ABSTRACT
Human sleep is characterized by the cyclic occurrence of periods of non-rapid eye movement (NREM) sleep and rapid eye movement (REM) sleep and by distinct patterns of the secretion of various hormones. During the first NREM sleep period the major portion of slow-wave sleep (SWS) and, as assessed by electroencephalographic (EEG) spectral analysis, of slow-wave activity (SWA) occur. Near to sleep onset, the growth hormone (GH) surge is found, whereas corticotropin (adrenocorticotropic hormone [ACTH]) and cortisol levels are low. During the second half of the night REM sleep and stage 2 sleep preponderate, ACTH and cortisol increase, whereas GH release is low.1 This pattern points to a reciprocal interaction of the hypothalamopituitary-somatotropic (HPS) and the hypothalamopituitary-adrenocortical (HPA) systems and to the existence of common regulating factors of the sleep EEG and the nocturnal hormone secretion. Indeed, there is a reciprocal interaction of the key hormones of the HPS and HPA systems, GH-releasing hormone (GHRH) and corticotropin-releasing hormone (CRH). Besides GHRH and CRH, various other peptides and steroids participate in sleep regulation.
