Sleep propensity is modulated by circadian and behavior-induced changes in cutaneous temperature

A close relation between sleep and body temperature has been noted already for a long time. Although a correlation is indisputable, there is at present hardly evidence for a causal involvement of sleep in changes in body temperature. Concerning the reverse, a causal involvement of body temperature in sleep has been demonstrated: if core or skin temperature changes activate thermoregulatory processes aimed at heat loss or heat preservation, sleep is usually disrupted. We have recently proposed that sleep propensity is also affected by more subtle changes in skin temperature, within the thermoneutral range (Van Someren (2000). Chronobiol. Int. 17, 313–354). These changes are likely to modulate the firing properties of thermosensitive neurons in brain areas involved in sleep regulation. Subtle changes in skin temperature occur daily under control of the circadian timing system. They could provide this system with an additional signal pathway to support its neuronal and neurohormonal signals to enforce circadian modulation of sleep propensity. Subtle changes in skin temperature also result from behavior, and could contribute to the changes in sleep propensity resulting from these behaviors. The present review summarizes the neurobiological background and correlational physiological and behavioral data in support of the involvement of skin temperature in the modulation of sleep propensity. It moreover points out the type of experimental investigations needed to support or refute the hypothesis.     

Sleep initiation and initial sleep intensity: interactions of homeostatic and circadian mechanisms

Sleep initiation and sleep intensity in humans show a dissimilar time course. The propensity of sleep initiation (PSI), as measured by the multiple sleep latency test, remains at a relatively constant level throughout the habitual period of waking or exhibits a midafternoon peak. When waking is extended into the sleep period, PSI rises rapidly within a few hours. In contrast, sleep intensity, as measured by electroencephalographic slow-wave activity during naps, shows a gradual increase during the period of habitual waking. In the two-process model of sleep regulation, it corresponds to the rising limb of the homeostatic Process S. We propose that PSI is determined by the difference between Process S and the threshold H defining sleep onset, which is modulated by the circadian process C. In contrast to a previous version of the model, the parameters of H (amplitude, phase, skewness) differ from those of threshold L, which defines sleep termination. The present model is able to simulate the time course of PSI under baseline conditions as well as following recovery sleep after extended sleep deprivation. The simulations suggest that during the regular period of waking, a circadian process counteracts the increasing sleep propensity induced by a homeostatic process. Data obtained in the rat indicate that during the circadian period of predominant waking, a circadian process prevents a major intrusion of sleep.     

The influence of night-time electronic device use on subsequent sleep and propensity to be physically active the following day

This study investigated the effect of acute night-time blue-light exposure through electronic device use on sleep quality/quantity, exercise motivation and perceived exertion during exercise the following day. In a randomised, crossover design, 14 participants read a book on an iPad (light) or a hard-copy book (control) one hour before bedtime. Small but not significant differences in perceived sleep quality and quantity and measured sleep efficiency were found between light and control trials, suggesting that sleep may be negatively affected following one night of electronic device use. This did not impact motivation to exercise or perceived exertion during exercise the following day.     

Effect of sleep and circadian cycle on sleep period energy expenditure

Energy expenditure is lower during sleep than relaxed wakefulness. However, there is disagreement as to the particular metabolic changes that produce the difference. The present study assessed the contribution of sleep, circadian cycle, and the specific dynamic action effect of the evening meal to the sleep period fall in metabolic rate. Five subjects were tested for a total of nine nights under three conditions in a repeated-measures design. Subjects were confined to bed throughout their usual sleep period but were instructed to go to sleep 0, 3, or 6 h after their usual time for lights out. O2 consumption was measured in all conditions for the 0.5 h before and after each of the times for lights out and then throughout the sleep period after lights out. The results demonstrated that changes in energy expenditure during the sleep period are a function of both sleep and circadian cycle. In this study, the contribution of the two components was approximately equal. However, the effect of sleep was rapid asymptoting within 15 min of sleep onset, whereas that of circadian cycle was constant over the assessment period.     

The influence of circadian rhythm during a sustained submaximal exercise and on recovery process.

The purpose of this study was to examine the time-of-day effects on muscle fatigue and recovery process following an isometric fatiguing contraction. Sixteen male subjects were tested at two times (06:00h and 18:00h) and were requested to perform a sustained submaximal contraction of the elbow flexors, consisting in maintaining 40% of their absolute strength as long as they could. Isometric maximal voluntary contractions (MVC) were performed before (Pre), immediately after (Post), and up to 10min after the endurance task. Endurance time, peak torque (PT) and electromyographic (EMG) activities of the biceps brachii and triceps brachii were recorded and analysed. Results showed that under Pre-test conditions, PT developed at 18:00h was higher than at 06:00h. No time-of-day effect appears for the endurance time and EMG activities during the test. No time-of-day effect was observed on either MVC or EMG recovery. From the results of this study, it seems that both muscle fatigue and recovery process are not time-of-day dependent. We conclude that circadian rhythm of the force do not influence the evaluation of muscle capacities during a submaximal exercise corresponding at 40% of MVC.     

Effects of thermal environment on sleep and circadian rhythm

ABSTRACT: The thermal environment is one of the most important factors that can affect human sleep. The stereotypical effects of heat or cold exposure are increased wakefulness and decreased rapid eye movement sleep and slow wave sleep. These effects of the thermal environment on sleep stages are strongly linked to thermoregulation, which affects the mechanism regulating sleep. The effects on sleep stages also differ depending on the use of bedding and/or clothing. In semi-nude subjects, sleep stages are more affected by cold exposure than heat exposure. In real-life situations where bedding and clothing are used, heat exposure increases wakefulness and decreases slow wave sleep and rapid eye movement sleep. Humid heat exposure further increases thermal load during sleep and affects sleep stages and thermoregulation. On the other hand, cold exposure does not affect sleep stages, though the use of beddings and clothing during sleep is critical in supporting thermoregulation and sleep in cold exposure. However, cold exposure affects cardiac autonomic response during sleep without affecting sleep stages and subjective sensations. These results indicate that the impact of cold exposure may be greater than that of heat exposure in real-life situations; thus, further studies are warranted that consider the effect of cold exposure on sleep and other physiological parameters.     

Impact of lifestyle on circadian orientation and sleep behaviour

Sleep and Biological Rhythms - Individual variability in preferred sleep timing is popularly described as chronotype. This study was conducted on 2105 subjects living in remote (500; without...     

Melatonin in circadian sleep disorders in the blind

Assessment of sleep patterns in blind people demonstrates a high prevalence of sleep disorders. Our studies have shown that subjects with no conscious light perception (NPL) have a higher occurrence and more severe sleep disorders than those with some degree of light perception (LP). A detailed study of 49 blind individuals showed that those with NPL are likely to have free-running (FR) circadian rhythms (aMT6s, cortisol) including sleep. Non-24-hour (or FR) sleep-wake disorder, characterised by periods of good and bad sleep is a condition that may benefit from melatonin treatment. Melatonin has been administered to NPL subjects with FR circadian rhythms and compared with placebo (or the no-treatment baseline) sleep parameters improved. The results suggest that prior knowledge of the subject's type of circadian rhythm, and timing of treatment in relation to the individual's circadian phase, may improve the efficacy of melatonin.     

蚤蝇的昼夜活动节律及睡眠行为研究

蚤蝇是重要的法医昆虫,同时是实验室中遗传、发育和生物测定等研究的重要对象。然而,蚤蝇的昼夜活动节律和睡眠行为及其在脑部的神经网络目前还不清晰。本文通过捕获本地蚤蝇并对其进行分子鉴定,研究了蚤蝇的昼夜活动节律和睡眠行为,同时表征了蚤蝇脑部核心钟神经元和多巴胺神经元。结果表明:蚤蝇在12h光照∶12h黑暗(12L∶12D)条件下不存在对开灯前或关灯前的活动预期,其双峰活动模式是对开关灯的光反应行为。在全黑暗(DD)条件下蚤蝇内源活动周期接近24h。黑腹果蝇神经肽PDF抗体免疫显示蚤蝇脑部核心钟神经元4~5个,不像黑腹果蝇一样存在明显的神经轴突。在睡眠行为上,蚤蝇雄虫和雌虫在整体活动强度、睡眠节律模式、总睡眠上均没有明显差异。相反,雄虫总睡眠次数和晚上睡眠次数低于雌虫,而总睡眠持续时间、晚上睡眠持续时间、总入睡时间和晚上入睡时间高于雌虫。此外,影响睡眠的重要多巴胺神经元在蚤蝇脑部的分布与黑腹果蝇类似。     

Modeling the influence of circadian rhythms on the acute inflammatory response

A wide variety of modeling techniques have been applied towards understanding inflammation. These models have broad potential applications, from optimizing clinical trials to improving clinical care. Models have been developed to study specific systems and diseases, but the effect of circadian rhythms on the inflammatory response has not been modeled. Circadian rhythms are normal biological variations obeying the 24-h light/dark cycle and have been shown to play a critical role in the treatment and progression of many diseases. Several of the key components of the inflammatory response, including cytokines and hormones, have been observed to undergo significant diurnal variations in plasma concentration. It is hypothesized that these diurnal rhythms are entrained by the cyclic production of the hormones cortisol and melatonin, as stimulated by the central clock in the suprachiasmatic nucleus. Based on this hypothesis, a mathematical model of the interplay between inflammation and circadian rhythms is developed. The model is validated by its ability to reproduce diverse sets of experimental data and clinical observations concerning the temporal sensitivity of the inflammatory response.     

Sleep quality and sleep duration,but not circadian parameters are associated with decreased insulin sensitivity in Type 1 diabetes

ABSTRACT

The objective of this cross-sectional analysis was to investigate in 109 adults with type 1 diabetes the relationship between sleep, circadian parameters and insulin sensitivity, as assessed by estimated glucose disposal rate (eGDR). In multiple regression analysis only poor sleep quality and sleep duration were negatively associated with eGDR (β = ?0.219 [95%CI:-1.977; ?0.445], p = .002 for poor sleep quality; β = ?0.183 [95%CI: ?0.645; ?0.111], p = .006 for sleep duration) independent of age, gender, smoking status and body mass index. In conclusion, poor sleep quality and longer sleep duration were significant predictors of decreased insulin sensitivity. Social jetlag, chronotype, and sleep debt had no effect on insulin sensitivity.     

Sleep homeostasis and models of sleep regulation

According to the two-process model of sleep regulation, the timing and structure of sleep are determined by the interaction of a homeostatic and a circadian process. The original qualitative model was elaborated to quantitative versions that included the ultradian dynamics of sleep in relation to the non-REM-REM sleep cycle. The time course of EEG slow-wave activity, the major marker of non-REM sleep homeostasis, as well as daytime alertness were simulated successfully for a considerable number of experimental protocols. They include sleep after partial sleep deprivation and daytime napping, sleep in habitual short and long sleepers, and alertness in a forced desynchrony protocol or during an extended photoperiod. Simulations revealed that internal desynchronization can be obtained for different shapes of the thresholds. New developments include the analysis of the waking EEG to delineate homeostatic and circadian processes, studies of REM sleep homeostasis, and recent evidence for local, use-dependent sleep processes. Moreover, nonlinear interactions between homeostatic and circadian processes were identified. In the past two decades, models have contributed considerably to conceptualizing and analyzing the major processes underlying sleep regulation, and they are likely to play an important role in future advances in the field.     

The effect of sleep upon human circadian rhythms

Subjects who slept for 4 h from 0000, and for a second 4 h variously distributed over the day, have provided values for rectal temperature and for urinary excretion of water, potassium, sodium, chloride, phosphate, creatinine, calcium and urate in the sleeping subject at all hours of the 24. These are compared with similar values in the wakeful subject. Temperature was lower during sleep at all hours except 1000 and 1200, and the difference was maximal shortly before 0000. At all hours potassium excretion was lower and phosphate excretion higher during sleep. Cosinor analysis of the different variables in the sleeping subject is compared with that in subjects following nycthemeral habits, and the interaction between endogenous rhythms and external influences such as sleep is discussed. The phasing of the temperature and urinary rhythms was essentially normal by the end of the observations. By contrast in a subject who slept at irregular hours mimicking the habits of an air pilot a free-running rhythm unrelated to the habits of sleep emerged. When he was finally living again on normal time his temperature and urinary acrophases had moved to the middle of the night. Phosphate excretion was largely exogenous, falling consistently when subjects rose after 8 h, but not after 4 h of sleep.     

Contribution of circadian physiology and sleep homeostasis to age-related changes in human sleep

The circadian pacemaker and sleep homeostasis play pivotal roles in vigilance state control. It has been hypothesized that age-related changes in the human circadian pacemaker, as well as sleep homeostatic mechanisms, contribute to the hallmarks of age-related changes in sleep, that is, earlier wake time and reduced sleep consolidation. Assessments of circadian parameters in healthy young (∼20-30 years old) and older people (∼65-75 years old)—in the absence of the confounding effects of sleep, changes in posture, and light exposure—have demonstrated that an earlier wake time in older people is accompanied by about a 1h advance of the rhythms of core body temperature and melatonin. In addition, older people wake up at an earlier circadian phase of the body temperature and plasma melatonin rhythm. The amplitude of the endogenous circadian component of the core body temperature rhythm assessed during constant routine and forced desynchrony protocols is reduced by 20-30% in older people. Recent assessments of the intrinsic period of the human circadian pacemaker in the absence of the confounding effects of light revealed no age-related reduction of this parameter in both sighted and blind individuals. Wake maintenance and sleep initiation are not markedly affected by age except that sleep latencies are longer in older people when sleep initiation is attempted in the early morning. In contrast, major age-related reductions in the consolidation and duration of sleep occur at all circadian phases. Sleep of older people is particularly disrupted when scheduled on the rising limb of the temperature rhythm, indicating that the sleep of older people is more susceptible to arousal signals genernpated by the circadian pacemaker. Sleep-homeostatic mechanisms, as assayed by the sleep-deprivation-induced increase of EEG slow-wave activity (SWA), are operative in older people, although during both baseline sleep and recovery sleep SWA in older people remains at lower levels. The internal circadian phase advance of awakening, as well as the age-related reduction in sleep consolidation, appears related to an age-related reduction in the promotion of sleep by the circadian pacemaker during the biological night in combination with a reduced homeostatic pressure for sleep. Early morning light exposure associated with this advance of awakening in older people could reinforce the advanced circadian phase. Quantification of the interaction between sleep homeostasis and circadian rhythmicity contributes to understanding age-related changes in sleep timing and quality. (Chronobiology International, 17(3), 285-311, 2000)     

Sleep on the job partially compensates for sleep loss in night-shift nurses

Nursing personnel in Brazil are usually submitted to fixed 12 h shifts with no consecutive working days or nights. Moonlighting is common in this group, with a consequent increase in the number of working hours. The possibility of sleeping on the job during the night shift in the studied hospitals had already been described. The present study aims to analyze whether the time devoted to daily activities (sleep, rest, leisure, housework, commuting, personal needs, care of children or other people, non-paid work, and study) is related to the number of worked hours and to nap-taking during the night shift. The field study took place at two public hospitals in Rio de Janeiro, Brazil. Workers filled out a structured form on time devoted to the above-mentioned activities for at least four consecutive days. The time devoted to sleep was analyzed according to its occurrence at home or on the job. Workers were classified according to the number of jobs (one job/two jobs) and the time dedicated to work according to the median of the whole series (below the median/above the median). All workers who had at least one working night were analyzed as to nap-taking on the job. They were classified according to the sleep occurrence during the night shift-the sleep group and the non-sleep group, both of which were compared to daytime workers. Statistical treatment of data included non-parametrical procedures. The study group comprised 144 workers (mean age: 35.7+/-10.5 years old; 91% women; 78% nurse assistants, the remainder registered nurses). They recorded their daily activities for 4-11 days; 829 cumulative days were analyzed for the whole group. A total of 165 working nights were analyzed; sleep or rest occurred during 112 (68%) of them, with mean sleep/rest duration of 141+/-86 min. Time devoted to sleep and leisure varied according to the number of working hours, being significantly reduced in those submitted to longer work hours (p < 0.001 and p = 0.002, respectively). Results close to significance point to a reduction in the time dedicated to housework among workers with long work hours (p = 0.053). The time spent on sleep/rest per working night did not differ according to the number of worked hours (p = 0.490). A tendency was observed for those who have two jobs to devote more time to sleep/rest on the job (p = 0.058). The time of personal needs was significantly lower among those who did not sleep on the job as compared to day workers (p = 0.036). The total sleep time was significantly lower among those who did not sleep on the job, as compared to day workers and to those who slept on the job (p = 0.004 and p = 0.05, respectively). As to home sleep length, workers who slept and those who did not sleep on the job were similar and slept significantly less than exclusively daytime workers (p < 0.001 and p = 0.002, respectively). Sleeping on the job during the night shift seems to partially compensate for the shorter sleep at home among night workers and may play a beneficial effect in coping with two jobs.     

Effect of sleep apnea syndrome on the circadian profile of cortisol in obese men

It has been hypothesized that sleep apnea syndrome (SAS) increases hypothalamic-pituitary-adrenal axis activity and, through increased cortisol levels, participates in the pathophysiology of metabolic and cardiovascular complications. We compared the circadian profiles of cortisol in obese men with [obSAS+; apnea-hypopnea index (AHI) >or= 20/h] and without SAS (obSAS-; AHI 相似文献