Influence of repeated passive body heating on subsequent night sleep in humans

Experiments were carried out on four healthy male subjects in two separate sessions: (a) A baseline period of two consecutive nights, one spent at thermoneutrality [operative temperature (To) = 30 degrees C, dew-point temperature (Tdp) = 7 degrees C, air velocity (Va) = 0.2 m.s-1] and the other in hot condition (To = 35 degrees C, Tdp = 7 degrees C, Va = 0.2 m.s-1). During the day, the subjects lived in their normal housing and were engaged in their usual activities. (b) An acclimation period of seven consecutive daily heat exposures from 1400 to 1700 hours (To = 44 degrees C, Tdp = 29 degrees C, Va = 0.3 m.s-1). During each night, the subjects slept in thermoneutral or in hot conditions. The sleep measurements were: EEG from two sites, EOG from both eyes, EMG and EKG. Esophageal and ten skin temperatures were recorded continuously during the night. In the nocturnal hot conditions, a sweat collection capsule recorded the sweat gland activity in the different sleep stages. Results showed that passive body heating had no significant effect on the sleep structure of subsequent nights at thermoneutrality. In contrast, during nights at To = 35 degrees C an effect of daily heat exposure was observed on sleep. During the 2nd night of the heat acclimation period, sleep was more restless and less efficient than during the baseline night. The rapid eye movement sleep duration was reduced, while the rate of transient activation phases observed in sleep stage 2 increased significantly. On the 7th night, stage 4 sleep increased (+68%) over values observed during the baseline night.(ABSTRACT TRUNCATED AT 250 WORDS)     

Thermoregulation, metabolism, and stages of sleep in cold-exposed men

Four naked men, selected for their ability to sleep in the cold, were exposed to an ambient temperature (Ta) of 21 degrees C for five consecutive nights. Electrophysiological stages of sleep, O2 consumption (VO2), and skin (Tsk), rectal (Tre), and tympanic (Tty) temperatures were recorded. Compared with five nights at a thermoneutral Ta of 29 degrees C, cold induced increased wakefulness and decreased stage 2 sleep, without significantly affecting other stages. Tre and Tty declined during each condition. The decrease in Tre was greater at 21 degrees C than at 29 degrees C, whereas Tty did not differ significantly between conditions. Increases in Tty following REM sleep onset at 21 degrees C were negatively correlated with absolute Tty. VO2 and forehead Tsk also increased during REM sleep at both TaS, whereas Tsk of the limb extremities declined at 21 degrees C. Unsuppressed REM sleep in association with peripheral vasoconstriction and increased Tty and VO2 in cold-exposed humans, do not signify an inhibition of thermoregulation during this sleep stage as has been observed in other mammals.     

Comparing Sleep‐Loss Sleepiness and Sleep Inertia: Lapses Make the Difference

To compare the behavioral effects of sleep‐loss sleepiness (performance impairment due to sleep loss) and sleep inertia (period of impaired performance that follows awakening), mean response latencies and number of lapses from a visual simple reaction‐time task were analyzed. Three experimental conditions were designed to manipulate sleepiness and sleep‐inertia levels: uninterrupted sleep, partial sleep reduction, and total sleep deprivation. Each condition included two consecutive nights (the first always a night of uninterrupted sleep, and the second either a night of uninterrupted sleep, a night when sleep was reduced to 3 h, or a night of total sleep deprivation), as well as two days in which performance was assessed at 10 different time points (08:00, 08:30, 09:00, 09:30, 10:00, 11:00, 14:00, 17:00, 20:00, and 23:00 h). From 08:00 to 09:00 h, reaction times in the partial sleep‐reduction and total sleep‐deprivation conditions were at a similar level and were slower than those observed in the uninterrupted sleep condition. In the same time period, the frequency of lapses in the total sleep‐deprivation condition was higher than in the partial sleep‐reduction condition, while this latter condition never differed from the uninterrupted sleep condition. The results indicate that both sleep inertia and sleep‐loss sleepiness lead to an increase in response latencies, but only extreme sleepiness leads to an increase in lapse frequency. We conclude that while reaction times slow as a result of both sleep inertia and sleep‐loss sleepiness, lapses appear to be a specific feature of sleep‐loss sleepiness.     

Low-dimensional dynamic self-organization in δ-sleep: effect of partial sleep deprivation

Studies on extended data including 37 electroencephalographic (EEG) records of -sleep, each 10³ s long (six subjects; up to seven nights per subject, comprising normal sleep, partial deprivation and recovery), confirmed earlier conclusions that rare episodes of low-dimensional dynamic self-organization, with lifetimes between 10 and 20 s, are present in stage 4 sleep. Particular care was taken of the Theiler correction which, in some -sleep signals, required the deletion of trajectory points covering nearly one pseudo-period. The percentage of segments showing an episode, i.e. the attractor probability, decreased with a change in sleep conditions — either deprivation or recovery prior to the next deprivation. Repetition of deprivation over three nights resulted in an adaptation process, manifested by an increase in attractor probability. After the sharp decrease in probability observed when recovery was established prior to the next deprivation, and on return to normal conditions of sleep at 2200 hours, the probability was immediately close to that observed in normal baseline sleep conditions free of any interference. The observation of a definite effect of sleep deprivation and recovery upon the number of stage 4 attractors observed provides a line of approach to the physiological significance of the probability of such attractors.     

Changes of pulse rate caused by sonic bomms during sleep (author's transl)]

In two experimental series (19 resp. 53 nights, 2 different persons in each series, test-time 10.30 p.m. to 3.00 a.m.) pulse rate after sonic booms had been recorded during sleep. In the first 3 nights the subjects slept undisturbed by noise. In the following 11 resp. 30 nights sonic booms were applied alternately 2 or 4 times. In the main series after 10 more nights without any noise 4 nights with 8 and 16 sonic booms alternately followed. The last 6 undisturbed nights in both series were used as comparison phase. The interval between two sonic booms was 40 min in nights with 2 booms, 20 min in nights with 4 sonic booms and in the nights with 8 and 16 sonic booms 8.6 resp. 4.6 min. Sound level of the sonic booms ranged from 0.48 mbar to 1.45 mbar, 1 mbar [83.5 dB (A)] in the average. The first sonic boom was applied if one of the two subjects had entered the deepest stage of sleep. Sonic booms induced a biphasic reaction in pulse rate. After an initial increase in frequency with a maximum in the 4th sec pulse rate decreased below the value before sonic boom; it was followed by a slow increase towards the baseline value. This reaction was analysed with special regard to the following factors: 1. Intensity. Due to very fast increase of noise intensity there was no significant correlation between the intensity of sonic boom and the pulse reaction. 2. Exogenic variables. There is no significant connection between postboom pulse rate and noiseless time before the sonic boom, the duration of the test series and the ambient temperature. 3. Endogenic variables. No correlation could be found between the stage of sleep and the reaction. On the contrary a very significant correlation was found between the maximum of postboom increase of pulse rate and the pulse rate before boom. With increasing pulse rate the extent of reaction becomes smaller.     

Daytime noise and subsequent night sleep in man

The effects of daytime noise on recovery processes during subsequent undisturbed night sleep were studied in six healthy men (21-27 years), exposed to 80 dB (A) pink noise 8 h per day for 2 days. Sleep EEG, ECG, and respiration were recorded in the laboratory for five consecutive nights: two baseline nights, two nights following noise stimulation, and again one baseline night. Additionally questionnaire data were collected, reflecting a subjective impairment of the recovery function of sleep after noise exposure. EEG sleep data of the first post-noise night showed an increase in slow wave sleep with a simultaneous decrease in stage 2 sleep. During the second post-noise night these changes were less prominent. Three subjects additionally showed an instability in the sleep course coinciding with elevated heart and respiration rates. However, altogether the autonomic parameters were not clearly affected by the noise exposure. The findings support the assumption that strong daytime noise may interfere with subsequent sleep processes.     

Comparing sleep-loss sleepiness and sleep inertia: lapses make the difference

To compare the behavioral effects of sleep-loss sleepiness (performance impairment due to sleep loss) and sleep inertia (period of impaired performance that follows awakening), mean response latencies and number of lapses from a visual simple reaction-time task were analyzed. Three experimental conditions were designed to manipulate sleepiness and sleep-inertia levels: uninterrupted sleep, partial sleep reduction, and total sleep deprivation. Each condition included two consecutive nights (the first always a night of uninterrupted sleep, and the second either a night of uninterrupted sleep, a night when sleep was reduced to 3 h, or a night of total sleep deprivation), as well as two days in which performance was assessed at 10 different time points (08:00, 08:30, 09:00, 09:30, 10:00, 11:00, 14:00, 17:00, 20:00, and 23:00 h). From 08:00 to 09:00 h, reaction times in the partial sleep-reduction and total sleep-deprivation conditions were at a similar level and were slower than those observed in the uninterrupted sleep condition. In the same time period, the frequency of lapses in the total sleep-deprivation condition was higher than in the partial sleep-reduction condition, while this latter condition never differed from the uninterrupted sleep condition. The results indicate that both sleep inertia and sleep-loss sleepiness lead to an increase in response latencies, but only extreme sleepiness leads to an increase in lapse frequency. We conclude that while reaction times slow as a result of both sleep inertia and sleep-loss sleepiness, lapses appear to be a specific feature of sleep-loss sleepiness.     

Acute sleep restriction alters neuroendocrine hormones and appetite in healthy male adults

This study examined the effects of two nights of sleep restriction on neuroendocrine hormones (i.e. peptide YY [PYY], ghrelin, glucagon-like peptide-1, adiponectin, and leptin) involved in regulating body weight. Ten healthy male adults aged 18 to 23 years were subjected to two consecutive nights of sleep restriction. Compared to a night of normal sleep, sleep restriction was associated with a significant reduction in PYY levels (P = 0.047) and a significant reduction in satiety levels (P = 0.033). These results suggest that sleep restriction alters the hormonal regulation of appetite in a manner predictive of increased energy intake.

     

Sleep in the surgical intensive care unit: continuous polygraphic recording of sleep in nine patients receiving postoperative care.

Sleep was studied in nine patients for two to four days after major non-cardiac surgery by continuous polygraphic recording of electroencephalogram, electrooculogram, and electromyogram. Presumed optimal conditions for sleep were provided by a concerted effort by staff to offer constant pain relief and reduce environmental disturbance to a minimum. All patients were severely deprived of sleep compared with normal. The mean cumulative sleep time (stage 1 excluded) for the first two nights, daytime sleep included, was less than two hours a night. Stages 3 and 4 and rapid eye movement sleep were severely or completely suppressed. The sustained wakefulness could be attributed to pain and environmental disturbance to only minor degree. Sleep time as estimated by nursing staff was often grossly misjudged and consistently overestimated when compared with the parallel polygraphic recording. The grossly abnormal sleep pattern observed in these patients may suggest some fundamental disarrangement of the sleep-wake regulating mechanism.     

Cardiovascular effects of partial sleep deprivation in healthy volunteers

Sleep deprivation is common in Western societies and is associated with increased cardiovascular morbidity and mortality in epidemiological studies. However, the effects of partial sleep deprivation on the cardiovascular system are poorly understood. In the present study, we evaluated 13 healthy male volunteers (age: 31 ± 2 yr) monitoring sleep diary and wrist actigraphy during their daily routine for 12 nights. The subjects were randomized and crossover to 5 nights of control sleep (>7 h) or 5 nights of partial sleep deprivation (<5 h), interposed by 2 nights of unrestricted sleep. At the end of control and partial sleep deprivation periods, heart rate variability (HRV), blood pressure variability (BPV), serum norepinephrine, and venous endothelial function (dorsal hand vein technique) were measured at rest in a supine position. The subjects slept 8.0 ± 0.5 and 4.5 ± 0.3 h during control and partial sleep deprivation periods, respectively (P < 0.01). Compared with control, sleep deprivation caused significant increase in sympathetic activity as evidenced by increase in percent low-frequency (50 ± 15 vs. 59 ± 8) and a decrease in percent high-frequency (50 ± 10 vs. 41 ± 8) components of HRV, increase in low-frequency band of BPV, and increase in serum norepinephrine (119 ± 46 vs. 162 ± 58 ng/ml), as well as a reduction in maximum endothelial dependent venodilatation (100 ± 22 vs. 41 ± 20%; P < 0.05 for all comparisons). In conclusion, 5 nights of partial sleep deprivation is sufficient to cause significant increase in sympathetic activity and venous endothelial dysfunction. These results may help to explain the association between short sleep and increased cardiovascular risk in epidemiological studies.     

A Laboratory Study of Sleep and Dreaming in a Case of Asperger's Syndrome

Asperger's Syndrome (AS) is a pervasive developmental disorder whose continuity with High-Functioning Autism is still a matter of debate. Clinical observations suggest that patients with AS may present the same sleep disorders as autistic patients, including difficulties in initiating and maintaining sleep as well as poor dream recall. We recorded the sleep of a 25-year-old male patient with AS for two nights using a full EEG montage and compared the second night to that of a group of normal participants. We found low levels of slow wave sleep (SWS: stages 3 + 4), high levels of stage 1, and a large number of awakenings. The organization of REM sleep was unremarkable, including normal REM density. Analyses of phasic EEG events revealed a very low incidence of sleep spindles and a normal number of K-complexes over bilateral frontal and central EEG leads. In order to collect dream reports, the patient was awakened three times over two nights following at least 15 minutes of REM sleep in each case. On each occasion the patient was not aware of any mental activity happening just prior to awakening. These observations are discussed with regards to the connections that may exist between EEG sleep spindle activity, selective attention, and the capacity to generate a dream report.     

Sleep Deprivation Influences Diurnal Variation of Human Time Perception with Prefrontal Activity Change: A Functional Near-Infrared Spectroscopy Study

Human short-time perception shows diurnal variation. In general, short-time perception fluctuates in parallel with circadian clock parameters, while diurnal variation seems to be modulated by sleep deprivation per se. Functional imaging studies have reported that short-time perception recruits a neural network that includes subcortical structures, as well as cortical areas involving the prefrontal cortex (PFC). It has also been reported that the PFC is vulnerable to sleep deprivation, which has an influence on various cognitive functions. The present study is aimed at elucidating the influence of PFC vulnerability to sleep deprivation on short-time perception, using the optical imaging technique of functional near-infrared spectroscopy. Eighteen participants performed 10-s time production tasks before (at 21:00) and after (at 09:00) experimental nights both in sleep-controlled and sleep-deprived conditions in a 4-day laboratory-based crossover study. Compared to the sleep-controlled condition, one-night sleep deprivation induced a significant reduction in the produced time simultaneous with an increased hemodynamic response in the left PFC at 09:00. These results suggest that activation of the left PFC, which possibly reflects functional compensation under a sleep-deprived condition, is associated with alteration of short-time perception.     

Catechol-O-methyltransferase Val158Met polymorphism associates with individual differences in sleep physiologic responses to chronic sleep loss

Background

The COMT Val158Met polymorphism modulates cortical dopaminergic catabolism, and predicts individual differences in prefrontal executive functioning in healthy adults and schizophrenic patients, and associates with EEG differences during sleep loss. We assessed whether the COMT Val158Met polymorphism was a novel marker in healthy adults of differential vulnerability to chronic partial sleep deprivation (PSD), a condition distinct from total sleep loss and one experienced by millions on a daily and persistent basis.

Methodology/Principal Findings

20 Met/Met, 64 Val/Met, and 45 Val/Val subjects participated in a protocol of two baseline 10h time in bed (TIB) nights followed by five consecutive 4 h TIB nights. Met/Met subjects showed differentially steeper declines in non-REM EEG slow-wave energy (SWE)—the putative homeostatic marker of sleep drive—during PSD, despite comparable baseline SWE declines. Val/Val subjects showed differentially smaller increases in slow-wave sleep and smaller reductions in stage 2 sleep during PSD, and had more stage 1 sleep across nights and a shorter baseline REM sleep latency. The genotypes, however, did not differ in performance across various executive function and cognitive tasks and showed comparable increases in subjective and physiological sleepiness in response to chronic sleep loss. Met/Met genotypic and Met allelic frequencies were higher in whites than African Americans.

Conclusions/Significance

The COMT Val158Met polymorphism may be a genetic biomarker for predicting individual differences in sleep physiology—but not in cognitive and executive functioning—resulting from sleep loss in a healthy, racially-diverse adult population of men and women. Beyond healthy sleepers, our results may also provide insight for predicting sleep loss responses in patients with schizophrenia and other psychiatric disorders, since these groups repeatedly experience chronically-curtailed sleep and demonstrate COMT-related treatment responses and risk factors for symptom exacerbation.     

Sleep in chronic chorea patients after therapy with sodium valproate

In previous researches spontaneous nocturnal sleep in chronic chorea showed short total sleep time, prolonged sleep latency, several awakenings, reduction of REM sleep time, decrease in slow waves sleep, strong increase in sleep spindles. Some of these alterations improved after therapy with lithium, haloperidol and lithium, pimozide. Since the concentration of GABA has been found to be reduced in patients with Huntington's chorea, we studied the effect of sodium valproate, a drug that enhances GABA inhibition in cerebral cortex, on nocturnal sleep of six patients with chronic chorea, aged 35 to 60 years (mean 47,3). Nocturnal polygraphic records (EEG, EOG, EMG of chin muscles) were carried out after two consecutive adjustative nights, both before therapy and after sixty days of treatment with sodium valproate (800-2000 mg four times a day, orally). Moreover, chorea, finger dexterity and gait were each rated once a week by three members of the research team and by one independent observer, using a five points rating scale from 0 (normal) to 4 (very severely abnormal). Before therapy the sleep parameters were in accordance with our previous results in chronic choreic patients. After two months therapy we observed a statistically significant (P less than 0.05) reduction of awakenings and of wake time. Sodium valproate produced no objective change in any of the parameters of motor function studied. If singularly examined, however, a reduction of chorea was obtained only in a patient, whose favourable response to therapy was also demonstrated by the normalization of other sleep parameters. These data stress the importance of sleep study in extrapyramidal disorders and suggest a different involvement of GABA-mediated transmission in various patients with chronic chorea.     

EEG patterns and body temperatures in man during sleep in arctic winter nights

Two Caucasian males, aged 19 and 22, slept at night in sleeping bags (9.0 clo) in an unheated tent at ambient temperatures between –25 and –35°C in the Arctic. Electroencephalographic (EEG) sleep studies were conducted for two baseline nights (19–21°C), 10 cold exposure nights and 2 recovery nights (19–21°C). Rectal and skin temperatures, and heart rates were also recorded. The subjects suffered disturbances in sleep patterns involving an insomnia composed of an increased wakefulness, a decrease in slow wave sleep and a deprivation in rapid eye movement (REM) sleep. Dissimilarities appeared between the subjects which may be related to differences in thermoregulatory responses.     

Uncertain call likelihood negatively affects sleep and next-day cognitive performance while on-call in a laboratory environment

ABSTRACT

On-call working arrangements are employed in a number of industries to manage unpredictable events, and often involve tasks that are safety- or time-critical. This study investigated the effects of call likelihood during an overnight on-call shift on self-reported pre-bed anxiety, sleep and next-day cognitive performance. A four-night laboratory-based protocol was employed, with an adaptation, a control and two counterbalanced on-call nights. On one on-call night, participants were instructed that they would definitely be called during the night, while on the other on-call night they were told they may be called. The State-Trait Anxiety Inventory form x-1 was used to investigate pre-bed anxiety, and sleep was assessed using polysomnography and power spectral analysis of the sleep electroencephalographic analysis. Cognitive performance was assessed four times daily using a 10-min psychomotor vigilance task. Participants felt more anxious before bed when they were definitely going to be called, compared with the control and maybe conditions. Conversely, participants experienced significantly less non-rapid eye movement and stage two sleep and poorer cognitive performance when told they may be called. Further, participants had significantly more rapid eye movement sleep in the maybe condition, which may be an adaptive response to the stress associated with this on-call condition. It appears that self-reported anxiety may not be linked with sleep outcomes while on-call. However, this research indicates that it is important to take call likelihood into consideration when constructing rosters and risk-management systems for on-call workers.     

Immune alterations after selective rapid eye movement or total sleep deprivation in healthy male volunteers

We investigated the impact of two nights of total sleep deprivation (SD) or four nights of rapid eye movement (REM) SD on immunological parameters in healthy men. Thirty-two volunteers were randomly assigned to three protocols (control, total SD or REM SD). Both SD protocols were followed by three nights of sleep recovery. The control and REM SD groups had regular nights of sleep monitored by polysomnography. Circulating white blood cells (WBCs), T- (CD4/CD8) and B-lymphocytes, Ig classes, complement and cytokine levels were assessed daily. Two nights of total SD increased the numbers of leukocytes and neutrophils compared with baseline levels, and these levels returned to baseline after 24 h of sleep recovery. The CD4(+) T-cells increased during the total SD period (one and two nights) and IgA levels decreased during the entire period of REM SD. These levels did not return to baseline after three nights of sleep recovery. Levels of monocytes, eosinophils, basophils and cytokines (IL-1β, IL-2, IL-4, IL-6, IL-10, TNF-α and IFN-γ) remained unchanged by both protocols of SD. Our findings suggest that both protocols affected the human immune profile, although in different parameters, and that CD4(+) T-cells and IgA levels were not re-established after sleep recovery.     

Plasma testosterone during nocturnal sleep in normal men

Plasma testosterone was measured by a competitive protein binding procedure at 10 to 20 minute intervals in five normal adult men during two nights of sleep. Blood samples were obtained by means of an indwelling venous catheter while sleep was monitored polygraphically. There were 1–4 abrupt elevations of plasma testosterone concentration per night in each of the subjects with an average increase of 244 ng/100 ml ± 45.5 (SE) or 59% above the values present at the onset of the episode. The fluctuations in plasma testosterone were superimposed on a nocturnal rise of the hormone observed in seven of the nights. The average of all samples taken during each hour period through the ten nights revealed a highly significant (P<0.001) nocturnal increase in plasma testosterone. The findings did not support the existence of a relation between REM sleep and an increase in testosterone levels.     

On the Influence of Freight Trains on Humans: A Laboratory Investigation of the Impact of Nocturnal Low Frequency Vibration and Noise on Sleep and Heart Rate

Background

A substantial increase in transportation of goods on railway may be hindered by public fear of increased vibration and noise leading to annoyance and sleep disturbance. As the majority of freight trains run during night time, the impact upon sleep is expected to be the most serious adverse effect. The impact of nocturnal vibration on sleep is an area currently lacking in knowledge. We experimentally investigated sleep disturbance with the aim to ascertain the impact of increasing vibration amplitude.

Methodology/Principal Findings

The impacts of various amplitudes of horizontal vibrations on sleep disturbance and heart rate were investigated in a laboratory study. Cardiac accelerations were assessed using a combination of polysomnography and ECG recordings. Sleep was assessed subjectively using questionnaires. Twelve young, healthy subjects slept for six nights in the sleep laboratory, with one habituation night, one control night and four nights with a variation of vibration exposures whilst maintaining the same noise exposure. With increasing vibration amplitude, we found a decrease in latency and increase in amplitude of heart rate as well as a reduction in sleep quality and increase in sleep disturbance.

Conclusions/Significance

We concluded that nocturnal vibration has a negative impact on sleep and that the impact increases with greater vibration amplitude. Sleep disturbance has short- and long-term health consequences. Therefore, it is necessary to define levels that protect residents against sleep disruptive vibrations that may arise from night time railway freight traffic.     

Suppression of electroencephalogram Δ power density during non-rapid eye movement sleep as a result of a prolonged cognitive task prior to sleep onset

The effects of a prolonged cognitive task prior to sleep onset on subsequent sleep patterns were examined in 14 healthy subjects who were randomly assigned to two conditions. Those assigned to a working condition were asked to engage in a prolonged cognitive task until close to bedtime (0200 hours), whereas those assigned to a relaxing condition were instructed to perform the same task during the daytime and then to stay awake in a relaxed state until the same bedtime as the work group. Visual scoring of sleep stages showed no significant differences in the amounts of stage 4 and slow wave sleep (stage 3+4) between the two conditions. Power spectrum analysis of sleep electroencephalogram (EEG) revealed that the EEG (0.5–4.0 Hz) power density in the first non-rapid eye movement (REM)-REM sleep cycle was significantly lower following the prolonged cognitive task prior to sleep onset than following the relaxed wakefulness and that the decreased EEG power density in the first sleep cycle was not compensated for during the later part of the sleep. These findings would indicate that the prolonged cognitive task prior to sleep onset may suppress EEG power density during subsequent sleep, suggesting that such a task may interfere with the development of deep non-REM sleep.