Sleep Restriction Period Research Articles

Impact of sleep duration on food intake regulation: Different mechanisms by sex?

In this issue of the journal, Broussard et al. (1) report findings of elevated ghrelin concentrations after a period of severe sleep restriction in healthy young men. This increase in the food intake-stimulating hormone would explain the greater caloric intake of these men under sleep-restricted conditions relative to their normal sleep duration. Increased food intake, of similar order of magnitude as those reported by Broussard et al., has been observed by others (2, 3) and it is readily accepted that energy intake is increased by approximately 300 kcal/day when sleep is curtailed by 2.5-4 h/night. However, controversy exists with respect to the effects of sleep restriction on regulators of food intake. A recent meta-analysis concluded no effect of sleep restriction on ghrelin, with high heterogeneity among studies (4). Our own interpretation of the findings in this field is similar (5, 6). One source of heterogeneity may be sex. The paucity of studies enrolling sufficient participants of both sexes is striking in sleep research. In fact, most studies enroll men only or too few participants to perform sex-specific analyses. It is further noteworthy that studies enrolling exclusively males, including the report by Broussard et al. (1), report significant effects of sleep restriction on ghrelin concentrations whereas those including women do not. Could it be that sleep restriction affects different food intake regulators in men and women? This is very likely since the end result, increased food intake due to sleep restriction, occurs in both sexes yet ghrelin seems to be elevated only in men. We have proposed the possibility of two separate mechanisms, one affecting appetite in men, and one affecting satiety in women, to explain the effects of sleep restriction on food intake. Results by Broussard et al. (1) seem to lend support to our hypothesis: the appetite-stimulating hormone ghrelin was increased with sleep restriction whereas the satiety-promoting hormone pancreatic polypeptide was largely unchanged. In a similar sleep restriction study conducted by our group, ghrelin was increased in men, whereas glucagon-like peptide 1, a satiety-signaling hormone, was reduced in women as a result of sleep restriction (7). Other factors related to the design of studies assessing the hormonal controls of food intake with sleep restriction may be responsible for between-study differences. One such factor may be the state of energy balance in which participants are maintained during the controlled feeding component of the study (6). Controlled feeding vs. ad libitum feeding conditions is another probable explanatory factor. However, the potential sex difference hypothesis needs further exploration, and future studies should enroll adequate numbers of both men and women to perform sex-specific analyses. Excluding women from sleep restriction studies is not justified. Further, additional information on other regulators of food intake, such as pancreatic polypeptide and glucagon-like peptide 1, but also cholecystokinin, peptide YY, and glucose-dependent insulinotropic polypeptide, to name a few, is needed. Maybe then we can have more definitive answers on the hormonal mechanisms underlying the increase in food intake resulting from sleep restriction.

The Impact of Sleep Restriction and Simulated Physical Firefighting Work on Acute Inflammatory Stress Responses.

ObjectivesThis study investigated the effect restricted sleep has on wildland firefighters’ acute cytokine levels during 3 days and 2 nights of simulated physical wildfire suppression work.MethodsFirefighters completed multiple days of physical firefighting work separated by either an 8-h (Control condition; n = 18) or 4-h (Sleep restriction condition; n = 17) sleep opportunity each night. Blood samples were collected 4 times a day (i.e., 06:15, 11:30, 18:15, 21:30) from which plasma cytokine levels (IL-6, IL-8, IL-1β, TNF-α, IL-4, IL-10) were measured.ResultsThe primary findings for cytokine levels revealed a fixed effect for condition that showed higher IL-8 levels among firefighters who received an 8-h sleep each night. An interaction effect demonstrated differing increases in IL-6 over successive days of work for the SR and CON conditions. Fixed effects for time indicated that IL-6 and IL-4 levels increased, while IL-1β, TNF-α and IL-8 levels decreased. There were no significant effects for IL-10 observed.ConclusionFindings demonstrate increased IL-8 levels among firefighters who received an 8-h sleep when compared to those who had a restricted 4-h sleep. Firefighters’ IL-6 levels increased in both conditions which may indicate that a 4-h sleep restriction duration and/or period (i.e., 2 nights) was not a significant enough stressor to affect this cytokine. Considering the immunomodulatory properties of IL-6 and IL-4 that inhibit pro-inflammatory cytokines, the rise in IL-6 and IL-4, independent of increases in IL-1β and TNF-α, could indicate a non-damaging response to the stress of simulated physical firefighting work. However, given the link between chronically elevated cytokine levels and several diseases, further research is needed to determine if firefighters’ IL-8 and IL-6 levels are elevated following repeated firefighting deployments across a fire season and over multiple fire seasons.

Repeated exposure to sleep restriction followed by recovery sleep – Effects on IL-6 expression and glucocorticoid (GC) sensitivity of monocytes

Restricting sleep on week days and catching up on sleep on weekend days is a highly prevalent pattern in work and school populations. We hypothesized that the repeated exposure to such patterns progressively increases the inflammatory response, due to reduced GC sensitivity of monocytes. Fourteen participants (age 25 ± 1 yrs) completed two 25-day-in-hospital periods; sleep-restriction and control-sleep in randomized order. The sleep-restriction condition consisted of three weekly cycles of 5 days with 4 h of sleep/night followed by 2 days with 8 h of sleep/night. Blood draws were taken at 11:30 h on the baseline day and the end of each sleep-restriction and recovery-sleep period. The inflammatory response was assessed by interleukin (IL)-6 positive monocytes (determined by flow cytometry); GC sensitivity of monocytes was determined by measuring the ability of dexamethasone to suppress lipopolysaccharide-stimulated IL-6 expression. IL-6 positive monocytes increased in the second and third week of sleep-restriction over control-sleep by 15% and 20%, respectively (both p 0.05), and did not return to baseline levels during intermittent recovery-sleep. GC sensitivity of monocytes was increased across all 3 weeks of sleep-restriction when compared to control-sleep, and did not normalize during intermittent recovery-sleep periods (all p 0.05). In conclusion, despite an increase in the sensitivity of monocytes to the counter-inflammatory GC signal, monocytes still express more IL-6 in response to repeated exposure of sleep-restriction. Importantly, recovery-sleep does not normalize these changes.

Prolonged REM sleep restriction induces metabolic syndrome-related changes: Mediation by pro-inflammatory cytokines.

Chronic sleep restriction in human beings results in metabolic abnormalities, including changes in the control of glucose homeostasis, increased body mass and risk of cardiovascular disease. In rats, 96h of REM sleep deprivation increases caloric intake, but retards body weight gain. Moreover, this procedure increases the expression of pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), which may be involved with the molecular mechanism proposed to mediate insulin resistance. The goal of the present study was to assess the effects of a chronic protocol of sleep restriction on parameters of energy balance (food intake and body weight), leptin plasma levels and its hypothalamic receptors and mediators of the immune system in the retroperitoneal adipose tissue (RPAT). Thirty-four Wistar rats were distributed in control (CTL) and sleep restriction groups; the latter was kept onto individual narrow platforms immersed in water for 18h/day (from 16:00h to 10:00h), for 21days (SR21). Food intake was assessed daily, after each sleep restriction period and body weight was measured daily, after the animals were taken from the sleep deprivation chambers. At the end of the 21day of sleep restriction, rats were decapitated and RPAT was obtained for morphological and immune functional assays and expression of insulin receptor substrate 1 (IRS-1) was assessed in skeletal muscle. Another subset of animals was used to evaluate blood glucose clearance. The results replicated previous findings on energy balance, e.g., increased food intake and reduced body weight gain. There was a significant reduction of RPAT mass (p<0.001), of leptin plasma levels and hypothalamic leptin receptors. Conversely, increased levels of TNF-α and IL-6 and expression of phosphorylated NFκ-β in the RPAT of SR21 compared to CTL rats (p<0.01, for all parameters). SR21 rats also displayed reduced glucose clearance and IRS-1 expression than CTL rats (p<0.01). The present results indicated that 21days of sleep restriction by the platform method induced metabolic syndrome-related alterations that may be mediated by inflammation of the RPAT.

Factors related with the ability to maintain wakefulness in the daytime after fast and forward rotating shifts

The aim of this study was to explore changes in cognitive function, sleep propensity, and sleep-related hormones (growth hormone, cortisol, prolactin, and thyrotropin) and to investigate the factors related to the ability to maintain wakefulness in the daytime after one block of fast forward rotating shift work (2 days, 2 evenings, and 2 nights). Twenty female nurses (mean age: 26.0 ± 2.0 years; range: 22–30 years) were recruited from an acute psychiatric ward. The nurses completed the Maintenance of Wakefulness Test (MWT), State Anxiety Inventory (SAI), Stanford Sleepiness Scale (SSS), Digit Symbol Substitution Test, Symbol Searching Test, Taiwan University Attention Test, Wisconsin Card Sorting Test (WCST), and Multiple Sleep Latency Test (MSLT) four times throughout the day at 2-hour intervals, and their hormone levels were measured at the same time. There was no time of day effect on sleep propensity as measured by the MWT or MSLT despite an increase in self-reported sleepiness. Anxiety state and neuropsychological tasks, including executive function, attention, and perceptual and motor abilities were not affected during the daytime sleep restriction period. The number of omissions and perceptual and motor abilities showed a practice effect. The thyrotropin levels were significantly elevated, and cortisol levels significantly decreased during the daytime sleep restriction period. There were no significant changes in growth hormone or prolactin throughout the daytime period. Age was negatively associated with the mean sleep latency (MSL) of the MWT and positively associated with the MSL of the MSLT. The perseverative errors in WCST and SSS scores were negatively associated with the MSL of the MWT. SAI scores and thyrotropin levels were positively associated with the MSL of the MWT. In conclusion, there was no change in sleep propensity in the daytime after one block of rotating shift work. An attempt to preserve daytime alertness was also related to maintaining neuropsychological performance. Maintaining this ability was related to thyrotropin and age, and this cognition required a high attentive load.

Sleep allostasis in chronic sleep restriction: The role of the norepinephrine system

Sleep responses to chronic sleep restriction may be very different from those observed after acute total sleep deprivation. Specifically, when sleep restriction is repeated for several consecutive days, animals express attenuated compensatory increases in sleep time and intensity during daily sleep opportunities. The neurobiological mechanisms underlying these adaptive, or more specifically, allostatic, changes in sleep homeostasis are unknown. Several lines of evidence indicate that norepinephrine may play a key role in modulating arousal states and NREM EEG delta power, which is widely recognized as a marker for sleep intensity. Therefore, we investigated time course changes in brain adrenergic receptor mRNA levels in response to chronic sleep restriction using a rat model. Here, we observed that significantly altered mRNA levels of the α1- adrenergic receptor in the basal forebrain as well as α2- and β1-adrenergic receptor in the anterior cingulate cortex only on the first sleep restriction day. On the other hand, the frontal cortex α1-, α2-, and β1-adrenergic receptor mRNA levels were reduced throughout the period of sleep restriction. Combined with our earlier findings on EEG that sleep time and intensity significantly increased only on the first sleep restriction days, these results suggest that alterations in the brain norepinephrine system in the basal forebrain and cingulate cortex may mediate allostatic changes in sleep time and intensity observed during chronic sleep restriction.

TRIB1 constitutes a molecular link between regulation of sleep and lipid metabolism in humans

Epidemiological studies show association between sleep duration and lipid metabolism. In addition, inactivation of circadian genes induces insulin resistance and hyperlipidemia. We hypothesized that sleep length and lipid metabolism are partially controlled by the same genes. We studied the association of total sleep time (TST) with 60 genetic variants that had previously been associated with lipids. The analyses were performed in a Finnish population-based sample (N=6334) and replicated in 2189 twins. Finally, RNA expression from mononuclear leucocytes was measured in 10 healthy volunteers before and after sleep restriction. The genetic analysis identified two variants near TRIB1 gene that independently contributed to both blood lipid levels and to TST (rs17321515, P=8.92*10−5, Bonferroni corrected P=0.0053, β=0.081 h per allele; rs2954029, P=0.00025, corrected P=0.015, β=0.076; P<0.001 for both variants after adjusting for blood lipid levels or body mass index). The finding was replicated in the twin sample (rs17321515, P=0.022, β=0.063; meta-analysis of both samples P=8.1*10−6, β=0.073). After the experimentally induced sleep restriction period TRIB1 expression increased 1.6-fold and decreased in recovery phase (P=0.006). In addition, a negative correlation between TRIB1 expression and slow wave sleep was observed in recovery from sleep restriction. These results show that allelic variants of TRIB1 are independently involved in regulation of lipid metabolism and sleep. The findings give evidence for the pleiotropic nature of TRIB1 and may reflect the shared roots of sleep and metabolism. The shared genetic background may at least partially explain the mechanism behind the well-established connection between diseases with disrupted metabolism and sleep.

Increased food intake and changes in metabolic hormones in response to chronic sleep restriction alternated with short periods of sleep allowance

Rodent models for sleep restriction have good face validity when examining food intake and related regulatory metabolic hormones. However, in contrast to epidemiological studies in which sleep restriction is associated with body weight gain, sleep-restricted rats show a decrease in body weight. This difference with the human situation might be caused by the alternation between periods of sleep restriction and sleep allowance that often occur in real life. Therefore, we assessed the metabolic consequences of a chronic sleep restriction protocol that modeled working weeks with restricted sleep time alternated by weekends with sleep allowance. We hypothesized that this protocol could lead to body weight gain. Male Wistar rats were divided into three groups: sleep restriction (SR), forced activity control (FA), and home cage control (HC). SR rats were subjected to chronic sleep restriction by keeping them awake for 20 h per day in slowly rotating drums. To model the human condition, rats were subjected to a 4-wk protocol, with each week consisting of a 5-day period of sleep restriction followed by a 2-day period of sleep allowance. During the first experimental week, SR caused a clear attenuation of growth. In subsequent weeks, two important processes occurred: 1) a remarkable increase in food intake during SR days, 2) an increase in weight gain during the weekends of sleep allowance, even though food intake during those days was comparable to controls. In conclusion, our data revealed that the alternation between periods of sleep restriction and sleep allowance leads to complex changes in food intake and body weight, that prevent the weight loss normally seen in continuous sleep-restricted rats. Therefore, this "week-weekend" protocol may be a better model to study the metabolic consequences of restricted sleep.

Age-related changes during a paradigm of chronic sleep restriction

Fragmented and restricted sleep is a common problem for the human elderly. There is evidence that aging impairs sleep in animals as well. After sleep deprivation, older animals have less sleep rebound. Despite increasing complaints of reduced time for sleep in contemporary society, few studies have examined chronic sleep restriction protocols in animals. Therefore, the aim of the present study was to evaluate the effects of chronic sleep restriction on the sleep patterns of aged rats. Using the single platform method, 22-month-old male rats were submitted to 18 h of sleep restriction followed by 6 h of total sleep opportunity. The sleep–wake cycles of these rats were recorded for 6 h/day throughout the 12-day procedure. The results showed that total sleep time and NREM sleep were reduced during the 12-day sleep restriction period. However, rebound REM sleep was only significant on day 6. A negative rebound was also seen, particularly during the last days of the chronic sleep restriction period. Furthermore, sleep latency and mean wake bout length progressively increased during the protocol. These findings indicate that older rats have an inability to restore their sleep patterns during extended sleep deprivation.

Sleep Restriction Is Associated With Increased Morning Plasma Leptin Concentrations, Especially in Women

We evaluated the effects of sleep restriction on leptin levels in a large, diverse sample of healthy participants, while allowing free access to food. Prospective experimental design. After 2 nights of baseline sleep, 136 participants (49% women, 56% African Americans) received 5 consecutive nights of 4 hours time in bed (TIB). Additionally, one subset of participants received 2 additional nights of either further sleep restriction (n = 27) or increased sleep opportunity (n = 37). Control participants (n = 9) received 10 hr TIB on all study nights. Plasma leptin was measured between 10:30 a.m. and 12:00 noon following baseline sleep, after the initial sleep-restriction period, and after 2 nights of further sleep restriction or recovery sleep. Leptin levels increased significantly among sleep-restricted participants after 5 nights of 4 hr TIB (Z = -8.43, p < .001). Increases were significantly greater among women compared to men (Z = -4.77, p < .001) and among participants with higher body mass index (BMI) compared to those with lower (Z = -2.09, p = .036), though participants in all categories (sex, race/ethnicity, BMI, and age) demonstrated significant increases. There was also a significant effect of allowed TIB on leptin levels following the 2 additional nights of sleep restriction (p < .001). Participants in the control condition showed no significant changes in leptin levels. These findings suggest that sleep restriction with ad libitum access to food significantly increases morning plasma leptin levels, particularly among women.

Effects of different sleep restriction protocols on sleep architecture and daytime vigilance in healthy men

Sleep is regulated by complex biological systems and environmental influences, neither of which is fully clarified. This study demonstrates differential effects of partial sleep deprivation (SD) on sleep architecture and psychomotor vigilance task (PVT) performance using two different protocols (sequentially) that each restricted daily sleep to 3 hours in healthy adult men. The protocols differed only in the period of sleep restriction; in one, sleep was restricted to a 3-hour block from 12:00 AM to 3:00 AM, and in the other, sleep was restricted to a block from 3:00 AM to 6:00 AM. Subjects in the earlier sleep restriction period showed a significantly lower percentage of rapid-eye-movement (REM) sleep after 4 days (17.0 vs. 25.7 %) and a longer latency to the onset of REM sleep (L-REM) after 1 day (78.8 vs. 45.5 min) than they did in the later sleep restriction period. Reaction times on PVT performance were also better (i.e. shorter) in the earlier SR period on day 4 (249.8 vs. 272 ms). These data support the view that earlier-night sleep may be more beneficial for daytime vigilance than later-night sleep. The study also showed that cumulative declines in daytime vigilance resulted from loss of total sleep time, rather than from specific stages, and underscored the reversibility of SR effects with greater amounts of sleep.

Banking Sleep: Realization of Benefits During Subsequent Sleep Restriction and Recovery

Determine whether sleep extension (a) improves alertness and performance during subsequent sleep restriction and (b) impacts the rate at which alertness and performance are restored by post-restriction recovery sleep. Participants were randomly assigned to an Extended (10 h time in bed [TIB]) or Habitual TIB [mean (SD) hours = 7.09 (0.7)] sleep group for one week, followed by 1 Baseline (10 hours or habitual TIB), 7 Sleep Restriction (3 h TIB), and 5 Recovery Sleep nights (8 h TIB). Performance and alertness tests were administered hourly between 08:00-18:00 during all in-laboratory phases of the study. Residential sleep/performance testing facility. Twenty-four healthy adults (ages 18-39) participated in the study. Extended vs. habitual sleep durations prior to sleep restriction. Psychomotor vigilance task (PVT) lapses were more frequent and modified maintenance of wakefulness (MWT) sleep latency was shorter in the Habitual group than in the Extended group across the sleep restriction phase. During the Recovery phase, PVT speed rebounded faster (and PVT lapsing recovered significantly after the first night of recovery sleep) in the Extended group. No group differences in subjective sleepiness were evident during any phase of the study. The extent to which sleep restriction impairs objectively measured alertness and performance, and the rate at which these impairments are subsequently reversed by recovery sleep, varies as a function of the amount of nightly sleep obtained prior to the sleep restriction period. This suggests that the physiological mechanism(s) underlying chronic sleep debtundergo long-term (days/weeks) accommodative/adaptive changes.

Banking Sleep: Realization of Benefits During Subsequent Sleep Restriction and Recovery

Determine whether sleep extension (a) improves alertness and performance during subsequent sleep restriction and (b) impacts the rate at which alertness and performance are restored by post-restriction recovery sleep. Participants were randomly assigned to an Extended (10 h time in bed [TIB]) or Habitual TIB [mean (SD) hours = 7.09 (0.7)] sleep group for one week, followed by 1 Baseline (10 hours or habitual TIB), 7 Sleep Restriction (3 h TIB), and 5 Recovery Sleep nights (8 h TIB). Performance and alertness tests were administered hourly between 08:00-18:00 during all in-laboratory phases of the study. Residential sleep/performance testing facility. Twenty-four healthy adults (ages 18-39) participated in the study. Extended vs. habitual sleep durations prior to sleep restriction. Psychomotor vigilance task (PVT) lapses were more frequent and modified maintenance of wakefulness (MWT) sleep latency was shorter in the Habitual group than in the Extended group across the sleep restriction phase. During the Recovery phase, PVT speed rebounded faster (and PVT lapsing recovered significantly after the first night of recovery sleep) in the Extended group. No group differences in subjective sleepiness were evident during any phase of the study. The extent to which sleep restriction impairs objectively measured alertness and performance, and the rate at which these impairments are subsequently reversed by recovery sleep, varies as a function of the amount of nightly sleep obtained prior to the sleep restriction period. This suggests that the physiological mechanism(s) underlying chronic sleep debt undergo long-term (days/weeks) accommodative/adaptive changes.

Sleep Restriction Increases the Risk of Developing Cardiovascular Diseases by Augmenting Proinflammatory Responses through IL-17 and CRP

BackgroundSleep restriction, leading to deprivation of sleep, is common in modern 24-h societies and is associated with the development of health problems including cardiovascular diseases. Our objective was to investigate the immunological effects of prolonged sleep restriction and subsequent recovery sleep, by simulating a working week and following recovery weekend in a laboratory environment.Methods and FindingsAfter 2 baseline nights of 8 hours time in bed (TIB), 13 healthy young men had only 4 hours TIB per night for 5 nights, followed by 2 recovery nights with 8 hours TIB. 6 control subjects had 8 hours TIB per night throughout the experiment. Heart rate, blood pressure, salivary cortisol and serum C-reactive protein (CRP) were measured after the baseline (BL), sleep restriction (SR) and recovery (REC) period. Peripheral blood mononuclear cells (PBMC) were collected at these time points, counted and stimulated with PHA. Cell proliferation was analyzed by thymidine incorporation and cytokine production by ELISA and RT-PCR. CRP was increased after SR (145% of BL; p<0.05), and continued to increase after REC (231% of BL; p<0.05). Heart rate was increased after REC (108% of BL; p<0.05). The amount of circulating NK-cells decreased (65% of BL; p<0.005) and the amount of B-cells increased (121% of BL; p<0.005) after SR, but these cell numbers recovered almost completely during REC. Proliferation of stimulated PBMC increased after SR (233% of BL; p<0.05), accompanied by increased production of IL-1β (137% of BL; p<0.05), IL-6 (163% of BL; p<0.05) and IL-17 (138% of BL; p<0.05) at mRNA level. After REC, IL-17 was still increased at the protein level (119% of BL; p<0.05).Conclusions5 nights of sleep restriction increased lymphocyte activation and the production of proinflammatory cytokines including IL-1β IL-6 and IL-17; they remained elevated after 2 nights of recovery sleep, accompanied by increased heart rate and serum CRP, 2 important risk factors for cardiovascular diseases. Therefore, long-term sleep restriction may lead to persistent changes in the immune system and the increased production of IL-17 together with CRP may increase the risk of developing cardiovascular diseases.

Interaction of chronic sleep restriction and circadian system in humans

Nocturnal sleep restriction and compensation with daytime naps is common in today's society. In a between-participants design, we examined the effects of chronic (10 nights) sleep restriction on 24 h plasma melatonin profiles in humans. Following a baseline period with 8.2 h time in bed (TIB) for sleep, participants were randomized to a control (8.2 h TIB) or sleep-restriction condition (4.2 h TIB), with and without diurnal naps. Sleep restriction was achieved via delaying bedtime and advancing wake time by 2 h each relative to the baseline sleep period. Participants were maintained in a controlled, time isolated laboratory environment throughout the protocol, with light levels below 40 lx at all times. Twenty-four hour plasma melatonin profiles were assessed at baseline and at the end of the sleep-restriction period, with subjects maintained in a constant posture protocol. Compared with the baseline assessment and the 8.2 h TIB control group, a significant phase delay in melatonin onset (1.2 +/- 0.9 h) occurred in all sleep-restriction (4.2 h TIB) groups (P < 0.05). There was no evidence of a phase advance or shortening of the period of melatonin secretion associated with the advanced waking time. These results suggest that nocturnal light and dark exposure may be more potent in effecting circadian phase shifts than exposure to morning light, at least in conditions of controlled, dim lighting in the laboratory.

Effects of sleep restriction periods on serum cortisol levels in healthy men

Objectives To clarify effects of partial sleep deprivation (SD) on morning (07:00) serum cortisol concentrations in two protocols that restricted sleep to 3 h/day in healthy adult men. The study was also designed to delineate the relationship between anxiety levels in the morning and slow wave sleep (SWS) periods at night. Methods Ten young adult Han Chinese males were recruited to participate in an ‘earlier-night’ sleep restriction (SR) period (sleep from 00:00 to 03:00) and then a ‘later-night’ SR period (sleep from 03:00 to 06:00). The duration of each SR period was 4 days, followed by a recovery night. The SR periods were separated by 10 days of normal sleep. Blood samples of serum cortisol were drawn at 07:00 during each of two SR periods for six consecutive mornings (for a total of 12 measurements per subject), and anxiety levels were also assessed over the same period by the State portion of the State-Trait Anxiety Inventory (STAI). Sleeping processes were monitored by polysomnogram. Results Serum cortisol levels decreased after SR ( P < 0.05) in both paradigms, with greater decreases evident after later-night sleep loss than after earlier-night sleep loss. Cortisol levels were significantly, negatively correlated to the number of days of earlier-night SR, but not to later-night SR. Anxiety scores increased gradually in both conditions. The time of SWS changed indiscriminately in both paradigms. Cortisol levels returned to baseline after one night of recovery sleep. Conclusions Cortisol decreased in both SR conditions, especially in the earlier-night SR protocol, even though SWS time and anxiety levels changed roughly in the same manner in both conditions. Data suggested that sleep loss at different times of the night affects the hypothalamic–pituitary–adrenal axis (HPA-axis) differentially.

Consequences of subchronic and chronic exposure to intermittent hypoxia and sleep deprivation on cardiovascular risk factors in rats

Since studies suggest that both hypoxia and sleep fragmentation are related to cardiovascular alterations induced by obstructive sleep apnea, the present study was designed to evaluate the effects of hypoxia, sleep deprivation, and their combination on biochemical blood parameters in rats. In subchronic experiments (4 days), rats were exposed to intermittent hypoxia (IH) during the light period (2min room air-2min 10% O(2) for 12h/day) and/or paradoxical sleep deprivation (PSD, 24h/day). Consequences of chronic intermittent hypoxia (CIH) exposure were examined after 21 consecutive days of hypoxia protocol from 10:00 to 16:00 followed by a sleep restriction (SR) period of 18h (16:00-10:00). Rats were randomly assigned to seven treatment groups: (1) control (2) IH (3) PSD (4) IH-PSD (5) SR (6) CIH and (7) CIH-SR. PSD reduced triglycerides and very low-density lipoprotein (VLDL) cholesterol concentrations and increased total cholesterol and high-density lipoprotein (HDL) cholesterol. IH did not alter any of these parameters. The combination of IH-PSD did not modify the values of total cholesterol and HDL compared to control group. In the chronic experiment, the animals exposed to CIH displayed a reduction of Vitamin B(6) and an increase of triglycerides and VLDL. Our findings show a duration-dependent effect of hypoxia on triglycerides. Rats in the SR and CIH-SR groups showed a diminished concentration of triglycerides and VLDL. SR rats showed a reduction in the concentration of homocysteine but the animals in the CIH-SR treatment condition did not display any alterations in this parameter. In this latter group, an augmentation of cysteine concentration was observed. These results suggest that sleep deprivation and hypoxia modify biochemical blood parameters in distinct ways.

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.