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Selection of a single dominant follicle is morphologically manifested by diameter deviation between the future dominant follicle (F1) and the future largest subordinate follicle (F2). Conventional deviation is defined as F2≥7 mm when F1 reaches ∼8.5 mm whereas, undersized deviation is if F27 mm when F1 reaches ∼8.5 mm. Greater frequency of undersized deviation has been temporally associated with greater circulating progesterone (P4) and greater FSH but reduced LH in observational studies. Experiment 1 was conducted to directly test if elevating P4 increased the likelihood of undersized deviation and altered circulating concentrations of LH and FSH. Experiment 2 was conducted to test if increasing LH action by treatment with exogenous porcine LH or human chorionic gonadotropin (hCG) in the presence of elevated P4, would stimulate growth of F2 and increase the likelihood of conventional deviation. Ovaries were evaluated by ultrasound and blood samples collected every 12 h after development of a new wave following follicle ablation on D6 (D0 = ovulation). Data were normalized to F1≥7.5 mm and compared using SAS software. In experiment 1 (n = 20), the CL was regressed by prostaglandin F2α treatment and heifers were randomized on D6 into control (no P4 treatment) or P4 treatment (75 mg every 12 h for 5.5 d) beginning when F1 reached ∼3 mm (P4-3 mm group) or ∼6 mm (P4-6 mm group). The P4 treatment significantly increased the frequency of undersized deviation from 0% (controls) to 54%, decreased LH by 44%, and increased FSH by 32%. In experiment 2 (n = 27) heifers were randomized on D6 into control (saline) or treatment with the LH analogs - pLH (1.25 mg porcine LH/12 h) or hCG (160 IU initially and subsequently 96 IU/24 h). Treatment with LH analogs significantly increased P4 (control, 4.6 ± 0.3 ng/mL; pLH, 6.6 ± 0.4 ng/mL; and hCG, 8.9 ± 0.4 ng/mL) and decreased FSH (control, 0.46 ± 0.03 ng/mL; combined-pLH/hCG, 0.34 ± 0.02 ng/mL). However, F1 and F2 diameter and frequency of conventional (37%) and undersized (48%) deviations were similar between the control and combined-pLH/hCG groups. In conclusion, elevated P4 was directly linked to undersized deviation but the P4 effect on decreasing F2 diameter occurred independently of the P4 effects on FSH and LH concentrations.

In order to evaluate GnRH administration for the treatment of infertile men with elevated serum FSH levels we administered GnRH in pulses via portable electronic infusion pumps initially to seven patients with low sperm counts and high FSH values over 12 weeks and later to nine further patients over 24 weeks who also underwent testicular biopsies. Fifty microlitres containing 5 micrograms GnRH were infused subcutaneously for 1 min every 120 min in the short-term study and every 90 min in the long-term study. Although FSH levels could be lowered in both groups of patients, none showed any improvement in sperm count or other seminal parameters. Therefore, pulsatile GnRH treatment cannot be recommended for therapy of severe oligozoospermia with elevated FSH levels.

Immunization against oestrogen resulted in elevated LH concentrations, in the form of a pulsatile release, which rose from 3 to as much as 41 ng/ml approximately every 1.5 h, even in the presence of high plasma progesterone concentrations. Elevated FSH concentrations showed only minor oscillations without consistent synchrony to the LH pulses. Injection of 250 microgram stilboestrol did not abolish the LH pulses but in 2 out of 8 ewes FSH was initially lowered. Injection of 1 mg stilboestrol abolished the LH pulses within 11 h and decreased FSH values in 2 out of 4 ewes. Between 16 and 35 h after injection there was a large increase in LH and FSH concentrations. Thus, in the ewe, the tonic secretion of LH and FSH is controlled by a negative feedback action of oestrogen, and diethylstilboestrol will exert both dose. Infusion of LH was unable to alter the frequency or height of the LH pulses, thereby excluding regulation of the LH pulses by a short feedback mechanism.

Subjects with GD have elevated LH & FSH and achieve greater rise in both after LRF (Silver, Yen 1973). Estrogens exert inhibitory action on FSH & LH release (Yen et al 1972). To ascertain an effect of estrogen on LH and/or FSH to LRF in GD, 8 females 7-20 yrs, were studied; 4 XO, 1 XO/XY, constitutional delay, hypopituitarism, normal female. LRF, 50-100 ugm IV, was followed by 0.1 mgm EE daily 3-7 days, with 1-7 days off EE prior to second LRF test. In 3 young XO GD, 7 days EE decreased basal FSH (mean 17.6 mIU/ml before EE, 6.1 after EE) and the FSH peak to LRF (mean FSH peak 64.1 before EE, 16.1 after); LH was not significantly affected. With 3 days EE, a 7 yr. XO/XY had no change in LH, FSH responses. An older XO had an LH rise to LRF after 3 days EE, with a decreased FSH responsiveness. LH levels with LRF (after EE) were decreased in a normal female and constitutional delay. The younger child with GD lacks ovarian feedback mechanism and may have chronic endogenous secretion of LRF which induces pubertal LH response, as shown in these studies. LH & FSH responses to EE varied with age.