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The temporal pattern of growth hormone release at sleep onset was studied in six adult human subjects by frequent blood sampling combined with polygraphic sleep recording. HGH release was associated with sleep onset but not with the transition from waking to sleep. Delta activity consistently preceded the first elevation of plasma HGH.

Relaxin was secreted episodically in all 6 human subjects studied. A 24-hr rhythm was detected in the pooled data, with maximum secretion in the early-midmorning hours and a nadir in the early evening.

A group of 7 healthy male subjects was studied in regard to sleep stages and 24 h plasma cortisol and growth hormone patterns during the 4 seasons of the year in an Arctic environment (Tromsø, Norway). No difference in total sleep or sleep stage per cents was found for any of the yearly seasons. A small but statistical significant increase in mean plasma cortisol concentration and amount secreted for 24 h was found for the autumn-winter seasons, as compared with the spring and summer. However, no difference in the circadian curve of cortisol hormonal pattern was found. All subjects secreted growth hormone shortly after sleep onset at night and no difference was found as a function of season of the year.

Human prolactin was measured in plasma by radioimmunoassay at 20 minute intervals for a 24-hour period in each of six normal adults, whose sleep-wake cycles were monitored polygraphically. A marked diurnal variation in plasma concentrations was demonstrated, with highest values during sleep; periods of episodic release occurred throughout the 24 hours.

Serial plasma growth hormone (GH) concentrations were measured every 20 min for 24 hr before and after the administration of clomiphene citrate (100 mg/day for 7 days) to four healthy young adult male subjects. The number of GH secretory episodes and the magnitude of the peak plasma concentrations during both wakefulness and sleep were decreased after the clomiphene treatment periods.

Further evidence that there is a relationship between prolactin rise and sleep is offered by this study that delayed sleep onset and inverted the normal sleep-waking cycle in 4 normal patients (3 women and 1 man). The inversion schedule lasted 3 weeks, and at its conclusion a final 12-hour laboratory study was carried out measuring the plasma levels of human prolactin and growth hormone by radioimmunoassay. In the first female subject, mean prolactin levels (ng/ml) were, for baseline and after shift, 7 and 8.3; for case 2 (female) the values were 7.3 and 5.9; for case 3 (male) the levels were 6.1 and 6.1; and for the last case, the levels were 4.7 and 4.3, respectively. Values for growth hormone were (ng/ml) 1.5 and 1.5 for Case 1 for baseline and after shift, respectively; 1.1 and 2.5 for Case 2, respectively; 1.8 and 1.1 for Case 3, respectively; and 7.3 and 5.2 for Case 4, respectively. Prolactin release shifted immediately and completely with shifts of sleep onset of 3, 6, and 12 hours. Thus, it is concluded that the nocturnal rise is dependent on the occurrence of sleep, not on the inherent rhythm related to time of day.

Human growth hormone (HGH) responses to insulin-induced hypoglycemia were measured in ten postmenopausal women suffering from primary unipolar depressive illness, and in ten age-matched normal postmenopausal women. The mean maximal HGH response in the depressed patients was 4.6 plus or minus 4.4 ng/ml, and in the normals 13.3 plus or minus 9.8 ng/ml (P less than .05). All of the normal subjects had clinically adequate HGH responses, in contrast to only four of the depressed patients (P less than .01). The blood glucose responses were virtually the same in the two groups. Since brain catecholamines play a major role in mediating HGH responses to hypoglycemia, the findings are consistent with the hypothesis of diminished functional catecholaminergic activity in the depressed patients.