How does gonadotropin release change from youth to adulthood

How does gonadotropin release change from youth to adulthood, and is the LH adulthood pattern solely responsible for gonadal steroid release?

a. Regarding changes to maturity: Sexual maturity is geared to enable men and women to achieve daily sperm and monthly egg production, respectively. There is a pulsatile release of both luteinizing hormone (LH) and follicle-stimulating hormone (FSH) before puberty and increased pulses occur with sleep. Gonadotropin secretion during the day is without circadian rhythm, differing from testosterone, which has a significant circadian rhythm. The gender-similar gonadotropin patterns diverge with puberty, with the menstrual cycle phase exerting unique influences on LH pulses. Indeed, one of the hallmarks of puberty is increased nocturnal pulse amplitudes of LH and FSH. Each LH pulse is in direct response to a hypothalamic gonadotropin-releasing hormone (GnRH) surge. However, GnRH pulses are not directly related to pituitary FSH secretion. With the advent of sexual maturity, the brisk LH and FSH pulses of puberty give way to lower amplitude, 90-minute interval LH surges without significant diurnal variation. Essentially, the male will continue his 90-minute interval LH pulses with little FSH pulsatility, whereas the female will show marked increases of LH pulse frequency during the follicular phase, with little change to the amplitude in either the follicular or luteal phases. There is a nocturnal LH pulse frequency decrease in the early follicular phase but not in the luteal phase. This slowing is sleep–wake related and is not circadian (i.e., seen in day-time sleep, but not seen in night-time wakefulness). Finally, FSH and LH secretion are increased in men and women as they age, with pulse frequency being increased, whereas amplitude is decreased. Additionally, in men age ≥ 30 years, there is a progressive decline in total testosterone associated with an increase in sex hormone binding globulin, resulting in an even greater decline in serum free testosterone levels; for this reason, free or bioavailable testosterone measurements may be warranted when evaluating older men for hypogonadism. The serum gonadotropin rise and pulse frequency increase are noted in menstruating women age > 40 years. One study showed a causal relationship between gonadotropin elevation, vasomotor symptoms (VMSs) and decreases in objective and subjective sleep quality. The North American Menopause Society published a 2017 position statement regarding the use of menopausal hormone replacement therapy (HRT). There, it is noted that the benefit–risk ratios for HRT are most favorable for women age < 60 years or who are within 10 years of the onset of menopause, and who have no contraindications for HRT treatment of bothersome VMSs and for those at elevated risk for bone loss or fracture.

b. Regarding gonad steroid release: FSH stimulates recruitment and growth of immature ovarian follicles and preservation of growing follicles in females. Once a follicle is in the 8- to 10-mm range, its estradiol secretion markedly increases. Mean monthly estrogen is essentially constant in eumenorrheic females, yet a diurnal free estradiol rhythm exists and consists of two major components: (1) an asymmetrically peaked diurnal cycle; (2) ultradian (shorter than a day) harmonics in the range of 6 to 12 hours. The diurnal and ultradian rhythms are remarkably consistent throughout the menstrual cycle in terms of 24-hour mean level, peak width, and amplitude. In contrast, there is less complicated diurnal variation in males. The early-morning rise in testosterone that started at sleep onset increases to maximum levels during the last half of sleep (REM predominant) and is not associated with corresponding LH surges. The characteristic male night-time LH surges occur later on, during the last half of sleep. Recently, a testosterone surge was observed during adult day-time recovery sleep, and a testosterone decrease followed as the patient remained awake after this day-time recovery sleep. All this suggests that sleep itself, independent of LH bursts, contributes to testosterone release. Therefore, the 24-hour testosterone profile and its response to sleep deprivation and daytime recovery sleep are more like the prolactin profile.

c. Tying this together by using an example: When a sleep-deprived male resident in internal medicine finally gets some sleep, his testosterone will surge during recovery sleep; remember that during the normal day, and in one who has not slept, testosterone levels are on a decline. So, if low testosterone is found in an individual, it may be from primary hypogonadism, but it may also be sleep deprivation, OSA, or even shift work. For the female shift worker, they will have the typical fragmented and shorter sleep, but the frequently associated menstrual irregularities could be from the altered sleep patterns. But in both genders with normal sleep–wake cycles there is no significant circadian pacemaker for the gonadotropins’ diurnal change. It is fair to tell patients to get their testosterone levels drawn first thing in the morning in a rested state, on the basis of the observations that sleep increases testosterone, wakefulness decreases it, and the circadian influence may be less potent than sleep–wake homeostasis.


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