Thus, small concentration of progesterone is required, after estrogen priming, and is an absolute prerequisite for the appearance of a FSH surge, in that they failed to elicit a FSH surge in with estrogen alone.
It seems logical that the preovulatory follicle is able to signal the pituitary that it is "ready" for the midcycle surge, after achieving the necessary LH receptor density and activity enabling" autonomous" progesterone production. .
Other ovarian steroids may be active in mid cycle dynamics. Small and medium sized antral follicles that undergo atresia during the follicular phase acquire LH receptors that are active in production of androstenedione, which fails to become aromatized to estrogen and partially undergoes metabolism to testosterone. Multiple small atretic follicles may contribute to high local androgen concentrations, which locally may inhibit follicular development and systemically may inhibit pituitary responsiveness to GnRH. Hyperandrogenism inhibits ovulation at both the hypothalamic and the pituitary levels. An ovarian derived nonsteroidal factor that inhibits LH secretion has been proposed to be a key factor in the regulation and timing of midcycle LH. This factor, termed gonadotrophin surge attenuating (inhibiting) factor has been characterized partially. This factor acts at the pituitary level to attenuate the LH response to GnRH pulses-endogenous or exogenous. It is a protein molecule of uncertain molecular weight in the range of 10 to 30 kD, or possibly 70 to 100 kD, and is distinct from inhibin. This factor attenuates both the GnRh-induced initial release of LH and the self-priming effect of additional exogenous GnRH administration on the pituitary. .
The duration of normal midcycle LH surge is in the range of 50 hours (48 to 54 hours). Its onset occurs abruptly and can be characterized by three phases: A rapid ascending phase of some 14 hours, a peak plateau phase of another 14 hours, and a longer descending phase of 20 hours.