Effect of sleep on nocturnal bronchoconstriction and ventilatory patterns in asthmatics

To assess the effect of sleep on airflow resistance and patterns of ventilation in asthmatic patients with nocturnal worsening, 10 adult subjects (6 asthmatic patients with nocturnal worsening, 4 normal controls) were monitored overnight in the sleep laboratory on two separate occasions. During 1 night, subjects were allowed to sleep normally, whereas during the other night all sleep was prevented. The six asthmatic patients demonstrated progressive increases in lower airway resistance (Rla) on both nights, but the rate of increase was twofold greater (P less than 0.0001) during the sleep night compared with the sleep prevention night. However, overnight decrements in forced expired volume in 1 s (FEV1) were similar over the 2 nights. The asthmatic patients maintained their minute ventilation as Rla increased during sleep, demonstrating a stable tidal volume with a mild increase in respiratory frequency. We conclude that in asthmatic patients with nocturnal worsening 1) Rla increases and FEV1 falls overnight regardless of sleep state, 2) sleep enhances the observed overnight increases in Rla, and 3) sleep does not abolish compensatory ventilatory responses to spontaneously occurring bronchoconstriction.     

Assessment of the reproducibility of nocturnal growth hormone secretion

The reproducibility of measurements of nocturnal spontaneous secretion of growth hormone (GH) was assessed. The study population consisted of 15 short children with a variety of pathological conditions. Blood samples were taken every 20 min from each subject during sleep on two consecutive nights. The analysis of variance of matched series indicated a global reproducibility, but also demonstrated significant individual variabilities (with-in-subject effect) of both peak amplitude (p = 0.05) and mean concentration (p = 0.02). We did not find any link between the variation of the GH parameters and the variations of the clinical sleep score in 11 patients.     

Amplification of nocturnal oscillations in PRA and aldosterone during continuous heat exposure

To assess the effect of continuous heat exposure on the nocturnal patterns of renin, aldosterone, adrenocorticotropic hormone (ACTH), and cortisol, six young men were exposed to thermoneutral environment for 5 days, followed by a 5-day acclimation period in a hot dry environment (35 degrees C). Blood was collected at 10-min intervals during the second night at thermoneutrality (N0) and during the first (N1) and the last (N5) nights of heat exposure. Polygraphic recordings of sleep were scored according to established criteria. Continuous heat exposure led to progressive decreases in the 24-h urinary volume and in Na excretion, whereas urinary osmolality increased. After 5 days of uninterrupted heat, significant increases were found in plasma volume (P less than 0.05), osmolality (P less than 0.01), plasma Na (P less than 0.01), and protein levels (P less than 0.05). Sweat gland output increased during the first 3 days and then declined without any concomitant increases in body temperature. Compared with N0, there were no differences in plasma renin activity (PRA) and aldosterone (PA) profiles during N1 at 35 degrees C. However, during N5 the mean PRA and PA levels were significantly (P less than 0.05) enhanced, and their nocturnal oscillations were amplified (P less than 0.05). This amplification occurred mainly in the second part of the night when regular rapid-eye-movement and non-rapid-eye-movement sleep cycles were observed, leading to a general upward trend in the nocturnal profiles. The relationship between the nocturnal PRA oscillations and the sleep cycles was not modified. ACTH and cortisol patterns were not affected by continuous heat exposure.(ABSTRACT TRUNCATED AT 250 WORDS)     

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)     

Nocturnal increase in plasma cGMP levels in humans.

The circadian dynamics of responses to cyclic guanosine 3',5'-monophosphate (cGMP) in in vitro experiments and the stimulating effects of the pineal hormone melatonin on cGMP levels both in vitro and in vivo provoked an investigation into the diurnal pattern of occurrence of this second messenger in human plasma and its correlation with plasma melatonin levels. Plasma cGMP levels were measured in 9 normal human subjects who were over 50 years of age. Samples were obtained hourly through a 20-h period (11 a.m. to 7 a.m.) that included the subjects' habitual hours of nocturnal sleep; physical activity was kept to a minimum during the daylight hours. The area under the time-plasma cGMP concentration curve showed a significant increase during the period of nocturnal sleep compared to that observed during the period of daytime wakefulness. The individual temporal pattern of the nocturnal rise in plasma cGMP differed among the subjects; however, the initial increase typically was observed soon after bedtime. No significant correlation was observed between individual nocturnal plasma melatonin levels and cGMP 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.     

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.     

Sleep enhances nocturnal plasma ghrelin levels in healthy subjects

Ghrelin, an endogenous ligand of the growth hormone secretagogue receptor, has been shown to promote slow-wave sleep (SWS, non-REM sleep stages 3 and 4). Plasma levels of ghrelin are dependent on food intake and increase in sleeping subjects during the early part of the night. It is unknown whether sleep itself affects ghrelin levels or whether circadian networks are involved. Therefore, we studied the effect of sleep deprivation on nocturnal ghrelin secretion. In healthy male volunteers, plasma levels of ghrelin, cortisol, and human growth hormone (hGH) were measured during two experimental sessions of 24 h each: once when the subjects were allowed to sleep between 2300 and 0700 and once when they were kept awake throughout the night. During sleep, ghrelin levels increased during the early part of the night and decreased in the morning. This nocturnal increase was blunted during sleep deprivation, and ghrelin levels increased only slightly until the early morning. Ghrelin secretion during the first hours of sleep correlated positively with peak hGH concentrations. We conclude that the nocturnal increase in ghrelin levels is more likely to be caused by sleep-associated processes than by circadian influences. During the first hours of sleep, ghrelin might promote sleep-associated hGH secretion and contribute to the promotion of SWS.     

Extraocular light exposure does not phase shift saliva melatonin rhythms in sleeping subjects

Preliminary work in humans suggests that extraocular light can shift circadian phase. If confirmed, extraocular light may be of therapeutic benefit in the treatment of circadian-related sleep disorders with the advantage over ocular exposure that it can be administered while subjects are asleep. In sleeping subjects, however, the effect of extraocular light exposure on circadian phase has yet to be fully tested. Likewise, there is limited data on the acute effects of extraocular light on sleep and body temperature that may influence its clinical utility Thirteen subjects [3F, 10M; mean (SD) age = 22.1 (3.0)y] participated in a protocol that totaled 7 nights in the laboratory consisting of a screening phase measurement night followed 1 week later by two counterbalanced experimental sessions each of 3 consecutive nights (habituation, treatment, and posttreatment phase measurement night) separated by 4 days. Saliva was collected for melatonin measurement every half hour from 1800 to 0300 h on the screening night and both the posttreatment phase measurement nights. On the treatment nights, continuous measures of rectal temperature and polysomnographic sleep were collected and overnight urine for measurement of total nocturnal urinary 6-sulphatoxymelatonin excretion. To test for the phase-delaying effects of extraocular light, subjects received either placebo or extraocular light (11,000 lux) behind the right knee from 0100 to 0400 h. Treatment had no significant effect on the onset of saliva melatonin secretion, phase of nocturnal core body temperature, or urinary 6-sulfatoxymelatonin excretion, but a small increase was observed in wakefulness over the light administration period. In summary, extraocular light was not shown to delay circadian phase but was shown to increase wakefulness. The authors suggest that the present protocol has limited application as a treatment for circadian-related sleep disorders.     

Human plasma DSIP decreases at the initiation of sleep at different circadian times

Nocturnal plasma delta sleep-inducing peptide-like immunoreactivity (DSIP-LI) was determined serially in seven healthy male subjects. Time courses during nocturnal sleep (2300-0800 h), nocturnal sleep deprivation (2300-0500 h), and morning recovery sleep (0500–0800 h) after sleep deprivation were compared. A significant decrease in plasma DSIP-LI was found at the transition from wakefulness to sleep in both evening sleep (2300 h) and morning recovery sleep (0500 h). Time courses were accompanied by physiological changes in sleep electroencephalographic slow-wave activity, and in plasma concentrations of cortisol and human growth hormone. No sleep stage specificity was found. It is concluded that DSIP is influenced by the initiation of sleep.     

Effect of bright light on EEG activities and subjective sleepiness to mental task during nocturnal sleep deprivation

The purpose of this study was to investigate the effect of the exposure to bright light on EEG activity and subjective sleepiness at rest and at the mental task during nocturnal sleep deprivation. Eight male subjects lay awake in semi-supine in a reclining seat from 21:00 to 04:30 under the bright (BL; >2500 lux) or the dim (DL; <150 lux) light conditions. During the sleep deprivation, the mental task (Stroop color-word conflict test: CWT) was performed each 15 min in one hour. EEG, subjective sleepiness, rectal and mean skin temperatures and urinary melatonin concentrations were measured. The subjective sleepiness increased with time of sleep deprivation during both rest and CWT under the DL condition. The exposure to bright light delayed for 2 hours the increase in subjective sleepiness at rest and suppressed the increase in that during CWT. The bright light exposure also delayed the increase in the theta and alpha wave activities in EEG at rest. In contrast, the effect of the bright light exposure on the theta and alpha wave activities disappeared by CWT. Additionally, under the BL condition, the entire theta activity during CWT throughout nocturnal sleep deprivation increased significantly from that in a rest condition. Our results suggest that the exposure to bright light throughout nocturnal sleep deprivation influences the subjective sleepiness during the mental task and the EEG activity, as well as the subjective sleepiness at rest. However, the effect of the bright light exposure on the EEG activity at the mental task diminishes throughout nocturnal sleep deprivation.     

Enuresis: A Three-Year Study of the Value of a Waking Apparatus

Over a three-year period (1959-1962), 122 children with essential nocturnal enuresis, observed at The Hospital for Sick Children, Toronto, used a waking apparatus for an average time of 3½ months. All were wet almost every night before the trial.At follow-up, the average duration of which was nine months, 50% were dry more than 7.5 nights out of 10. Thirty patients (40%) were completely dry.Since essential enuresis is probably due to an isolated maturational lag, progress in so-called “failures” of treatment can be measured in terms of an increasing initial dry interval between initiation of sleep and first voiding.     

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.     

Activity and migratory flights of individual free‐flying songbirds throughout the annual cycle: method and first case study

We describe a method and device (< 1.2 g) for recording, processing and storing data about activity and location of individuals of free‐living songbirds throughout the annual cycle. Activity level was determined every five minutes from five 100 ms samples of accelerometer data with 5 s between the sampling events. Activity levels were stored on an hourly basis throughout the annual cycle, allowing periods of resting/sleep, continuous flight and intermediate activity (foraging, breeding) to be distinguished. Measurements from a light sensor were stored from preprogrammed key stationary periods during the year to provide control information about geographic location. Successful results, including annual actogram, were obtained for a red‐backed shrike Lanius collurio carrying out its annual loop migration between northern Europe and southern Africa. The shrike completed its annual migration by performing > 66 (max. 73) nocturnal migratory flights (29 flights in autumn and > 37, max. 44, in spring) adding up to a total of > 434 (max. 495) flight hours. Migratory flights lasted on average 6.6 h with maximum 15.9 h. These flights were aggregated into eight travel episodes (periods of 4–11 nights when flights took place on the majority of nights). Daytime resting levels were much higher during the winter period compared to breeding and final part of spring migration. Daytime resting showed peaks during days between successive nocturnal flights across Sahara, continental Africa and the Arabian Peninsula, indicating that the bird was mostly sleeping between these long migratory flights. Annual activity and flight data for free‐living songbirds will open up many new research possibilities. Main topics that can be addressed are e.g. migratory flight performance (total flight investment, numbers and characteristics of flights), timing of stationary periods, activity patterns (resting/sleep, activity level) in different phases of the annual cycle and variability in the annual activity patterns between and within individuals.     

Diurnal variations in plasma testosterone concentrations in the male lesser mouse lemur (Microcebus murinus)

In 6 isolated adult male lesser mouse lemurs, concentrations of testosterone in plasma were determinated at 6-h intervals over a 24-h period. Blood samples were collected at monthly intervals and for a period of 12 months under natural photoperiod. In this nocturnal prosimian, there were no apparent diurnal changes in testosterone concentrations during the non-breeding season (autumn). During seasonal sexual activity (January-August), diurnal changes in testosterone concentrations were characterized by a significant rise during the light phase. The daily testosterone peak occurred about 8.5 h after sunrise from February to July, but at the beginning (January) or at the end (August) of the breeding season, the daily testosterone peak was displaced to the morning. A circannual testosterone rhythm occurred with the highest testosterone values in May/June and the lowest values 6 months later. The dramatic fall in testosterone concentrations after the summer solstice may be associated with a change in the peripheral metabolism of testosterone.     

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.     

Melatonin administration increased plasminogen activator activity in ram spermatozoa

The aim of the present study was to investigate the effect of melatonin on plasminogen activator activity (PAA), plasminogen activator inhibition (PAI) and plasmin inhibition (PI) in ram spermatozoa and seminal plasma, in correlation with changes in blood testosterone. Melatonin implants (18 mg) were placed subcutaneously in sixteen Chios rams in autumn and spring. Semen samples for spectrophotometrical assays were collected 36 h before the implantation of melatonin and thereafter once a week, for 17 weeks. Blood samples for testosterone assay (RIA) were collected 8h before implantation (one sample/30 min x 7.5 h) and thereafter every 15 days for 105 days after implantation. For each ram, six parameters of testosterone were estimated: mean value, basal level, number of peaks, peak amplitude, peak duration and mean testosterone concentration during peaks. Melatonin implantation during autumn induced an increase in PAA and t-PAI in spermatozoa; melatonin implantation in spring induced an additional increase in u-PAI and PI; no change in PAA, PAI or PI was found in seminal plasma, during autumn or spring. The melatonin-induced increase of PAA, PAI and PI in spermatozoa was in positive correlation with the increase of testosterone mean value, basal level and number of peaks; the increase of testosterone parameters was greater in autumn compared to spring. Changes of PAA, PAI and PI of spermatozoa, under the influence of melatonin, might indicate changes in the fertilizing ability of spermatozoa, since plasminogen activators and their inhibitors are present on the plasma and the outer acrosomal membrane of spermatozoa and are released during the acrosome reaction.     

The impact of training schedules on the sleep and fatigue of elite athletes

In any sport, successful performance requires a planned approach to training and recovery. While sleep is recognized as an essential component of this approach, the amount and quality of sleep routinely obtained by elite athletes has not been systematically evaluated. Data were collected from 70 nationally ranked athletes from seven different sports. Athletes wore wrist activity monitors and completed self-report sleep/training diaries for 2 weeks during normal training. The athletes also recorded their fatigue level prior to each training session using a 7-point scale. On average, the athletes spent 08:18?±?01:12?h in bed, fell asleep at 23:06?±?01:12?h, woke at 6:48?±?01:30?h and obtained 06:30?±?01:24?h of sleep per night. There was a marked difference in the athletes’ sleep/wake behaviour on training days and rest days. Linear mixed model analyses revealed that on nights prior to training days, time spent in bed was significantly shorter (p?=?0.001), sleep onset and offset times were significantly earlier (p?<?0.001) and the amount of sleep obtained was significantly less (p?=?0.001), than on nights prior to rest days. Moreover, there was a significant effect of sleep duration on pre-training fatigue levels (p?≤?0.01). Specifically, shorter sleep durations were associated with higher levels of pre-training fatigue. Taken together, these findings suggest that the amount of sleep an elite athlete obtains is dictated by their training schedule. In particular, early morning starts reduce sleep duration and increase pre-training fatigue levels. When designing schedules, coaches should be aware of the implications of the timing of training sessions for sleep and fatigue. In cases where early morning starts are unavoidable, countermeasures for minimizing sleep loss – such as strategic napping during the day and correct sleep hygiene practices at night – should be considered.