The relationship between the temporal organization of cortisol secretion and sleep structure is controversial. To determine whether the cortisol profile is modified by 4 hours of sleep deprivation, which shifts slow-wave sleep (SWS) episodes, 12 normal men were studied during a reference night, a sleep deprivation night and a recovery night. Plasma cortisol was measured in 10-minute blood samples. Analysis of the nocturnal cortisol profiles and the concomitant patterns of sleep stage distribution indicates that the cortisol profile is not influenced by sleep deprivation. Neither the starting time of the cortisol increase nor the mean number and amplitude of pulses was significantly different between the three nights. SWS episodes were significantly associated with declining plasma cortisol levels (p less than 0.01). This was especially revealed after sleep deprivation, as SWS episodes were particularly present during the second half of the night, a period of enhanced cortisol secretion. In 73% of cases, rapid eye movement sleep phases started when cortisol was reflecting diminished adrenocortical activity. Cortisol increases were not concomitant with a specific sleep stage but generally accompanied prolonged waking periods. These findings tend to imply that cortisol-releasing mechanisms may be involved in the regulation of sleep.

This study examines the relationships between vascular changes and endocrine responses to prolonged exercise in the heat, associated with dehydration and rehydration by fluids of different osmolarity. Five subjects were exposed, in a 34 degrees C environment for 4 h of intermittent exercise on a cycle ergometer at 85 +/- 12 Watts (SD). Fluid regulatory hormones and cortisol were analysed in 3 experimental sessions: one without any fluid supplement (NO FLUID), and two with progressive rehydration, either by spring water (WATER) or isotonic solution (ISO), given after 70 min of exercise. Results were expressed in terms of differences between the mean values observed at the end of the exercise and the first hour values taken as references. Dehydration (NO FLUID) elicited a 4.0 +/- 0.8% (SE) decrease in plasma volume (PV) and an increase in osmolarity (8.4 +/- 3.1 mosmol X l-1). Concomitantly, plasma aldosterone (PA), renin activity (PRA), arginin vasopressin (AVP) and cortisol (PC) levels increased greatly in response to exercise in the heat (PA: 37.2 +/- 10.8 ng. 100 ml-1; PRA: 13.4 +/- 2.5 ng X ml-1 X h-1; AVP: 3.8 +/- 1.3 pg X ml-1; PC: 12.2 +/- 2.7 micrograms X 100 ml-1). Rehydration with water led to decreased osmolarity (-8.2 +/- 2.1 mosmol X l-1) with no significant changes in PV. With ISO, PV increased by 6.0 +/- 1.3% and the decrease in osmolarity was-5.8 +/- 1.8 mosmol X l-1. With both modes of rehydration, the increases in PRA, AVP and cortisol were blunted; only ISO prevented the rise in PA.(ABSTRACT TRUNCATED AT 250 WORDS)

Six young men were exposed to a thermoneutral environment of air temperature (Ta) 20 degrees C for 5 days and nights followed by an acclimation period of 5 days and nights at Ta 35 degrees C and 2 recovery days and nights at Ta 20 degrees C. Electrophysiological measures of sleep, esophageal temperature, and mean skin temperature were continuously monitored. The total nocturnal body weight loss was measured by a sensitive platform scale. Compared with the 5 nights of the baseline period at 20 degrees C, sleep patterns showed disturbances at 35 degrees C. Total sleep time was significantly reduced, while the amount of wakefulness increased. The subjects exhibited fragmented sleep patterns. The mean duration of REM episodes was shorter at 35 degrees C than at 20 degrees C of Ta, while the REM cycle length shortened. In the acclimation period, there was no change in sleep pattern from night to night, despite adaptative adjustments of the thermoregulatory response. The protective mechanisms of deep body temperature occurring with heat adaptation did not interact with sleep processes. Upon return to baseline condition, a recovery effect was observed on a number of sleep parameters which were not significantly affected by the preceding exposure to prolonged heat. This would suggest that during exposure to dry heat, the demand for sleep could overcome that of other regulatory functions that are temperature-dependent. Therefore, a complete analysis of the effect of heat on sleep parameters can be assessed only if heat exposure is compared with both baseline and recovery periods.

No abstract

The changes in the central control of sweating were investigated in five sleeping subjects under neutral and warm conditions [operative temperature (To) = 30, 33, and 34 degrees C; dew-point temperature = 10 degrees C]. Esophageal (Tes) and mean skin (Tsk) temperatures, chest sweat rate (msw,1), and concomitant electroencephalographic data were recorded. Throughout the night, msw,1 was measured under a local thermal clamp of 38 degrees C. Results showed that the thermal environment exerted a strong influence on both the levels and the time patterns of body temperatures. Moreover, local sweating rate correlated positively with Tes, and this relationship varied according to sleep stages. For a given Tes level, there was a sleep stage-related gradation in msw,1 that was higher in slow-wave sleep (SWS) than in stage 1-2 and the lowest in rapid-eye-movement (REM) sleep. This is explained by a change in the excitability or the sensitivity of the thermoregulatory system. The msw,1 differences between stage 1-2 and SWS are accounted for by a decrease in the Tes threshold (Tset) for sweating while the slope of the msw,1-Tes relation remains unchanged. The lower msw,1 in REM sleep is explained by a lesser slope for the msw,1-Tes relation without any Tset change from stage 1-2.