Biological effect of bright light.

1. Five minute bright light exposures reduced plasma levels of melatonin in eight normal subjects. 2. No significant change in ACTH levels occurred. 3. These results raise the possibility that short intense light exposures can synchronize circadian rhythms as well as benefit patients with seasonal affective disorder. They also indicate that short pulses of bright light do not affect pituitary ACTH production.

Effect of 64-hour sleep deprivation on the circadian waveform of thyrotropin (TSH): further evidence of sleep-related inhibition of TSH release.

Half-hourly sampling of plasma TSH was done across 3 days in four normal young men. Sleep was denied for 64 h from 0700 h on awakening from accommodation sleep until polygraphic sleep was resumed at 7100 h of the third day (D3) such that 2 consecutive nights of usual 2300-0700 h sleep were missed. This protocol allowed examination of any modulatory effects on the daily patterns in TSH concentrations during sleep deprivation on D1-2 (1100-3500, 3500-5900 h) or during resumption of usual nightly sleep on D3 (5900-8300) compared to that of a previously studied group of normal young men. The circadian nature of the daily TSH waveform was evidenced by its daily repetition within a subject both basally and during D1-2 sleep deprivation and by its synchronization within the basal, deprived, or resumed sleep days. The peaks in each subject's daily TSH patterns on D1-2 were consistently longer, and the daily maxima and cosine acrophases on D1-2 were consistently later than those on D3 when basal sleep was resumed. About half the daily TSH concentration maxima and daily cosinor amplitudes on D1-2 were greater than those of the respective sleep-resumed TSH patterns of D3. Both the group mean TSH patterns and the cosinor 95% confidence ellipses also indicated the daily peak in the TSH waveform to be significantly longer, later, and larger during D1-2 sleep deprivation than during the basal or D3 periods. These results indicate that significant alteration of the daily TSH waveform can occur in response to absence of sleep and are compatible with the existence of an inhibitory effect in early nightly sleep on TSH release. The TSH patterns during the 1700-2300 h intervals of rising TSH levels were congruent in the basal, deprived, and resumed sleep periods. Prompt reversion to the basal TSH pattern also occurred when sleep was resumed on D3. Both of these observations suggest the alteration in TSH waveform during sleep deprivation to have arisen from an inhibitory effect in sleep rather than from a change in period or phase of a generating oscillator.

Pubertal sleep-wake patterns of episodic LH, FSH and testosterone release in twin boys.

On 2 consecutive nights, plasma LH, FSH and testosterone (T) were measured every20 min for 12 h during evening wakefulness and polygraphic sleep in 5 pairs of male monozygotic twins in pubertal stages 1-4, and in a male dizygotic also studied in 3 twins. During sleep, significant enhancement of episodic LH release was seen on 16 of 18 nights on the stage 1-4 twins. During wakefulness, minimal episodic LH release was observed in the stage 1-3 twins, which then gradually increased in the more mature twins, until finally the significant sleep-wake difference in mean LH was lost in the stage 5 male. Testosterone also rose significantly in sleep on 19 of 20 study nights in the stage 1-5 twins. In the early pubertal twins this nocturnal rise in T was small, but in the midpubertal pairs it was profound, as peaks in T occurred which lay in the normal range for adult males. In these less mature twins the majority of the episodic secretion of T also was limited to sleep. In wakefulness, the T levels gradually increased across puberty until, in the stage 5 twin, wakeful peaks in T finally reached the adult male range. In the midpubertal twins, a close temporal relationship was seen between initiation of sleep-enhanced LH release and the subsequent initial rise in T (mean lag time 29.1 min). In the stage 5 twin, this episodic LH-T relationship persisted into wakefulness where the largest increments in T were seen just prior to sleep onset. Evidence of sleep-enhanced FSH release was more equivocal, and was limited mainly to pubertal stage 1 and 3 pairs. Similarities in hormonal patterns were seen within the monozygotic twin pairs and probably contributed to the parallel progress in puberty of the pair. Thus, sleep-wake rhythmicity in release of gonadotropins, particularly LH and thereby of testosterone, was seen to evolve transiently in twin boys across puberty. The existence of such rhythmicity suggests that a fundamental, sleep-entrained CNS mechanism plays an important, if not a dominant, role in sexual maturation in boys.

Human growth hormone release: relation to slow-wave sleep and sleep-walking cycles.

Release of human growth hormone during sleep is significantly related to slow, synchronized stages of sleep and therefore would seem to be controlled by related neural mechanisms. When sleep-waking cycles are reversed by 12 hours, the release of growth hormone with sleep is reversed; thus release does not follow an inherent circadian rhythm independent of sleep.