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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↗
PubMed1991

EEG slow wave activity, REM sleep, and rectal temperature during night and day sleep in morning-type and evening-type subjects.

During 3 baseline nights (2 for adaptation) and during 3 days of a sleep-wake reversal, electrophysiological characteristics of sleep and rectal temperature were recorded in 8 morning-type (M-type) and 8 evening-type (E-type) subjects, living in a quiet sleep laboratory. Outcomes of visual sleep scoring revealed the following general tendencies for day-sleep as compared to night-sleep: shorter sleep latencies, shorter REM (rapid eye movement sleep) latencies, advance of the time of maximum REM duration, increased duration of slow wave sleep, more intermittent wakefulness, and decreased subjective sleep quality. Furthermore, for the M-types consistently shorter sleep latencies and--for day-sleep--longer REM latencies were observed than those for the E-types. With regard to the parabolic time course of REM duration, M-types appeared to be relatively phase advanced, in particular for their day-sleep. In addition, subjective sleep quality was consistently higher for the M-types, with the exception of the first day-sleep. The temporal distributions of EEG delta (0.5-3.5 Hz) energy over the first four NREM/REM cycles of day-sleep all deviated from a monotonically decreasing trend. Compared to night-sleep the M-types showed a relative increase of delta energy for Cycle 2, whereas for the E-types a relative increase for Cycles 3 and 4 was observed. An analysis of delta energy, employing a pattern-recognition technique independently from visual sleep scoring, revealed an overall faster rate of accumulation for the M-types. Following sleep onset, rectal temperature showed a decrement, which was larger for the M-types. Moreover, rectal temperature and delta energy were negatively related, as indicated by a negative mean intra-individual correlation. These results are discussed in relation to the characteristic sleep-wake behavior of M-types and E-types.

Adolescent↗
PubMedDate not supplied

Sleep quality and the role of sleep medications for veterans with chronic pain.

OBJECTIVE: The purpose of this study was to investigate the nature of sleep problems in veterans presenting to a pain clinic, factors that predict likelihood of being prescribed a sleep medication, types of medications prescribed, and the relationships between sleep medication use and sleep quality, pain, and depression. DESIGN/SETTING/PATIENTS: Participants were 201 consecutive patients referred to a Veterans Affairs outpatient pain clinic. They were administered the Pittsburgh Sleep Quality Index, Multidimensional Pain Inventory, and Beck Depression Inventory at intake and 2-month follow-up. Sleep and opioid medication prescriptions were also monitored. RESULTS: Pain severity did not predict global sleep quality; global sleep quality was not predictive of pain severity. Greater depression predicted both more severe pain and more sleep impairment. Having previously been prescribed such medications was the only significant predictor of being prescribed a sleep medication at the time of the 2-month assessment. For the 45% of participants on sleep medications, these medications were not associated with any significant change in pain factors or depression. However, sleep medication use was associated with worse global sleep quality, sleep duration, and sleep efficiency. Opioid prescription was not a significant predictor of sleep factors, pain-related variables, or depression symptoms. DISCUSSION: Results suggest depression may contribute more significantly to sleep problems than pain-related variables in this population. The data suggest the need for controlled, prospective studies of sleep medication to further investigate the impact of sleep medications on sleep components in patients with chronic pain.

Adult↗
PubMed1996

Relationships between intact parathyroid hormone 24-hour profiles, sleep-wake cycle, and sleep electroencephalographic activity in man.

To determine whether the 24-h intact PTH (iPTH) profile is influenced by the sleep-wake cycle, and whether iPTH pulses show a temporal relationship with internal sleep structure, eight normal young men were studied during 24 h under basal conditions, once with normal nighttime sleep from 2300-0700 h and once after a night of sleep deprivation followed by an 8-h period of daytime sleep from 0700-1500 h. During the 8-h nighttime sleep period, mean iPTH levels were significantly increased by +13% and mean iPTH pulse amplitudes by +31% as compared with the 8-h subsequent waking periods. During the 8 h of total sleep deprivation, mean iPTH levels were not significantly different from the corresponding period in nighttime sleep condition, but mean iPTH pulse amplitudes were significantly lower (P < 0.01). The 8-h daytime sleep period was associated with increased mean iPTH levels and mean iPTH pulse amplitudes (+15% and +57%, respectively, as compared with the corresponding period in nighttime sleep condition). The number of pulses was similar in both experimental series and was not influenced by sleep or by time of day. Analysis of coincidence between iPTH pulses, plasma ionized calcium and plasma phosphate pulses, and slow wave sleep, as well as with rapid eye movement sleep episodes, did not reveal any significant association. Cross-correlation analysis between iPTH, plasma ionized calcium, and plasma phosphate fluctuations during sleep also showed no systematic association. Seven other subjects were studied during a nighttime sleep period in which temporal relationships between iPTH and internal sleep structure were reevaluated using spectral analysis of the sleep electroencephalogram. Cross-correlation analysis between iPTH levels and delta-relative power fluctuations showed nonsignificant results, which confirms the lack of relationship with slow wave sleep. This study demonstrates that the iPTH 24-h profile is influenced by sleep processes with a weak circadian component. However, iPTH pulses are not temporally linked with sleep electroencephalographic activity nor with calcemia and phosphatemia fluctuations. This evidence raises questions about the origin of iPTH pulses.

Adult↗
PubMed2004

Sleep quantity, sleep difficulties and their perceived consequences in a representative sample of some 2000 British adults.

Sleep problems and sleep restriction are popular topics of discussion, but few representative data are available. We document Britain's sleep based on a nationally representative sample of 1997, 16-93 year olds, who participated in face-to-face interviews. Fifty-eight per cent of respondents reported sleep problems on one or more nights the previous week and 18% reported that the sleep they obtained was insufficient on the majority of nights. Sleep durations were longest in the youngest participants (16-24 years), who slept on average 1 h longer than the 7.04 (SD 1.55) sample average. Sleep duration showed no appreciable change beyond middle age. Men and women reported sleeping similar amounts but women reported more sleep problems. Men reported sleeping less when there were more children in their household. Workers (i.e. employees) reported sleeping less on workdays than on non-workdays, but those based at home and those not employed did not. Inability to switch off from work was related to sleep duration on non-workdays. Across all participants average sleep duration exhibited a non-monotonic association with quality of life (i.e. contribution of sleep to energy, satisfaction and success in work, home and leisure activities). Quality of life was positively associated with sleep duration, for durations up to 9 h, but negatively associated with quality of life beyond this. Comparison of our data with the US national sleep poll revealed that Britain sleeps as little or less, whereas a comparison with data reported 40 years ago revealed no statistically reliable reductions. Although we may not sleep less than four decades ago, when we report sleeping less we also tend to associate that lack of sleep with poor performance and quality of life.

Adolescent↗
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↗
PubMed2003

Association between sleep bruxism, swallowing-related laryngeal movement, and sleep positions.

STUDY OBJECTIVE: To describe the relationships of sleep bruxism to swallowing and sleep positions. DESIGN: Controlled descriptive study. SETTING: Polysomnography and audio-video recordings were done in a hospital sleep laboratory. PARTICIPANTS: Nine patients with sleep bruxism and 7 normal subjects were matched for age and sex. INTERVENTIONS: n/a. MEASUREMENTS AND RESULTS: During sleep, patients with sleep bruxism showed a higher frequency of rhythmic masticatory muscle activity episodes (6.8 +/- 1.0 [SEM]/h) than did normals (0.5 +/- 0.1/h, p < 0.01). Swallowing-related laryngeal movements occurred more frequently in sleep of patients with sleep bruxism (6.8 +/- 0.8/h) than in normals (3.7 +/- 0.3/h, p < 0.01). In both groups, during sleep, close to 60% of rhythmic masticatory muscle activity episodes were associated with swallowing. In sleep bruxism patients, 68% of swallowing events occurred during rhythmic masticatory muscle activity episodes, while only 10% of swallowing events were associated with rhythmic masticatory muscle activity in normal subjects. Sleep bruxism patients and normals spent 95.5% and 87.3% of sleeping time in the supine and lateral decubitus positions, respectively. In both groups, up to 96% of rhythmic masticatory muscle activity and swallowing were observed in the supine and lateral decubitus position. In sleep bruxism patients, although sleeping time did not differ between the 2 sleeping body positions, 74% of rhythmic masticatory muscle activity and swallowing events were scored in the supine position compared to 23% in the lateral decubitus position. CONCLUSIONS: During sleep, rhythmic masticatory muscle activity is often associated with swallowing. In sleep bruxism patients, most of these oromotor events are observed in the supine position. The physiologic link between rhythmic masticatory muscle activity and swallowing and the clinical relevance of sleep position in sleep bruxism management need to be investigated.

Adult↗
PubMed2000

Are periodic leg movements during sleep (PLMS) responsible for sleep disruption in insomnia patients?

On the basis of polygraphic findings, it has been suggested that periodic leg movements during sleep are not responsible for sleep impairment (Lugaresi et al., 1972). However, for some authors it is an important cause of insomnia (Guilleminault et al., 1975; Coleman, 1982). Thus, the relationship between periodic leg movements during sleep, sleep disruption and the complaint of patients is particularly complex. We investigated the macro- and micro-structure of sleep with and without leg movements in 10 PLMS patients complaining of insomnia to clarify whether periodic leg movements are responsible for sleep disruption. The total sleep time without periodic leg movements was significantly longer than sleep time with leg movements. Sleep time without leg movements was longer than sleep time with leg movements in stage 2, slow wave sleep (SWS) and rapid eye movement (REM) sleep. Short lasting awakenings were significantly more frequent during periodic leg movements associated sleep whilst long lasting awakenings were equally frequent during sleep with and without periodic leg movements. The percentage of the four electroencephalogram (EEG) activities (delta, theta, alpha and spindles) did not show any significant difference between periodic leg movements associated and not associated with sleep stages and total sleep time. The lack of significant differences in both the macro- and micro-structure of sleep and EEG activity content regarding the association with movements confirm the hypothesis that periodic leg movements did not primarily cause sleep disturbance.

Adult↗
PubMed2004

The effects of age, sex, ethnicity, and sleep-disordered breathing on sleep architecture.

BACKGROUND: Polysomnography is used to assess sleep quality and to gauge the functional effect of sleep disorders. Few population-based data are available to estimate the variation in sleep architecture across the population and the extent to which sleep-disordered breathing (SDB), a common health condition, contributes to poor sleep independent of other factors. The objective of this study was to describe the population variability in sleep quality and to quantify the independent associations with SDB. METHODS: Cross-sectional analyses were performed on data from 2685 participants, aged 37 to 92 years, in a community-based multicenter cohort study. Dependent measures included the percentage time in each sleep stage, the arousal index, and sleep efficiency. Independent measures were age, sex, ethnicity, comorbidity status, and the respiratory disturbance index. RESULTS: Lighter sleep was found in men relative to women and in American Indians and blacks relative to other ethnic groups. Increasing age was associated with impaired sleep in men, with less consistent associations in women. Notably, women had, on average, 106% more slow wave sleep. Sleep-disordered breathing was associated with poorer sleep; however, these associations were generally smaller than associations with sex, ethnicity, and age. Current smokers had lighter sleep than ex-smokers or never smokers. Obesity had little effect on sleep. CONCLUSIONS: Sleep architecture varies with sex, age, ethnicity, and SDB. Individual assessment of the effect of SDB on sleep quality needs to account for other host characteristics. Men, but not women, show evidence of poorer sleep with aging, suggesting important sex differences in sleep physiology.

Adult↗
PubMed1996

Advanced vs. normal sleep timing: effects on depressed mood after response to sleep deprivation in patients with a major depressive disorder.

Total sleep deprivation (TSD) exerts beneficial but only transient effects on mood in patients with a major depressive disorder (MDD). Though approximately 50 to 70% of depressed patients improve after sleep deprivation, the majority relapse after recovery sleep, some even after a short nap. One theoretical model postulates a critical period in the early morning hours where sleep is likely to induce a relapse, and nap studies indicate that sleep may be particularly 'depressogenic' at this time of day. A second model attributes the relapse to the release of non-REM sleep. We therefore compared the impact of an advanced sleep period (17:00-24:00 h) to a normal sleep period (23:00-06:00 h) on mood in patients who had responded to sleep deprivation. Less relapses into depression occurred after advanced sleep. Polysomnographic data showed that, as expected, normal sleep was characterized by a more pronounced improvement of sleep continuity and increased slow-wave sleep. The normal sleep group showed a stronger decrease in REM sleep density than the advanced sleep group compared with baseline. These data add to a growing body of evidence that the timing of sleep following successful sleep deprivation may be crucial for a stabilization of its antidepressant effect. Thus, avoidance of sleep during a "critical period' for more than a single night is necessary to provide a longer-lasting treatment modality.

Adult↗
PubMed2005

Partial sleep deprivation therapy combined with sertraline affects subjective sleep quality in major depressive disorder.

BACKGROUND AND PURPOSE: Earlier studies have shown an association between mood disorders and sleep regulation. Total or partial sleep deprivation was demonstrated to have rapid antidepressive effects in depression. Depressive symptoms recur after one night of recovery sleep, but relapse is less when patients are receiving medication. In this study, we examined the subjective sleep quality changes with the antidepressive therapy using partial sleep deprivation plus sertraline and sertraline monotherapy in patients with major depressive disorder. PATIENTS AND METHODS: Thirteen patients received six partial sleep deprivation therapies in addition to sertraline; the sleep schedule on deprivation nights started at 11:00 p.m. and ended at 3:00 a.m. Eleven patients were treated with sertraline monotherapy as a control group. Six nights of partial sleep deprivation were completed in the first two weeks. Subjective sleep quality was evaluated with the Pittsburgh Sleep Quality Index (PSQI); depression and the accompanying anxiety were also assessed at baseline and at the end of the fourth week. RESULTS: The late partial sleep deprivation (LPSD) group showed less increase in estimated sleep duration and less significant improvement in subjective sleep quality than the control group. Although decreased sleep latency and increased sleep efficiency are associated with the sleep deprivation, contrary results were found in our study. CONCLUSIONS: In conclusion, changes in subjective sleep quality could occur relative to the combined partial sleep deprivation therapy and to pharmacotherapy and must be differentiated from the rapid effects of sleep deprivation therapy and objective polysomnographic measures.

Adult↗
PubMed1997

The link between sleep and depression: the effects of antidepressants on EEG sleep.

The assumption that sleep dysregulation is more than a mere epiphenomenon of depression is based on several observations: sleep disturbances are strongly associated with the depressive state; a number of sleep manipulations can alleviate symptoms of depression in some patients; and the majority of antidepressants bring about remarkable changes in sleep polygraphic variables. An obvious question is whether changes in sleep physiological processes are intimately involved in the pathogenesis and recovery from depression. One way to elucidate the link between sleep and depression is to examine whether the influence of antidepressants on sleep is related to clinical improvements in depressives. For that purpose, the effects of antidepressants on EEG sleep and their importance for the treatment of depression are summarized against the background of two existing hypotheses concerning the link between sleep and depression: one hypothesis concerning the role of REM; the other concerning the role of non-REM sleep. EEG sleep studies on the use of antidepressants in depressives have not produced clear evidence of the involvement of REM sleep or non-REM sleep in the mechanisms underlying clinical change. Furthermore, the role of sleep physiological mechanisms during treatment with antidepressants is still unclear. To interpret the effects of antidepressants on EEG sleep in terms of sleep physiological processes more fundamental sleep research is necessary. Also, more comparative studies of antidepressants with similar therapeutic effects but different pharmacological profiles are needed in both healthy and depressed subjects to further quantify the impact of EEG sleep modification in the recovery from depression and to differentiate between pharmacological and sleep-related aspects.

Antidepressive Agents↗
PubMed2006

Effects of caffeine are more marked on daytime recovery sleep than on nocturnal sleep.

Caffeine is often used to counteract sleepiness generated by sleep deprivation, jet lag, and shift-work, and is consumed at different times of day. Caffeine also has effects on sleep. However, little is known about the interaction between sleep deprivation, circadian timing, and caffeine consumption on sleep. In this study, we compared the effects of caffeine on nocturnal sleep initiated at habitual circadian time and on daytime recovery sleep. Thirty-four moderate caffeine consumers participated in both caffeine (200 mg) and placebo (lactose) conditions in a double-blind crossover design. Seventeen subjects followed their habitual sleep-wake cycle and slept in the laboratory during the night (Night), while 17 subjects were sleep deprived for one night and recovery sleep started in the morning (DayRec). All subjects received a capsule of 100 mg of caffeine (or placebo) 3 h before bedtime, and the remaining dose 1 h before bedtime. Compared to placebo, caffeine lengthened sleep latency, increased stage 1, and reduced stage 2 and slow-wave sleep (SWS) in both groups. However, caffeine reduced sleep efficiency more strongly in the DayRec group, and decreased sleep duration and REM sleep only in that group. The stronger effects of caffeine on daytime recovery sleep compared to nocturnal sleep are probably the consequence of the combined influence of increasing circadian wake propensity drive and the dissipation of homeostatic sleep pressure. We propose that the reduction of SWS by caffeine during daytime sleep increases the impact of the circadian wake signal on sleep. These results have implications for individuals using caffeine during night time.

Adult↗
PubMed1999

Comparison between subjective and actigraphic measurement of sleep and sleep rhythms.

Sleep is often assessed in circadian rhythm studies and long-term monitoring is required to detect any changes in sleep over time. The present study aims to investigate the ability of the two most commonly employed methods, actigraphy and sleep logs, to identify circadian sleep/wake disorders and measure changes in sleep patterns over time. In addition, the study assesses whether sleep measured by both methods shows the same relationship with an established circadian phase marker, urinary 6-sulphatoxymelatonin. A total of 49 registered blind subjects with different types of circadian rhythms were studied daily for at least four weeks. Grouped analysis of all study days for all subjects was performed for all sleep parameters (1062-1150 days data per sleep parameter). Good correlations were observed when comparing the measurement of sleep timing and duration (sleep onset, sleep offset, night sleep duration, day-time nap duration). However, the methods were poorly correlated in their assessment of transitions between sleep and wake states (sleep latency, number and duration of night awakenings, number of day-time naps). There were also large and inconsistent differences in the measurement of the absolute sleep parameters. Overall, actigraphs recorded a shorter sleep latency, advanced onset time, increased number and duration of night awakenings, delayed offset, increased night sleep duration and increased number and duration of naps compared with the subjective sleep logs. Despite this, there was good agreement between the methods for measuring changes in sleep patterns over time. In particular, the methods agreed when assessing changes in sleep in relation to a circadian phase marker (the 6-sulphatoxymelatonin (aMT6s) rhythm) in both entrained (n = 30) and free-running (n = 4) subjects.

Circadian Rhythm↗
PubMed2002

Effects of treatment by laser-assisted uvuloplasty on sleep energy expenditure in obstructive sleep apnea patients.

The purpose of this study was to evaluate the effect of successful laser-assisted uvulopalatoplasty (LAUP) on sleep energy expenditure (EE) in obstructive sleep apnea syndrome (OSAS) patients. Fifteen healthy subjects (group I) and 25 patients with moderately severe or severe OSAS (group II) proven by overnight sleep study and who wanted LAUP were enrolled. During the night of the sleep studies, EE was measured with a metabolic cart (indirect calorimetry with canopy), including basal metabolic rate (BMR), mean sleep EE, lowest sleep EE, ratios of mean sleep EE/BMR, and lowest sleep EE/BMR. For the OSAS patients, a second sleep study with EE measurement was performed 3 months after LAUP. Based on this assessment of their sleep architecture, they were divided into 2 groups: responders (group IIa) and nonresponders (group IIb). The mean sleep EE, the ratio of mean sleep EE/BMR and lowest EE/BMR were significantly higher in group II than group I. After LAUP in group II, 6 patients were found to be responders (group IIa) and 19 patients were nonresponders (group IIb). Group IIa had decreased mean sleep EE, ratios of mean sleep EE/BMR, and lowest sleeping EE/BMR after LAUP than before LAUP compared with no significant changes in group IIb after LAUP. In conclusion, there is increased sleep EE in moderately severe OSAS patients when compared with normal controls. LAUP, when effective in reversing the sleep abnormalities, also normalizes the sleep EE. If it does not adequately treat the OSAS, however, the sleep EE remains abnormal.

Adult↗
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↗
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↗
PubMed2001

Selected Contribution: Regulation of sleep-wake states in response to intermittent hypoxic stimuli applied only in sleep.

Recurrent sleep-related hypoxia occurs in common disorders such as obstructive sleep apnea (OSA). The marked changes in sleep after treatment suggest that stimuli associated with OSA (e.g., intermittent hypoxia) may significantly modulate sleep regulation. However, no studies have investigated the independent effects of intermittent sleep-related hypoxia on sleep regulation and recovery sleep after removal of intermittent hypoxia. Ten rats were implanted with telemetry units to record the electroencephalogram (EEG), neck electromyogram, and body temperature. After >7 days recovery, a computer algorithm detected sleep-wake states and triggered hypoxic stimuli (10% O2) or room air stimuli only during sleep for a 3-h period. Sleep-wake states were also recorded for a 3-h recovery period after the stimuli. Each rat received an average of 69.0 +/- 6.9 hypoxic stimuli during sleep. The non-rapid eye movement (non-REM) and rapid-eye-movement (REM) sleep episodes averaged 50.1 +/- 3.2 and 58.9 +/- 6.6 s, respectively, with the hypoxic stimuli, with 32.3 +/- 3.2 and 58.6 +/- 4.8 s of these periods being spent in hypoxia. Compared with results for room air controls, hypoxic stimuli led to increased wakefulness (P < 0.005), nonsignificant changes in non-REM sleep, and reduced REM sleep (P < 0.001). With hypoxic stimuli, wakefulness episodes were longer and more frequent, non-REM periods were shorter and more frequent, and REM episodes were shorter and less frequent (P < 0.015). Hypoxic stimuli also increased faster frequencies in the EEG (P < 0.005). These effects of hypoxic stimuli were reversed on return to room air. There was a rebound increase in REM sleep, increased slower non-REM EEG frequencies, and decreased wakefulness (P < 0.001). The results show that sleep-specific hypoxia leads to significant modulation of sleep-wake regulation both during and after application of the intermittent hypoxic stimuli. This study is the first to determine the independent effects of sleep-related hypoxia on sleep regulation that approximates OSA before and after treatment.

Animals↗