic discharges no real difference was found between the 2 methods (generalized: 29.5 vs. 29.5%, generalized with lateral emphasis: 11.1 vs. 9.5%, focal: 12.1 vs. 14.2%). Only in the waking EEG, recorded immediately before the sleep EEG after sleep deprivation, a few more patients showed epileptic discharges (33.6 vs. 27.4%). Without there being any significant differences between the 2 methods there were some different results in comparing the EEG with the clinical findings: significantly more epileptic activity was shown in patients who had their first seizure before the age of 20 (55.6 and 55.6% vs. 26.3 and 31.6%), amongst females (59.8 and 61.9% vs. 45.2 and 44.1%), in awakening grand mal (= primary generalized tonic-clonic seizures, 76.5 and 70%) and in absences (69 and 72.4%). The higher activation rates in young subjects, in patients with a family history of seizures, with pathological neurological findings, mental retardation and delayed psychomotoric development in early childhood, were not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1997

Differences in sleep variables, blood adenosine, and body temperature between hypothyroid and euthyroid rats before and after REM sleep deprivation.

Sleep deprivation causes an increase in energy expenditure in animals. Thyroid gland function has been related to metabolic function, and this may be compromised in sleep manipulations. The objectives of the present study were the following: 1) to develop a model of hypothyroid rats by surgical removal of thyroid glands without extirpation of the parathyroid; 2) to observe the sleep architecture in euthyroid (Etx) and hypothyroid (Htx) rats, both before and after rapid eye movement (REM) sleep deprivation (96 hours); 3) to challenge both groups (i.e. Etx and Htx) with REM sleep deprivation (96 hours) and then evaluate the effects on temperature; and 4) to measure the levels of adenosine and thyroid hormones in blood. One-month-old Wistar male rats (weight 90-100 g) were studied. The thyroid gland was removed, and the parathyroid glands were reimplanted within the neck muscle (Htx) under halothane anesthesia. A sham-operated group was also included (Etx). Four months later, the animals were studied according to the following protocols. Protocol 1: Animals of both groups (i.e. Etx and Htx) were implanted for sleep recordings. After a baseline polysomnography, these animals were REM sleep deprived by the platform method (96 hours). Protocol 2. An intraperitoneal temperature transducer was placed into animals of both groups under deep halothane anesthesia. They were studied at baseline, during 96 hours of REM sleep deprivation, and on the rebound period. Protocol 3: Plasma thyroid hormones [T3, T4, and thyroid-stimulating hormone (TSH)] and plasma adenosine were determined in both groups. Results of protocol 1 indicated that the main difference observed in Htx rats during the baseline sleep was an increase in delta sleep (slow-wave sleep 2) and a reduction in waking time compared with Etx animals. REM sleep rebound after 96 hours of REM sleep deprivation was similar in both groups. In protocol 2, the main finding was that Htx animals had reduced body temperature. A significant difference in body temperature between Etx and Htx animals was found mainly during lights-on period. REM sleep deprivation in the Etx group produced an increase in body temperature. Htx animals showed the opposite effect, with a reduction in body temperature during and after REM sleep deprivation. In protocol 3, the main findings were that Htx animals exhibited a significant reduction in blood thyroid hormones (T3, T4), and that they also had high levels of plasma adenosine. REM sleep deprivation produces changes in temperature regulation. The increase in body temperature during REM sleep deprivation may require thyroid integrity. Absence of the thyroid gland does not seem to influence REM sleep recovery after its deprivation. The high plasma adenosine levels found in the Htx group may explain the increase in delta sleep in this group.

Adenosine↗
PubMed2000

Progression of influenza viral infection through the murine respiratory tract: the protective role of sleep deprivation.

Sleep deprivation is reported to have both beneficial and harmful effects upon host defenses. In the work reported herein, we address the effects of sleep deprivation on the mucosal anti-influenza defenses of both immune and nonimmune BALB/c mice. Sleep deprivation does not depress existing mucosal antiviral defenses in the respiratory tracts of BALB/c mice; in fact, it may actually be beneficial. Nasal mucosal immunity is not adversely affected in immune mice by sleep deprivation. In nonimmune mice, sleep deprivation slows or prevents the progress of nasal influenza viral infection down the trachea into the lungs. By 72 hours post-infection, 12 of 12 control mice shed virus into bronchioalveolar lavages (BAL) while only 2 of 12 sleep deprived mice shed virus (p<0.001). BAL levels of IL-1beta and interferon alpha were increased in sleep deprived animals, suggesting that sleep deprivation may exert its beneficial effects on the respiratory tract by upregulating the production of antiviral cytokines.

Animals↗
PubMed2005

EEG spectral power and cognitive performance during sleep inertia: the effect of normal sleep duration and partial sleep deprivation.

Sleep inertia (SI) is a transient period occurring immediately after awakening, usually characterized by performance decrement. When sleep is sufficient, SI is moderate, and produces few or no deficit. When it is associated with prior sleep deprivation, SI shows dose-dependent negative effects on cognitive performance, especially when subjects have been awaken in slow wave sleep (SWS). In the present study, spectral analysis was applied during the last 10 min before and the first 10 min after awakening, and during 1 h after awakening while subjects performed the Stroop test. Seventeen subjects were divided into a Control group who slept 8 h, and a Sleep Deprived group who slept only 2 h. The results show that performance was normal in the Control group, whereas reaction time was increased during the first half hour and error level during the second half hour in the Sleep Deprived group. Spectral analysis applied on the waking EEG during the whole test session showed that alpha activity was increased in both groups, but theta power only in the Sleep Deprived group. There was a high positive correlation in sleep deprived subjects between delta power during the last 10 min of sleep and subsequent performance decrement in speed and accuracy. Comparison of individual records showed a high positive correlation between spectral power before and after awakening in the Control group (generally in the sense of an increased frequency band), but no correlation was found in the Sleep Deprived group who exhibited a rather disorganized pattern. We discuss these results in terms of incoherence in the EEG continuity during sleep offset after prior sleep loss, which could partly account for the performance decrement observed during SI in sleep deprived subjects.

Adult↗
PubMed2003

A comparison of tyrosine against placebo, phentermine, caffeine, and D-amphetamine during sleep deprivation.

Sleep deprivation can impair alertness and cognitive and motor performance. We hypothesized that the amino acid tyrosine might reduce deleterious effects of sleep deprivation. Seventy-six healthy males, age 18-35 years, participated in a four-day protocol that included a habituation night, a baseline night, a 40.5 h period without sleep, and a recovery night. Tyrosine 150 mg/kg, caffeine 300 mg/70 kg, phentermine 37.5 mg, D-amphetamine 20 mg and placebo were administered in a double-blind, randomized fashion to compare their effects on the time it took to fall asleep, on endocrine responses during sleep deprivation, and on sleep quantity, quality and architecture as measured by polysomnography during recovery sleep. When given after 36 h without sleep, tyrosine had no significant effect on any parameter of sleep. D-amphetamine produced marked decrease in sleep drive but caused deleterious effects on many aspects of recovery sleep. Still, D-amphetamine was associated with increased alertness on the first recovery day. Phentermine and caffeine both decreased sleep drive during sleep deprivation, but phentermine impaired rapid-eye-movement (REM) recovery sleep. Tyrosine (when compared to placebo) had no effect on any sleep related measure, but it did stimulate prolactin release.

Adolescent↗
PubMed2002

Hypothalamic thyrotropin-releasing hormone mRNA responses to hypothyroxinemia induced by sleep deprivation.

Sleep deprivation in rats results in progressive declines in circulating concentrations of both total and free thyroxine (T(4)) and triiodothyronine (T(3)) without an expected increase in plasma thyroid-stimulating hormone (TSH). Administration of thyrotropin-releasing hormone (TRH) results in appropriate increases in plasma TSH, free T(4), and free T(3) across experimental days, suggesting deficient endogenous TRH production and/or release. This study examined transcriptional responses related to TRH regulation following sleep deprivation. In situ hybridization was used to detect and quantitate expression of mRNAs encoding prepro-TRH and 5'-deiodinase type II (5'-DII) in brain sections of six rats sleep deprived for 16-21 days, when there was marked hypothyroxinemia, and in sections from animals yoked to the experimental protocol as well as from sham controls. TRH transcript levels in the paraventricular nucleus (PVN) were essentially unchanged at 15-16 days but increased to about threefold control levels in three of four rats sleep deprived for 20-21 days, a change comparable to that typically found in prolonged experimental hypothyroidism. There was no evidence for suppression of 5'-DII mRNA levels, which would be a sign of T(3) feedback downregulation of neurons in the PVN. A failure to increase serum TSH in response to hypothyroxinemia and to increased prepro-TRH mRNA expression indicates that alterations in posttranscriptional stages of TRH synthesis, processing, or release likely mediate the central hypothyroidism induced by sleep deprivation.

Animals↗
PubMed2002

Increases in amino-cupric-silver staining of the supraoptic nucleus after sleep deprivation.

Sleep deprived rats undergo a predictable sequence of physiological changes, including changes in skin condition, increased energy expenditure, and altered thermoregulation. Amino-cupric-silver staining was used to identify sleep deprivation related changes in the brain. A significant increase in staining was observed in the supraoptic nucleus (SON) of the hypothalamus of rats with high sleep loss (>45 h) vs. their yoked controls. Follow-up experiments showed that staining was not significantly different in rats sleep deprived for less than 45 h, suggesting that injurious sleep deprivation-related processes occur above a threshold quantity of sleep loss. These anatomical changes suggest that the effects of sleep deprivation may be related to protein metabolism in certain brain regions.

Animals↗
PubMed1996

The effect of sleep deprivation on sleep states, breathing events, peripheral chemoresponsiveness and arousal propensity in healthy 3 month old infants.

We wished to investigate the effects of sleep deprivation on sleep, arousal propensity, respiratory events and peripheral chemoresponses in healthy infants, since these effects might be relevant to mechanisms concerned with some cases of sudden infant death syndrome. Paired observations were made overnight during natural sleep and following sleep deprivation, in a randomized fashion, in 15 healthy infants aged 78 (7) days (mean (SD)). Polysomnograms were recorded and sleep was scored using Anders' criteria. Respiratory events were categorized into central, mixed and obstructive apnoeas. Peripheral chemoresponses were measured during quiet sleep from the respiratory response to two-breath alternations in fractional inspiratory oxygen (F1, O2) (0.42 and 0.00). Arousal propensity was determined from awakening and arousal thresholds to graded photic and auditory stimuli during quiet sleep, and from spontaneous awakenings and limb movements. Compared with natural sleep, following sleep deprivation infants maintained a greater proportion of quiet sleep (39 vs 44%). There was no measurable change in arousal propensity. During quiet sleep, obstructed breathing events tended to be more common after sleep deprivation (0.1 vs 0 events.h-1) and the expiratory time during baseline breathing increased significantly (1.27 vs 1.58 s) although the decrease in respiratory rate was not significant (32 vs 30 breaths.min-1). Peripheral chemoresponses altered significantly, alternations in tidal volume/inspiratory time (VT/tI) as a measure of inspiratory drive increased after sleep deprivation (9 vs 21%). In conclusion, following short-term sleep deprivation in infancy, respiratory control alters, peripheral chemoresponsiveness increases in magnitude and the timing of baseline breathing alters, without any detectable alteration in arousal propensity. This state may be associated with an increased vulnerability to obstructive respiratory events.

Arousal↗
PubMed2006

Impaired decision making following 49 h of sleep deprivation.

Sleep deprivation reduces regional cerebral metabolism within the prefrontal cortex, the brain region most responsible for higher-order cognitive processes, including judgment and decision making. Accordingly, we hypothesized that two nights of sleep loss would impair decision making quality and lead to increased risk-taking behavior on the Iowa Gambling Task (IGT), which mimics real-world decision making under conditions of uncertainty. Thirty-four healthy participants completed the IGT at rested baseline and again following 49.5 h of sleep deprivation. At baseline, volunteers performed in a manner similar to that seen in most samples of healthy normal individuals, rapidly learning to avoid high-risk decks and selecting more frequently from advantageous low-risk decks as the game progressed. After sleep loss, however, volunteers showed a strikingly different pattern of performance. Relative to rested baseline, sleep-deprived individuals tended to choose more frequently from risky decks as the game progressed, a pattern similar to, though less severe than, previously published reports of patients with lesions to the ventromedial prefrontal cortex. Although risky decision making was not related to participant age when tested at rested baseline, age was negatively correlated with advantageous decision making on the IGT, when tested following sleep deprivation (i.e. older subjects made more risky choices). These findings suggest that cognitive functions known to be mediated by the ventromedial prefrontal cortex, including decision making under conditions of uncertainty, may be particularly vulnerable to sleep loss and that this vulnerability may become more pronounced with increased age.

Adult↗
PubMed2006

The neural basis of interindividual variability in inhibitory efficiency after sleep deprivation.

Sleep deprivation results in the loss of our ability to suppress a prepotent response. The extent of decline in this executive function varies across individuals. Here, we used functional magnetic resonance imaging to study the neural correlates of sleep deprivation-induced differences in inhibitory efficiency. Participants performed a go/no-go task after normal sleep and after 24 h of total sleep deprivation. Regardless of the extent of change in inhibitory efficiency, sleep deprivation lowered go/no-go sustained, task-related activation of the ventral and anterior prefrontal (PFC) regions bilaterally. However, individuals better able to maintain inhibitory efficiency after sleep deprivation could be distinguished by lower stop-related, phasic activation of the right ventral PFC during rested wakefulness. These persons also showed a larger rise in such activation both here and in the right insula after sleep deprivation relative to those whose inhibitory efficiency declined.

Adult↗
PubMed2005

Metabolic and endocrine effects of sleep deprivation.

Sleep deprivation has multiple effects on endocrine and metabolic function. In particular, sleep restriction is accompanied by increased cortisol levels in the afternoon and early evening and a shorter quiescent period compared with extended sleep periods. Those alterations could facilitate central and peripheral disturbances that are associated with glucocorticoid excess, such as memory deficits, and are similar to those observed in aging. Thus, chronic sleep loss could contribute to acceleration of the aging process. Sleep restriction is also associated with an impairment of carbohydrate tolerance, similar to that observed in individuals with clinically significant impaired glucose tolerance. Thus, chronic sleep deprivation may increase the risk for diabetes. Finally, sleep plays an important role in energy balance. Partial sleep deprivation was found to be associated with a decrease in plasma levels of leptin and a concomitant increase in plasma levels of ghrelin; subjective ratings of hunger and appetite also increased (the appetite for protein-rich foods was not significantly affected). Moreover, a remarkable correlation was found between the increase in hunger and the increase in the ghrelin:leptin ratio. Thus, the neuroendocrine regulation of appetite and food intake appears to be influenced by sleep duration, and sleep restriction may favor the development of obesity.

Appetite↗
PubMed2005

The wake-promoting hypocretin/orexin neurons change their response to noradrenaline after sleep deprivation.

Sleep deprivation is accompanied by the progressive development of an irresistible need to sleep, a phenomenon whose mechanism has remained elusive. Here, we identified for the first time a reflection of that phenomenon in vitro by showing that, after a short 2 h period of total sleep deprivation, the action of noradrenaline on the wake-promoting hypocretin/orexin neurons changes from an excitation to an inhibition. We propose that such a conspicuous modification of responsiveness should contribute to the growing sleepiness that accompanies sleep deprivation.

Animals↗
PubMed2006

Paradoxical sleep deprivation and sleep recovery: effects on the hypothalamic-pituitary-adrenal axis activity, energy balance and body composition of rats.

Numerous studies indicate that sleep deprivation alters energy expenditure. However, this conclusion is drawn from indirect measurements. In the present study, we investigated alterations of energy expenditure, body composition, blood glucose levels, plasma insulin, adrenocorticotropic hormone (ACTH) and corticosterone levels immediately after 4 days of sleep deprivation or after 4 days of sleep recovery. Rats were sleep deprived or maintained in a control environment (groups sleep-deprived/deprivation and control/deprivation). One half of these animals were sacrificed at the end of the deprivation period and the other half was transported to metabolic cages, where they were allowed to sleep freely (groups sleep-deprived/recovery and control/recovery). At the end of the sleep recovery period, these rats were sacrificed. After sleep deprivation, sleep-deprived rats exhibited loss of body weight, augmented energy expenditure and reduced metabolic efficiency compared to control rats. These alterations were normalised during the sleep recovery period. The body composition of sleep-deprived rats was altered insofar as there was a loss of fat content and gain of protein content in the carcass compared to control rats. However, these alterations were not reversed by sleep recovery. Finally, plasma levels of insulin were reduced during the sleep deprivation period in both control and sleep deprived groups compared to the recovery period. After the deprivation period, plasma ACTH and corticosterone levels were increased in sleep-deprived rats compared to control rats, and although ACTH levels were similar between the groups after the sleep recovery period, corticosterone levels remained elevated in sleep-deprived rats after this period. By means of direct measurements of metabolism, our results showed that sleep deprivation produces increased energy expenditure and loss of fat content. Most of the alterations were reversed by sleep recovery, except for corticosterone levels and body composition.

Adipose Tissue↗
PubMed1996

Overnight human plasma melatonin, cortisol, prolactin, TSH, under conditions of normal sleep, sleep deprivation, and sleep recovery.

Early investigations of the effect of sleep deprivation on plasma melatonin reported no major changes. Recently, 36 hrs of sleep deprivation was reported to elevate melatonin levels on the post-sleep deprivation night. Given these contradictions melatonin, cortisol, prolactin, and thyroid stimulating hormone before, during, and, after sleep deprivation were examined in nine healthy young males following one night of sleep deprivation. Hormone levels at hourly intervals, for each night, were statistically analyzed by a repeated measures, two-way factorial ANOVA. ANOVA was also performed for measures of area under the curve (AUC). No significant differences were observed for melatonin levels. Cortisol was significantly higher on the sleep deprivation night presumably reflecting the aroused state accompanying being awake; however, there were several time points on the control night when it was elevated also. Prolactin was higher on the post-sleep deprivation and control nights but did not rise on the deprivation night, indicating a useful nonpolysomnographic index for discriminating overnight sleep and awake states. TSH levels showed a similar rise during the control and sleep deprivation nights, but remained flat on the post-sleep deprivation night. It appears that the pineal is insulated against feedback from changes to the level of arousal accompanying sleep and wakefulness. In comparison, cortisol, prolactin, and TSH levels vary with these states and are, therefore, useful indices of arousal and sleep-wake.

Adult↗
PubMed1994

Effects of sleep deprivation and sleep fragmentation on upper airway collapsibility in normal subjects.

Sleep deprivation can induce or worsen nocturnal respiratory disturbances. In patients with sleep apnea hypopnea, sleep abnormalities consist of repetitive episodes of arousals and awakenings that lead to sleep fragmentation. Because the propensity for upper airway collapse is increased in these patients, we wondered if sleep fragmentation could increase upper airway collapsibility and contribute to the pathogenesis of this disease. In eight normal subjects, upper airway collapsibility was assessed during sleep by progressively decreasing the pressure in a nasal mask while recording airflow, mask, and esophageal pressures. The critical pressure was determined by the relationship between breath-by-breath values of maximal inspiratory airflow of each flow-limited inspiratory cycle and the corresponding mask pressure. Critical pressure was measured twice in each subject: after one night of total sleep deprivation and after one night of sleep fragmentation using auditory stimuli. The two measures were done in random order 1 wk apart. A polysomnographic recording was obtained the night after each measurement of critical pressure. Sleep architecture was identical after sleep deprivation and fragmentation. Sleep-related breathing abnormalities were more frequent after sleep fragmentation than after sleep deprivation. Critical pressure was -17.1 +/- 6.8 cm H2O (mean +/- SEM) after sleep deprivation, and -12.3 +/- 6.3 cm H2O after sleep fragmentation (p < 0.05), corresponding to an earlier closing of the upper airway. We conclude that sleep fragmentation leads to a higher upper airway collapsibility than does sleep deprivation.

Adult↗
PubMed2004

Cellular adhesion molecule expression, nocturnal sleep, and partial night sleep deprivation.

Sleep is hypothesized to have a role in the regulation of the immune system. This study evaluated the nocturnal expression of cellular adhesion molecules, Mac-1 and L-selectin on monocytes and lymphocytes during a full nights sleep and following a partial night of sleep deprivation (PSD). Healthy male subjects (n=16) had an increase in the percentage of Mac-1 positive lymphocytes across the baseline night. Whereas, the percentage of Mac-1 positive lymphocytes was reduced and L-selectin positive lymphocytes and monocytes were greater during the PSD night as compared to the baseline night. These data indicate that acute sleep disruption is associated with alterations in cellular adhesion molecule expression, with implications for the regulation of immune cell trafficking.

Adult↗