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Roman, Viktor; Walstra, Irene; Luiten, Paul G. M.; Meerlo, Peter
doi: 10.1093/sleep/28.12.1505pmid: N/A
AbstractStudy Objectives:In our 24-hour society, frequently disrupted and restricted sleep is a rapidly increasing problem that may contribute to the development of diseases such as depression. One of the proposed neurobiological mechanisms underlying depression is a disturbance in the brain's serotonergic neurotransmission, particularly a desensitization of the serotonin (5-HT)1A receptor system. However, a relationship between chronic sleep loss and changes in 5-HT1A receptors has not been established yet. Therefore, in the present study, we experimentally tested the hypothesis that chronic sleep restriction leads to desensitization of the 5-HT1A receptor system.Design:Rats were subjected to a schedule of restricted sleep allowing them 4 hours of sleep per day. Sleep restriction was achieved by placing the animals in slowly rotating wheels. The sensitivity of the 5-HT1A receptor system was examined by measuring the hypothermic response to a standard injection of a 1A agonist.Results:After 2 days of restricted sleep, the sensitivity of the 5-HT1A receptor system was not yet affected; however, after 8 days of sleep restriction, it was desensitized. Control experiments indicated that the effect of sleep restriction was not due to forced activity or stress. Importantly, the desensitization of the 5-HT1A system persisted for many days even with unlimited recovery sleep. Normalization occurred gradually but required at least 7 days.Conclusions:Chronic sleep restriction causes a gradual and persistent desensitization of the 5-HT1A receptor system. This finding provides a link between chronic sleep loss and sensitivity for disorders that are associated with altered serotonergic neurotransmission.
Philip, Pierre; Sagaspe, Patricia; Taillard, Jacques; Valtat, Cédric; Moore, Nicholas; Åkerstedt, Torbjorn; Charles, André; Bioulac, Bernard
doi: 10.1093/sleep/28.12.1511pmid: 16408409
AbstractStudy Objectives:To determine whether real-life driving would produce different effects from those obtained in a driving simulator on fatigue, performances and sleepiness.Design:Cross-over study involving real driving (1200 km) or simulated driving after controlled habitual sleep (8 hours) or restricted sleep (2 hours).Setting:Sleep laboratory and open French Highway.Participants:Twelve healthy men (mean age ± SD = 21.1 ± 1.6 years, range 19–24 years, mean yearly driving distance ± SD = 6563 ± 1950 miles) free of sleep disorders.Measurements:Self-rated fatigue and sleepiness, simple reaction time before and after each session, number of inappropriate line crossings from the driving simulator and from video-recordings of real driving.Results:Line crossings were more frequent in the driving simulator than in real driving (P < .001) and were increased by sleep deprivation in both conditions. Reaction times (10% slowest) were slower during simulated driving (P = .004) and sleep deprivation (P = .004). Subjects had higher sleepiness scores in the driving simulator (P = .016) and in the sleep restricted condition (P = .001). Fatigue increased over time (P = .011) and with sleep deprivation (P = .000) but was similar in both driving conditions.Conclusions:Fatigue can be equally studied in real and simulated environments but reaction time and self-evaluation of sleepiness are more affected in a simulated environment. Real driving and driving simulators are comparable for measuring line crossings but the effects are of higher amplitude in the simulated condition. Driving simulator may need to be calibrated against real driving in various condition.
Latta, Federica; Leproult, Rachel; Tasali, Esra; Hofmann, Elisa; L'Hermite-Balériaux, Mireille; Copinschi, Georges; Van Cauter, Eve
doi: 10.1093/sleep/28.12.1519pmid: 16408410
AbstractStudy Objectives:To examine sex differences in nocturnal growth hormone and prolactin release in older adults.Design:Sleep was polygraphically recorded for 2 consecutive nights, and blood was sampled at frequent intervals during the last 24 hours.Setting:The University of Chicago Clinical Research Center.Participants:Two groups of healthy nonobese older subjects: 10 men (59 ± 2 years, mean ± SEM), and 10 postmenopausal women (63 ± 2 years).Interventions:N/A.Measurements and Results:A spectral analysis of the electroencephalogram was performed in the delta and alpha bands. When delta activity was normalized for the activity in rapid eye movement sleep, women had lower delta activity than men. Growth hormone secretion was estimated by deconvolution. The prolactin profile was quantified by a best-fit curve. In both sexes, growth hormone was released both before and after sleep onset. In men, there was no relationship between presleep growth hormone release and subsequent sleep quality and postsleep growth hormone release correlated with delta activity. In women, presleep growth hormone release appeared to inhibit both postsleep growth hormone release and sleep consolidation. Prolactin release was related to rapid eye movement sleep and was lower in men than in women. Women with poor sleep maintenance had a lower prolactin acrophase.Conclusions:Major sex differences in the nocturnal profiles of growth hormone and prolactin and their relationship to sleep electroencephalogram variables are present in healthy older adults. Our analyses suggest that lower sleep-onset release of growth hormone in women as compared with men could be related to lower levels of delta activity. Improvements in the homeostatic control of sleep could have hormonal benefits in older adults.
Latta, Federica; Leproult, Rachel; Tasali, Esra; Hofmann, Elisa; Van Cauter, Eve
doi: 10.1093/sleep/28.12.1525pmid: 16408411
AbstractStudy Objectives:To examine sex effects on sleep stages and electroencephalogram (EEG) spectral power in older adults.Design:Sleep was polygraphically recorded for 2 consecutive nights, and blood was sampled during the last 24 hours.Setting:The University of Chicago Clinical Research Center.Participants:Two groups of healthy nonobese older subjects: 10 men (59 ± 2 years), and 10 postmenopausal women (63 ± 2 years).Interventions:N/A.Measurements and Results:A spectral analysis of the EEG was performed in the delta and alpha bands. There were no sex differences in sleep stages. Blood sampling resulted in reductions of total sleep time, sleep maintenance, slow-wave sleep, and absolute delta activity that were all larger in women than in men. In absolute values, delta and alpha activities in non-rapid eye movement (NREM) and rapid eye movement (REM) sleep were higher in women than in men, but, for delta activity, the sex differences were larger in REM than in NREM sleep. In women, but not in men, absolute delta activity in REM was decreased during blood sampling and was strongly correlated with absolute delta activity in NREM. Delta activity in REM did not dissipate across the night in either group. When normalized for the activity in REM sleep, the sex difference in delta activity in NREM sleep was reversed, with lower activity in women.Conclusions:Sex differences in sleep EEG variables are present in older adults. When normalized, delta activity in older women is lower than in older men, which may be more consistent with sex differences in subjective complaints, in fragility of sleep in the presence of environmental disturbances, and in the relationship to growth-hormone release.
Brandenberger, Gabrielle; Ehrhart, Jean; Buchheit, Martin
doi: 10.1093/sleep/28.12.1535pmid: 16408412
AbstractStudy Objectives:It is generally thought that the electroencephalogram of sleep stage 2 is not uniform, depending on whether sleep stage 2 evolves toward slow-wave sleep (SWS) or toward rapid eye movement (REM) sleep. We provide here further evidence of the duality of sleep stage 2 on the basis of its autonomic and hormonal background.Participants:Fourteen healthy men (aged 21–29 years) underwent 1 experimental night.Interventions:Sleep and cardiac recordings were taken from 11:00 PM to 7:00 AM. Blood was sampled continuously over 10-minute periods.Measurements and Results:Autonomic activity, as inferred from heart rate variability analysis and hormone profiles, were examined with regard to the normalized hypnograms. We found a dual activity of the autonomic nervous system during sleep stage 2, with a progressive decrease in heart rate variability sympathetic indexes during the transition toward SWS contrasting with high and rather stable levels during sleep stage 2 that evolve toward REM sleep. Also, different profiles were observed in 2 major hormone systems, the activating adrenocorticotropic system and the renin-angiotensin system. Cortisol, in its active period of circadian secretion, was stable during sleep stage 2 preceding SWS and increased significantly when sleep stage 2 preceded REM sleep. For plasma renin activity, sleep stage 2 played a transitional role, initiating increasing levels that peaked during SWS and decreasing levels that reached a nadir during REM sleep.Conclusions:These results indicate an autonomic and hormonal duality of sleep stage 2 that is characterized by a “quiet” period preparing SWS and an “active” period preceding REM sleep. These differences may confer a fundamental role on this sleep stage in ultradian sleep regulation.
Leung, Richard S. T.; Huber, Matthias A.; Rogge, Thomas; Maimon, Nimrod; Chiu, Kuo-Liang; Bradley, T. Douglas
doi: 10.1093/sleep/28.12.1543pmid: 16408413
AbstractBackground:We previously described an association between atrial fibrillation and central sleep apnea in a group of patients with congestive heart failure. We hypothesized that the prevalence of atrial fibrillation might also be increased in patients with central sleep apnea in the absence of other cardiac disease.Methods and Results:We compared the prevalence of atrial fibrillation in a series of 60 consecutive patients with idiopathic central sleep apnea (apnea-hypopnea index > 10 events per hour, > 50% central events) with that in 60 patients with obstructive sleep apnea (apnea-hypopnea index > 10, > 50% obstructive events) and 60 patients without sleep apnea (apnea-hypopnea index < 10), matched for age, sex, and body mass index. Subjects with a history of congestive heart failure, coronary artery disease, or stroke were excluded from the study. The prevalence of atrial fibrillation among patients with idiopathic central sleep apnea was found to be significantly higher than the prevalence among patients with obstructive sleep apnea or no sleep apnea (27%, 1.7%, and 3.3%, respectively, P<.001). However, hypertension was most common and oxygen desaturation most extreme among patients with obstructive sleep apnea.Conclusions:We conclude that there is a markedly increased prevalence of atrial fibrillation among patients with idiopathic central sleep apnea in the absence of congestive heart failure. Moreover, the high prevalence of atrial fibrillation among patients with idiopathic central sleep apnea is not explainable by the presence of hypertension or nocturnal oxygen desaturation, since both of these were more strongly associated with obstructive sleep apnea.
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