Age-Dependent Suppression of Nocturnal Growth Hormone Levels during Sleep Deprivation

Abstract

Although the major daily peak in plasma growth hormone (GH) level normally occurs during the early part of nocturnal sleep, it is known that in about one quarter of young healthy men, peaks in circulating human GH occur before sleep onset. Possible factors associated with these nocturnal peaks were investigated in the absence of sleep, including subjectively defined sleepiness, electroencephalographically defined drowsiness and short lapses into sleep, measures of cortisol and temperature. Healthy men between the ages of 20 and 34 years were studied in a between-subjects design, 16 assigned to a sleep deprivation group, and 16 age matched and assigned to a group permitted to sleep. The average GH peak level in the sleeping subjects was 19.9 µg/1 ( ± 8.4 SD). In the sleep-deprivation group there was a wide range of nocturnal GH patterns, from no detectable rise to normal nocturnal levels (average peak of 10.5 ± 10.0 µg/1). Within the narrow age range sampled, age, body mass index, temperature and cortisol failed to predict nocturnal GH peak in the sleeping group, but regression analysis found age to be a significant negative predictor of nocturnal GH peak level in sleep-deprived subjects. All sleep-deprived subjects who had peak GH levels over 7 µg/1 were 24 years of age or less. Subjective sleepiness and electroencephalographically defined drowsiness failed to predict either the peak level of GH during sleep deprivation or the cumulative amount measured across the night. These results suggest that the well-known suppressive effect of sleep deprivation on GH secretion is an age-dependent phenomenon which evolves during early adulthood.

Effect of sleep loss on C-Reactive protein, an inflammatory marker of cardiovascular risk

“…Nonlinear mixedmodels regression found significant increases in daily cortisol levels during the 88-h vigil of Experiment 1 (t ϭ 2.82, p ϭ 0.018). Furthermore, the circadian nadir in cortisol concentrations has been shown to increase during sleep deprivation (42,43), and evening cortisol levels were also elevated in a PSD study (34).…”

Reciprocal interactions between the GH axis and sleep

“…This increase is probably because of a reduction in somatostatinergic activity [10], which may be occurring concurrent with an increase in ghrelin levels. Pre-sleep GH pulses are frequently observed in older adults [11] and in younger subjects in a state of sleep debt [9], and it has been argued that they simultaneously suppress GH secretion and slow-wave activity in early sleep via inhibition of central GHRH release [9]. The existence of a robust relationship between slowwave activity and increased GH release raised the possibility that pharmacological agents that increase SWS may also stimulate GH release and represent a novel class of orally active GH ''secretagogues'' distinct from that represented by the compounds that bind to the GHS receptor (e.g., ghrelin and the synthetic compound MK-0677).…”

Central effects of the somatotropic system

“…In premenopausal women the GH peak at sleep onset also occurs but does not normally constitute the main part of the 24-h secretion. In shifts of sleep onset the GH peak still normally occurs at sleep onset (136), but in about 25% of young men a GH peak occurs before sleep onset (137). The somatotropic axis interacts with sleep on many levels: there is a close relationship between the occurrence of slow wave sleep (SWS) of the sleep phases III and IV, and pulsatile GH secretion.…”