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.     

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.     

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)     

Metabolism during normal, fragmented, and recovery sleep.

Average metabolic data (O2 uptake and CO2 output) were obtained for each 3-min period during consecutive nights of normal, experimentally fragmented, and recovery sleep in a group of 12 normal young adult males. Naturally occurring arousals and awakenings resulted in a characteristic increase in metabolism on the baseline night. The placement of brief frequent experimental arousals on the following night resulted in significantly increased metabolism throughout the night and significantly decreased sleep restoration as measured by morning performance, mood, and alertness tests, even though total sleep time was minimally reduced. Metabolic variables were significantly decreased compared with baseline on the nondisturbed recovery night that followed the sleep fragmentation night. The data cannot be used to infer that increased metabolism during sleep causes nonrestorative sleep, but the direction and time course of metabolic change accompanying arousal are consistent with that hypothesis.     

Effects of short- and long-term pulsed radiofrequency electromagnetic fields on night sleep and cognitive functions in healthy subjects

There has been wide public discussion on whether the electromagnetic fields of mobile telephones and their base stations affect human sleep or cognitive functioning. As there is evidence for learning and memory-consolidating effects of sleep and particularly of REM sleep, disturbance of sleep by radiofrequency electromagnetic fields might also impair cognitive functions. Previously realized sleep studies yielded inconsistent results regarding short-term exposure. Moreover, data are lacking on the effect that short- and long-term exposure might have on sleep as well as on cognitive functions. Therefore, 10 healthy young male subjects were included and nocturnal sleep was recorded during eight consecutive nights. In the second, third, and last night, we investigated polysomnographic night sleep and cognitive functions. After the adaptation and baseline nights, the participants were exposed to a defined radiofrequency electromagnetic field during the following six nights. We analyzed polysomnographic night sleep according to Rechtschaffen and Kales [1968, Manual of Standardized Terminology, Techniques and Scoring System for Sleep of Human Subjects] as well as by power spectra and correlation dimension. Cognitive functions were investigated by an array of neuropsychological tests. Data analysis was done by comparing the baseline night with the first and last exposure night and the first two sleep cycles of the respective nights. We did not find significant effects, either on conventional sleep parameters or on power spectra and correlation dimension, nor were there any significant effects on cognitive functions. With our results, we are unable to reveal either short-term or cumulative long-term effects of radiofrequency electromagnetic fields on night sleep and cognitive functions in healthy young male subjects.     

Growth hormone-releasing hormone and corticotropin-releasing hormone enhance non-rapid-eye-movement sleep after sleep deprivation

The neuropeptides growth hormone (GH)-releasing hormone (GHRH) and corticotropin-releasing hormone (CRH) regulate sleep and nocturnal hormone secretion in a reciprocal fashion, at least in males. GHRH promotes sleep and GH and inhibits hypothalamo-pituitary-adrenocortical (HPA) hormones. CRH exerts opposite effects. In women, a sexual dimorphism was found because GHRH impairs sleep and stimulates HPA hormones. Sleep deprivation (SD) is the most powerful stimulus for inducing sleep. Studies in rodents show a key role of GHRH in sleep promotion after SD. The effects of GHRH and CRH on sleep-endocrine activity during the recovery night after SD are unknown. We compared sleep EEG, GH, and cortisol secretion between nights before and after 40 h of SD in 48 normal women and men aged 19-67 yr. During the recovery night, GHRH, CRH, or placebo were injected repetitively. After placebo during the recovery night, non-rapid-eye-movement sleep (NREMS) and rapid-eye-movement sleep (REMS) increased and wakefulness decreased compared with the baseline night. After GHRH, the increase of NREMS and the decrease of wakefulness were more distinct than after placebo. Also, after CRH, NREMS increased higher than after placebo, and a positive correlation was found between age and the baseline-related increase of slow-wave sleep. REMS increased after placebo and after GHRH, but not after CRH. EEG spectral analysis showed increases in the lower frequencies and decreases in the higher frequencies during NREMS after each of the treatments. Cortisol and GH did not differ between baseline and recovery nights after placebo. After GHRH, GH increased and cortisol decreased. Cortisol increased after CRH. No sex differences were found in these changes. Our data suggest that GHRH and CRH augment NREMS promotion after SD. Marked differences appear to exist in peptidergic sleep regulation between spontaneous and recovery sleep.     

Temporal dissociation between myeloperoxidase (MPO)-modified LDL and MPO elevations during chronic sleep restriction and recovery in healthy young men

Objectives

Many studies have evaluated the ways in which sleep disturbances may influence inflammation and the possible links of this effect to cardiovascular risk. Our objective was to investigate the effects of chronic sleep restriction and recovery on several blood cardiovascular biomarkers.

Methods and Results

Nine healthy male non-smokers, aged 22–29 years, were admitted to the Sleep Laboratory for 11 days and nights under continuous electroencephalogram polysomnography. The study consisted of three baseline nights of 8 hours sleep (from 11 pm to 7 am), five sleep-restricted nights, during which sleep was allowed only between 1 am and 6 am, and three recovery nights of 8 hours sleep (11 pm to 7 am). Myeloperoxidase-modified low-density lipoprotein levels increased during the sleep-restricted period indicating an oxidative stress. A significant increase in the quantity of slow-wave sleep was measured during the first recovery night. After this first recovery night, insulin-like growth factor-1 levels increased and myeloperoxidase concentration peaked.

Conclusions

We observed for the first time that sleep restriction and the recovery process are associated with differential changes in blood biomarkers of cardiovascular disease.     

模拟高海拔低氧对人体睡眠的影响

在模拟不同海拔高度的低氧条件暴露下,我们记录和测定了6名对象的睡眠生理各项指标。结果如下:在急性低氧暴露下所有对象均出现了睡眠障碍,主要是在夜间规定睡眠时间中觉醒期和觉醒次数增加,深睡眠期和快眼动期减少,睡眠各期的呼吸频率和心率增加。随着低氧暴露时间的延长和多次空气潜水后,各睡眠生理指标有向海平对照值水平发展的趋势。4500m以上的低氧暴露下,所有对象在睡眠中都有周期性呼吸现象出现,并影响体内的缺氧。     

Changes in the heart rate variability in patients with obstructive sleep apnea and its response to acute CPAP treatment

Introduction

Obstructive Sleep Apnea (OSA) is a major risk factor for cardiovascular disease. The goal of this study was to demonstrate whether the use of CPAP produces significant changes in the heart rate or in the heart rate variability of patients with OSA in the first night of treatment and whether gender and obesity play a role in these differences.

Methods

Single-center transversal study including patients with severe OSA corrected with CPAP. Only patients with total correction after CPAP were included. Patients underwent two sleep studies on consecutive nights: the first night a basal study, and the second with CPAP. We also analyzed the heart rate changes and their relationship with CPAP treatment, sleep stages, sex and body mass index. Twenty-minute segments of the ECG were selected from the sleep periods of REM, no-REM and awake. Heart rate (HR) and heart rate variability (HRV) were studied by comparing the R-R interval in the different conditions. We also compared samples from the basal study and CPAP nights.

Results

39 patients (15 females, 24 males) were studied. The mean age was 50.67 years old, the mean AHI was 48.54, and mean body mass index was 33.41 kg/m² (31.83 males, 35.95 females). Our results showed that HRV (SDNN) decreased after the use of CPAP during the first night of treatment, especially in non-REM sleep. Gender and obesity did not have any influence on our results.

Conclusions

These findings support that cardiac variability improves as an acute effect, independently of gender or weight, in the first night of CPAP use in severe OSA patients, supporting the idea of continuous use and emphasizing that noncompliance of CPAP treatment should be avoided even if it is just once.     

Assessment of running velocity at maximal oxygen uptake

The purpose of the study was to compare the cardiovascular, respiratory and metabolic responses to exercise of highly endurance trained subjects after 3 different nights i.e. a baseline night, a partial sleep deprivation of 3 h in the middle of the night and a 0.25-mg triazolam-induced sleep. Sleep-waking chronobiology and endurance performance capacity were taken into account in the choice of the subjects. Seven subjects exercised on a cycle ergometer for a 10-min warm-up, then for 20 min at a steady exercise intensity (equal to the intensity corresponding to 75% of the predetermined maximal oxygen consumption) followed by an increased intensity until exhaustion. The night with 3 h sleep loss was accompanied by a greater number of periods of wakefulness (P less than 0.01) and fewer periods of stage 2 sleep (P less than 0.05) compared with the results recorded during the baseline night. Triazolam-induced sleep led to an increase in stage 2 sleep (P less than 0.05), a decrease in wakefulness (P less than 0.05) and in stage 3 sleep (P less than 0.05). After partial sleep deprivation, there were statistically significant increases in heart rate (P less than 0.05) and ventilation (P less than 0.05) at submaximal exercise compared with results obtained after the baseline night. Both variables were also significantly enhanced at maximal exercise, while the peak oxygen consumption (VO2) dropped (P less than 0.05) even though the maximal sustained exercise intensity was not different.(ABSTRACT TRUNCATED AT 250 WORDS)     

Comparing the response to acute and chronic exposure to short wavelength lighting emitted from computer screens

The use of electronic devices with light-emitting screens has increased exponentially in the last decade. As a result, humans are continuously exposed to unintentional artificial light. We explored the effects of acute and chronic exposure to artificial light at night (ALAN) via screen illumination on sleep, circadian rhythms, and related functional outcomes. Nineteen participants (11 female and 8 males, mean age 28.1 ± 7.2 years) underwent a six-night study with three experimental conditions using a repeated-measures design: baseline (first night, no light exposure), acute ALAN exposure (second night), and chronic ALAN exposure (third to sixth nights). Each light exposure lasted for 2 hours (21:00–23:00). Participants underwent an overnight polysomnography at the end of each condition (nights 1, 2, and 6). We collected urine samples (for melatonin metabolite analysis), while body (oral) temperatures were measured before and after exposure. Each morning, the participants filled out questionnaires and conducted a computerized attention test. Both acute and chronic illumination significantly disrupted sleep continuity and architecture and led to greater self-reported daytime sleepiness, negative emotions, and attention difficulties. Both exposure types also altered circadian rhythms, subduing the normal nocturnal decline in body temperature and dampening nocturnal melatonin secretion. In sum, ALAN exposure from electronic screens has an immediate, detrimental, yet stable effect on sleep, circadian regulation, and next-day functional outcomes. Given the widespread use of electronic devices today, our findings suggest that even one night of screen light exposure may be sufficient to cause adverse effects on health and performance.     

Effects of exhaustive submaximal exercise on cardiovascular function during sleep

The influence of an afternoon bout of exhaustive submaximal exercise on cardiovascular function and catecholamine excretion during sleep was examined in five female and four male subjects. Subjects walked on a treadmill for successive 50-min periods at 50, 60, and 70% maximal O2 consumption, separated by 10-min rest periods. Exercise terminated with volitional exhaustion. Following an adaptation night, electroencephalographic and impedance cardiographic measures were obtained during three successive nights of sleep, with exercise preceding night 3. Relative to the base-line night (night 2), exhaustive exercise resulted in a sustained elevation of heart rate and cardiac output throughout the entire night's sleep. The magnitude of these elevations was unaffected by sleep stage but decreased over the night. The typical pattern of circadian decline in cardiac output was unaltered. However, the decline in heart rate with sleep onset was greater on the exercise night. Changes in impedance dZ/dt and R-Z interval suggested an enhanced myocardial contractility during the first 3 h of sleep postexercise. Analysis of morning urine samples revealed that in seven of nine subjects norepinephrine excretion increased, epinephrine excretion decreased, and dopamine excretion was unchanged during sleep on the exercise night. It is suggested that these cardiac changes reflect a sustained increase in myocardial beta-receptor activity.     

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.     

Diurnal Emotional States Impact the Sleep Course

Background

Diurnal emotional experiences seem to affect several characteristics of sleep architecture. However, this influence remains unclear, especially for positive emotions. In addition, electrodermal activity (EDA), a sympathetic robust indicator of emotional arousal, differs depending on the sleep stage. The present research has a double aim: to identify the specific effects of pre-sleep emotional states on the architecture of the subsequent sleep period; to relate such states to the sympathetic activation during the same sleep period.

Methods

Twelve healthy volunteers (20.1 ± 1.0 yo.) participated in the experiment and each one slept 9 nights at the laboratory, divided into 3 sessions, one per week. Each session was organized over three nights. A reference night, allowing baseline pre-sleep and sleep recordings, preceded an experimental night before which participants watched a negative, neutral, or positive movie. The third and last night was devoted to analyzing the potential recovery or persistence of emotional effects induced before the experimental night. Standard polysomnography and EDA were recorded during all the nights.

Results

Firstly, we found that experimental pre-sleep emotional induction increased the Rapid Eye Movement (REM) sleep rate following both negative and positive movies. While this increase was spread over the whole night for positive induction, it was limited to the second half of the sleep period for negative induction. Secondly, the valence of the pre-sleep movie also impacted the sympathetic activation during Non-REM stage 3 sleep, which increased after negative induction and decreased after positive induction.

Conclusion

Pre-sleep controlled emotional states impacted the subsequent REM sleep rate and modulated the sympathetic activity during the sleep period. The outcomes of this study offer interesting perspectives related to the effect of diurnal emotional influences on sleep regulation and open new avenues for potential practices designed to alleviate sleep disturbances.     

Effect of sleep restriction on orthostatic cardiovascular control in humans.

We hypothesized that sleep restriction (4 consecutive nights, 4 h sleep/night) attenuates orthostatic tolerance. The effect of sleep restriction on cardiovascular responses to simulated orthostasis, arterial baroreflex gain, and heart rate variability was evaluated in 10 healthy volunteers. Arterial baroreflex gain was determined from heart rate responses to nitroprusside-phenylephrine injections, and orthostatic tolerance was tested via lower body negative pressure (LBNP). A Finapres device measured finger arterial pressure. No difference in baroreflex function, heart rate variability, or LBNP tolerance was observed with sleep restriction (P > 0.3). Systolic pressure was greater at -60 mmHg LBNP after sleep restriction than before sleep restriction (110 +/- 6 and 124 +/- 3 mmHg before and after sleep restriction, respectively, P = 0.038), whereas heart rate decreased (108 +/- 8 and 99 +/- 8 beats/min before and after sleep restriction, respectively, P = 0.028). These data demonstrate that sleep restriction produces subtle changes in cardiovascular responses to simulated orthostasis, but these changes do not compromise orthostatic tolerance.     

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.     

Pimozide attentuates d-amphetamine-induced sleep changes in man.

Pretreatment with pimozide (mean dose = 13 mg/day) blocked the effect of d-amphetamine (20 mg base, administered by intravenous bolus infusion at 0815) on all-night EEG sleep patterns in seven hospitalized psychiatric patients. Each patient was studied for five nights (2 nights baseline, 1 night on the day of the infusion, and 2 nights recovery) with and without pretreatment with pimozide. Without treatment with pimozide, d-amphetamine significantly reduced duration of total sleep, REM and nonREM sleep, Stage I, and Stage II. With coadministration of pimozide, d-amphetamine had no effect on sleep. These results suggest that the d-amphetamine induced changes in sleep are mediated by dopaminergic neurons.     

Effect of hyoscine butylbromide and atropine on heart rate during nocturnal sleep

This is a single blind crossover study designed to test the effects of hyoscine butylbromide (HBB), an anticholinergic which does not cross the blood brain barrier (BBB), on the temporal changes in heart rate during nocturnal sleep. The effects were compared with atropine sulphate which is known to cross the BBB. Ten healthy male volunteers slept in the JIPMER sleep disorders laboratory for three nights and received either saline, atropine sulphate (0.4 mg, i.v.) or HBB (10 mg, i.v.) just prior to sleep onset. All night polysomnography recording was done to monitor heart rate during the specific stages of sleep. The normal physiological fall in heart rate is blunted by both drugs during slow wave sleep whereas only HBB prevented the fall in rapid eye movement sleep. Therefore, HBB may be a better choice as pre-anaesthetic medication for patients with cardiac abnormalities since it does not alter heart rate during both slow wave sleep and rapid eye movement sleep.     

Effects of nighttime low frequency noise on the cortisol response to awakening and subjective sleep quality

The effects of night-time exposure to traffic noise (TN) or low frequency noise (LFN) on the cortisol awakening response and subjective sleep quality were determined. Twelve male subjects slept for five consecutive nights in a noise-sleep laboratory. After one night of acclimatisation and one reference night, subjects were exposed to either TN (35dB L(Aeq), 50dB L(Amax)) or LFN (40dB L(Aeq)) on alternating nights (with an additional reference night in between). Salivary free cortisol concentration was determined in saliva samples taken immediately at awakening and at three 15-minute intervals after awakening. The subjects completed questionnaires on mood and sleep quality. The awakening cortisol response on the reference nights showed a normal cortisol pattern. A significant interaction between night time exposure and time was found for the cortisol response upon awakening. The awakening cortisol response following exposure to LFN was attenuated at 30 minutes after awakening. Subjects took longer to fall asleep during exposure to LFN. Exposure to TN induced greater irritation. Cortisol levels at 30 minutes after awakening were related to "activity" and "pleasantness" in the morning after exposure to LFN. Cortisol levels 30 minutes after awakening were related to sleep quality after exposure to TN. This study thus showed that night time exposure to LFN may affect the cortisol response upon wake up and that lower cortisol levels after awakening were associated with subjective reports of lower sleep quality and mood.     

Cardiovascular responses and electroencephalogram disturbances to intermittent noises: effects of nocturnal heat and daytime exposure

During sleep, in thermoneutral conditions, the noise of a passing vehicle induces a biphasic cardiac response, a transient peripheral vasoconstriction and sleep disturbances. The present study was performed to determine whether or not the physiological responses were modified in a hot environment or after daytime exposure to both heat and noise. Eight young men were exposed to a nocturnal thermoneutral (20 degrees C) or hot (35 degrees C) environment disturbed by traffic noise. During the night, the peak intensities were of 71 dB(A) for trucks, 67 dB(A) for motorbikes and 64 dB(A) for cars. The background noise level (pink noise) was set at 30 dB(A). The noises were randomly distributed at a rate of 9.h-1. Nights were equally preceded by daytime exposure to combined heat and noise or to no disturbance. During the day, the noises as well as the background noise levels were increased by 15 dB(A) and the rate was 48.h-1. Electroencephalogram (EEG) measures of sleep, electrocardiograms and finger pulse amplitudes were continuously recorded. Regardless of the day condition, when compared with undisturbed nights, the nocturnal increase in the level of heart rate induced by heat exposure disappeared when noise was added. Percentages, delays, magnitudes and costs of cardiac and vascular responses as well as EEG events such as transient activation phases (TAP) due to noise were not affected by nocturnal thermal load or by the preceding daytime exposure to disturbances.(ABSTRACT TRUNCATED AT 250 WORDS)