The impact of sleep on gonadotropin secretion

Abstract

Comparable to the period of pubertal transition, sleep also exerts profound effects on episodic gonadotropin secretion in adult women. During the early follicular phase of the menstrual cycle, a sleep-induced slowing of luteinizing hormone (LH) secretion occurs concurrently with a rise in LH pulse amplitude. A selective increase in opioidergic, but not in dopaminergic or serotoninergic activity may account for this decline in LH pulsatility. In addition, sleep-reversal studies have confirmed that the presence of sleep is essential for the expression of this neuroendocrine function. Since pituitary gonadotropin responsiveness to gonadotropin-releasing hormone (GnRH) is virtually unchanged during sleep, the reasons for the enhanced LH pulse amplitude remain unresolved. This sleep-associated increase in opioidergic activity may be restricted to a hypothalamic site, since opiate blockade does not modify the gonadotropin response to GnRH stimulation. In addition, circadian variability is shown in terms of gonadotropin secretion in regularly cycling women; this may again represent sleep-associated effects on gonadotropin release. Although the physiological importance of sleep-associated neuroendocrine phenomena remains basically unexplained, the observed changes in LH secretory profiles during sleep in adult women suggest close functional links between the endocrine secretion and the rest-activity cycle of the brain.