No abstract

In a counter-balanced design, the effects of daytime and/or nighttime exposure to heat and/or traffic noise on night sleep were studied in eight healthy young men. During the day, the subjects were exposed to baseline condition (ambient temperature = 20 degrees C; no noise) or to both heat (35 degrees C) and noise. The duration of the daytime exposure was 8 h ending 5 h before sleep onset. The following nights, the subjects slept either in undisturbed (20 degrees C; no noise) or in noise, heat, or noise plus heat-disturbed environments. During the day, the various types of traffic noise were distributed at a rate of 48/h with peak intensities ranging between 79 and 86 dB(A). The background noise level was at 45 dB(A). At night, the peak intensities were reduced by 15 dB(A), the rate was diminished to 9/h, and the background noise was at 30 dB(A). Electrophysiological measures of sleep and esophageal and mean skin temperatures were continuously recorded. The results showed that both objective and subjective measures of sleep were more disturbed by heat than by noise. The thermal load had a larger impact on sleep quality than on sleep architecture. In the nocturnal hot condition, total sleep time decreased while duration of wakefulness, number of sleep stage changes, stage 1 episodes, number of awakenings, and transitions toward waking increased. An increase in the frequency of transient activation phases was also found in slow-wave sleep and in stage 2. In the nocturnal noise condition, only total number of sleep stage changes, changes to waking, and number of stage 1 episodes increased.(ABSTRACT TRUNCATED AT 250 WORDS)

The principal nocturnal GH peak normally coincides with the first episode of slow wave sleep (SWS). Obstructive sleep apnea (OSA) patients have low nocturnal GH levels which may be explained by their poor quality fragmented sleep but other factors are possibly involved. Obesity is frequently associated with OSA, and obese patients also manifest reduced GH secretion. The mechanisms reducing GH levels in obese subjects are not understood, but hyperinsulinaemia is a suggested factor. In this study nocturnal plasma and secretory GH profiles of OSA patients were examined in relation to the quality and quantity of sleep, together with plasma glucose and insulin levels. Eight OSA patients, (BMI 32.7 +/- 2.3 kg/m2), underwent 2 night studies. For one night no treatment was given and for the other continuous positive airway pressure (CPAP) treatment was administered for the first time. Blood was collected continuously throughout each night and plasma GH, insulin and glucose profiles established in 10 min interval samples. From the plasma data a deconvolution model was used to calculate GH secretion rates. Sleep was recorded during the studies. For the non-treatment night GH levels were low and increased significantly with treatment, p = 0.008 for plasma levels and p = 0.02 for secretion rates. Treatment significantly decreased the cumulative apnea duration and increased the quantity of SWS and Rapid Eye Movement (REM) sleep (p = 0.008), but the mean insulin and glucose profiles did not differ between the two nights. Individual GH plasma and secretion rates, on treatment, showed a tendency to correlate with the amount of SWS (p = 0.09).(ABSTRACT TRUNCATED AT 250 WORDS)

SUMMARYThe thyrotropin (TSH) nycthemeral pattern is known to be strongly influenced by sleep, but previous studies have failed to demonstrate any link between sleep structure and TSH variations. Using 10-min blood sampling, nocturnal TSH profiles were analysed in 24 young healthy subjects during normal sleep. Six of the subjects then underwent a partial sleep deprivation experiment, sleep was permitted from 03.00 hours to 07.00 hours. Descending slopes of TSH values were observed for the first 20 minutes of SWS episodes, whereas no significant trend was found for other sleep stages. During the period of sleep deprivation, nocturnal TSH levels increased and then declined immediately after sleep onset; however, the association between SWS and descending TSH slopes persisted. This temporal concordance suggests that some particular mechanisms associated with SWS may modulate TSH release, or conversely that increasing TSH levels prevent the occurrence of SWS.

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)