Experimental Immunomodulation, Sleep, and Sleepiness in Humans
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A bstract : Infection, inflammation, and autoimmune processes are accompanied by serious disturbances of well‐being, psychosocial functioning, cognitive performance, and behavior. Here we review those studies that have investigated the effects of experimental immunomodulation on sleep and sleepiness in humans. In most of these studies bacterial endotoxin was injected intravenously to model numerous aspects of infection including the release of inflammatory cytokines. These studies show that human sleep‐wake behavior is very sensitive to host defense activation. Small amounts of endotoxin, which affect neither body temperature nor neuroendocrine systems but slightly stimulate the secretion of inflammatory cytokines, promote non‐rapid‐eye‐movement sleep amount and intensity. Febrile host responses, in contrast, go along with prominent sleep disturbances. According to present knowledge tumor necrosis factor‐α (TNF‐α) is most probably a key mediator of these effects, although it is likely that disturbed sleep during febrile host responses involves endocrine systems as well. There is preliminary evidence from human studies suggesting that inflammatory cytokines such as TNF‐α not only mediate altered sleep‐wake behavior during infections, but in addition are involved in physiological sleep regulation and in hypnotic effects of established sedating drugs.Keywords:
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Because of on-call responsibilities, many medical residents are subjected to chronic partial sleep deprivation, a form of sleep restriction whereby individuals have chronic patterns of insufficient sleep. It is unclear whether deterioration in cognitive processing skills due to chronic partial sleep deprivation among medical residents would influence educational exposure or patient safety.Twenty-six medical residents were recruited to participate in the study. Participants wore an Actigraph over a period of 5 consecutive days and nights so their sleep pattern could be recorded. Thirteen participants worked on services that forced chronic partial sleep deprivation (<6 hours of sleep per 24h for 5 consecutive days and nights). The other thirteen residents worked on services that permitted regular and adequate sleep patterns. Following the 5-day sleep monitoring period, the participants completed the three following cognitive tasks: (a) the Wisconsin Card Sorting Test (WCST) to assess abstract reasoning and prefrontal cortex performance; (b) the Time Perception Task (TPT) to assess time estimation and time reproduction skills; and (c) the Iowa Gambling Task (IGT) to assess decision-making ability.The results of independent samples t-tests found no significant differences between the group who was chronically sleep deprived and the group who rested adequately (all ps > .05).THESE RESULTS MAY HAVE EMERGED FOR SEVERAL POSSIBLE REASONS: (a) chronic partial sleep deprivation may have a lesser impact on prefrontal cortex function than on other cognitive functions; (b) fairly modest chronic sleep restriction may be less harmful than acute and more significant sleep restriction; or (c) our research may have suffered from poor statistical power. Future research is recommended.
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Chronic sleep insufficiency is common in our society and has negative cognitive and health impacts. It can also alter sleep regulation, yet whether it affects subsequent homeostatic responses to acute sleep loss is unclear. We assessed sleep and thermoregulatory responses to acute sleep deprivation before and after a '3/1' chronic sleep restriction protocol in adult male Wistar rats. The 3/1 protocol consisted of continuous cycles of wheel rotations (3 h on/1 h off) for 4 days. Sleep latency in a 2-h multiple sleep latency test starting 26 h post-3/1 was unchanged, whereas non-rapid eye movement sleep (NREMS) and associated electroencephalogram delta power (a measure of sleep need) over a 24-h period beginning 54 h post-3/1 were reduced, compared to respective pre-3/1 baseline levels. However, in response to acute sleep deprivation (6 h by 'gentle handling') starting 78 h post-3/1, the compensatory rebounds in NREMS and rapid eye movement sleep (REMS) amounts and NREMS delta power were unaltered. Body temperature increased progressively across the 3/1 protocol and returned to baseline levels on the second day post-3/1. The acute sleep deprivation also increased body temperature, followed by a decline below baseline levels, with no difference between before and after 3/1 sleep restriction. Non-sleep-restricted control rats showed responses to acute sleep deprivation similar to those observed in the sleep-restricted animals. These results suggest that the process of sleep homeostasis is altered on the third recovery day after a 4-day 3/1 sleep restriction protocol, whereas subsequent homeostatic sleep and temperature responses to brief sleep deprivation are not affected.
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Background: Chronic sleep restriction and performance on the Psychomotor Vigilance Task (PVT) have been well documented in humans. Results demonstrate significantly impaired PVT performance. An analogous task in rodents, the rat Psychomotor Vigilance Task (rPVT), cites similar results. However, few studies have examined the effect of caffeine to ameliorate the effects of sleep restriction on rPVT performance as demonstrated in human PVT literature. Materials and Methods: After baseline, animals experienced three conditions for 1 week each: 6 hours/day sleep deprivation, 10 mg/kg intraperitoneal (i.p.) caffeine, and 6 hours/day sleep deprivation followed by 10 mg/kg i.p. caffeine. Performance on the rPVT was measured daily at 15:00. Results: Significant results were found for all rPVT metrics. Six hours per day sleep deprivation significantly impaired rPVT performance, but 10 mg/kg caffeine did not counteract the sleep deprivation. Conclusion: Caffeine administration did not counteract the effects of sleep deprivation on rPVT performance. Future research should explore dose–response effects of stimulants on rPVT performance following chronic sleep restriction.
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Objective Sleep deficiency which is prevalent in shift work has been associated with an increased metabolic disease risk. Experimentally induced sleep restriction has been shown to impair glucose metabolism and has been linked to reduced slow wave sleep (SWS) as a possible causal factor. This study examined (i) whether total sleep deprivation exhibits similar effects on glucose tolerance and insulin sensitivity as sleep restriction, (ii) whether one recovery night after sleep restriction is sufficient to restore impaired glucose metabolism, and (iii) whether the combination of total sleep deprivation with prior sleep restriction shows cumulative effects. Methods Thirty‐six healthy volunteers participated in a 12‐day study. After one adaptation night and two baseline nights with 8 h of scheduled sleep each, sleep opportunities were restricted for 5 nights either to 5 h (21 participants, 9 females, mean ± SD, age 26 ± 4 yrs, BMI 23.1 ± 1.9) or maintained at 8 h (control, 15 participants, 5 females, age 28 ± 6 yrs, BMI 23.6 ± 2.9). Then, both groups underwent a single 8‐h night of recovery sleep, a 38‐h period of wakefulness, and a final recovery night. Oral glucose tolerance tests (OGTT) were conducted in the morning following lights on (>10 h fasting) after the second baseline night, after 5 nights of sleep restriction, after the first recovery night, and after 24 h of sleep deprivation. Blood was sampled immediately prior to the OGTT and then at 30‐min intervals for 2 h. Polysomnograms were recorded. SWS per night and areas under the curve (AUC) for glucose, insulin, and HOMA were analyzed in each of the two groups with mixed ANOVAs with ‘sleep condition’ (4x) and ‘sex’ (2x) as factors (post‐hoc Bonferroni‐Holm adjustment). Results Glucose tolerance and insulin sensitivity decreased after sleep restriction (mean ± SEM, glucose Δ 32.5 ± 7.0 mg*h/dl, p<0.0001; insulin Δ 44.9 ± 9.2 mU*h/dl, p<0.0001; HOMA Δ 20.7 ± 3.9, p<0.0001) and remained low after recovery sleep (glucose Δ 17.3 ± 6.8 mg*h/dl, p=0.0139; insulin Δ 24.7 ± 9.2 mU*h/dl, p=0.0102; HOMA Δ 11.3 ± 3.8, p=0.0053) compared to baseline. After 24 h awake, these parameters were not different from baseline in both groups. The amount of SWS in the final sleep restriction night (Δ 0.6 ± 4.7 min, p=0.8949) and the recovery night (Δ 9.2 ± 4.7 min, p=0.0534) did not significantly differ from baseline. Conclusion Sleep restriction for 5 nights negatively impacts glucose metabolism. This impairment appears to occur independently of SWS, and to outlast a single night of recovery sleep. In contrast, prolonged wakefulness does neither acutely affect glucose metabolism nor exhibit cumulative effects with prior sleep restriction. Chronic sleep loss and acutely extended wake duration appear to activate different regulatory responses in glucose metabolism. Support or Funding Information Funded by the German Aerospace Center and the Research Center Juelich This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .
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Positive affect helps people in coping with difficult situations. People with high positive affect have been shown to be happier, have more success in life and better relationships than people scoring low. Positive affect is reduced during chronic and acute sleep loss. The aims of the present study were 1) to establish the adverse effect of 5 days of sleep restriction on positive affect, 2) to test whether one night of recovery sleep reverses this effect, and 3) to test whether the combined effects of prior sleep restriction and acute sleep deprivation are cumulative. In an ongoing investigation, 27 healthy volunteers completed two baseline nights (8h TIB) and either five nights of sleep restriction (experimental group: 5h TIB, N=18, mean age 26 ± 3 years, 9 females) or regular sleep (control group: 8h TIB, N=9, mean age 25 ± 5 years, 3 females). Thereafter, all participants had 8h of recovery sleep and 38h of total sleep deprivation. Participants filled out the mood scale PANAS at 9 a.m. on all days. Differences in the positive affect subscale between experimental days and the second baseline day were calculated. Wilcoxon signed-rank tests with Bonferroni-adjusted alpha-level showed a decrease in positive affect after one night of sleep restriction (Δ5.06 ± 3.78; p<.001). Positive affect scores of the last day of chronic sleep restriction and of the day after recovery sleep did not differ (Δ1.33 ± 4.67; p=.18). Positive affect decreased from the last day of chronic sleep restriction to acute sleep deprivation (Δ4.11 ± 4.27; p=.001) for the experimental group. No significant difference was found between chronic sleep restriction (last day) in the experimental group and total sleep deprivation in the control group (Mann-Whitney-U-Test, z(26)=-1.24; p=.5). Chronic sleep loss for five days exhibited long-lasting effects on the reduction of positive affect which were not reset by one recovery night. Positive affect decreased further following acute sleep deprivation, indicating that people’s sleep curtailing lifestyles make them more vulnerable to additional acute sleep loss. Five days of chronically reduced sleep exhibited a comparable reduction in positive affect as a sleepless night.
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To identify features in the compensatory mechanisms of sleep regulation in response to acute sleep deprivation after chronic sleep restriction in rats.Male Wistar rats 7-8 months old underwent 5-day sleep restriction: 3 h of sleep deprivation and 1 h of sleep opportunity repeating throughout each day. Six-hour acute total sleep deprivation was performed at the beginning of daylight hours on the 3rd day after sleep restriction. Polysomnogramms were recorded throughout the day before chronic sleep restriction, on the 2nd recovery day after chronic sleep restriction and after acute sleep deprivation. The control group was not subjected to chronic sleep restriction.The animals after chronic sleep restriction had the compensatory increase in total sleep time in response to acute sleep deprivation weaker than in control animals. Animals after sleep restriction had the compensatory increase in the time of slow-wave sleep (SWS) only in the first 6 hours after acute sleep deprivation, whereas in control animals the period of compensation of SWS lasted 12 hours. A compensatory increase in slow-wave activity (SWA) was observed in both groups of animals, but in animals experiencing chronic sleep restriction the amplitude of SWA after acute sleep deprivation was less than in control animals. A compensatory increase in REM sleep in sleep restricted animals occurred immediately after acute sleep deprivation and coincides with a compensatory increase in SWS and SWA, whereas in control conditions these processes are spaced in time.Compensatory reactions in response to acute sleep deprivation (sleep homeostasis) are weakened in animals subjected to chronic sleep restriction, as the reaction time and amplitude are reduced.Выявить особенности в проявлении компенсаторных механизмов регуляции сна в ответ на острую депривацию сна после хронического недосыпания у крыс.У самцов крыс популяции Вистар (7—8 мес) хронический недостаток сна вызывался 5-дневным циклическим режимом ограничения сна: 3 ч депривации сна и 1 ч покоя непрерывно в течение суток. Шестичасовую острую тотальную депривацию сна проводили в начале светлого времени суток на 3-й день после ограничения сна. Полисомнографические данные регистрировали в течение суток до хронического ограничения сна, на 2-й день после хронического ограничения сна и после острой депривации сна. Контрольную группу хроническому ограничению сна не подвергали.У животных, подвергнутых хроническому ограничению сна, компенсаторное увеличение общего времени сна в ответ на острую депривацию было меньше, чем у контрольных животных. Компенсаторное увеличение времени медленноволнового сна (МВС) наблюдалось только в первые 6 ч после острой депривации сна, тогда как у контрольных животных период компенсации МВС продолжался 12 ч. Компенсаторное повышение медленноволновой активности (МВА) наблюдалось в обеих группах, но у животных, испытавших хроническое ограничение сна, амплитуда МВА после острой депривации была меньше, чем у контрольных животных. Компенсаторное возрастание продолжительности парадоксального сна (ПС) у животных, подвергнутых хроническому ограничению сна, наступало сразу после острой депривации и совпадало с компенсаторным увеличением МВС и МВА, тогда как в контрольных условиях эти процессы разнесены во времени.В целом можно резюмировать, что компенсаторные реакции сна в ответ на его острую депривацию (гомеостаз сна) оказываются ослаблены у животных, подвергнутых хроническому недосыпанию, так как сокращается время и амплитуда реакции.
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The relationship between chronic sleep restriction and performance on the Psychomotor Vigilance Task (PVT) has been well documented in human literature with chronic sleep restriction as little as 7 hours per night resulting in significant impairment in PVT performance. However, there is considerable variability in individual responses to sleep deprivation that potentially correspond to genetic differences. Recently, an analogous version of the PVT has been developed for use with rodent models (rPVT). The purpose of this study is to compare performance on the rPVT following chronic restriction in Wistar Han (WH) and Sprague Dawley (SD) rats, two rat strains commonly used for behavioral testing. After meeting baseline criterion on the rPVT, WH (n=7) and SD (n=7) rats were subjected to 6hr/day sleep restriction in forced exercise wheels for one week. Performance on the rPVT was measured daily at 1500. Data indicates WH rats show more prominent impairment in rPVT performance following sleep restriction compared to SD rats. WH rats show increased reaction times and decreased accuracy while SD rats show little to no change performance following chronic sleep restriction. The results of this study suggest that SD rats may be more resilient to the effects of sleep loss on vigilant attention measured via the rPVT than WH rats. These results have significant implications for the choice of strain when conducting behavioral tasks following sleep restriction as well as implications for research concerning genetic differences underlying resiliency to sleep loss. Future research on this topic in our laboratory will explore the distinct genetic differences between these strains and others to provide further insight into the relationship between genetics, sleep loss, and cognitive performance. N/A
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