The significance of sleep onset and slow wave sleep for nocturnal release of growth hormone (GH) and cortisol.

The present experiments were designed to compare the influences of delayed sleep onset and temporary slow wave sleep (SWS) deprivation on nocturnal GH and cortisol release in humans. Polysomnographic recordings and blood samples were obtained from 10 male subjects each participating on three experimental nights. On all nights the subjects went to bed at 2300 h and were wakened at 0700 h. On the baseline night, the lights were turned off at 2300 h, enabling the subject to fall asleep. To delay sleep onset, on the second night, the subjects were kept awake until 0200 h. On the third night, the subjects were deprived of SWS between 2300 h and 0200 h. SWS deprivation was accomplished by sounding a tone as soon as it appeared the subject was going into stage 3 sleep. The order of experimental conditions was randomized. On the baseline nights, the occurrence of SWS was closely associated with the occurrence of GH secretory bursts, and plasma cortisol concentrations were low at that time. Delaying sleep onset after 0200 h substantially delayed the GH secretory bursts, which again coincided with the initial periods of SWS. Deprivation of SWS between 2300 h and 0200 h did not significantly reduce the time spent in SWS, because it recovered after the deprivation was discontinued. On these nights, the GH secretory peaks were not significantly changed in amplitude. However, they were dissociated from SWS, because they occurred mostly subsequent to sleep onset rather than during the main epochs of SWS occurring after 0200 h. Nocturnal cortisol release was distinctly delayed with delayed sleep onset, whereas temporary SWS suppression had no significant effect. Thus, the timing of both nocturnal GH and cortisol secretion seems more dependent on sleep onset than on SWS.

RCT Entities:   Population Interventions Outcomes