This study was designed to test the hypothesis that treatment with sup
erovulatory drugs suppresses endogenous pulsatile LH secretion. Heifer
s (n=5/group) were superovulated with eCG (2500 IU) or FSH (equivalent
to 400 mg NIH-FSH-P1), starting on Day 10 of the estrous cycle, and w
ere injected with prostaglandin F-2 alpha on Day 12 to induce luteolys
is. Control cows were injected only with prostaglandin. Frequent blood
samples were taken during luteolysis (6 to 14 h after PG administrati
on) for assay of plasma LH, estradiol, progesterone, testosterone and
androstenedione. The LH pulse frequency in eCG-treated cows was signif
icantly lower than that in control cows (2.4 +/- 0.4 & 6.4 +/- 0.4 pul
ses/8 h, respectively; P<0.05), and plasma progesterone (3.4 +/- 0.4 v
s 1.8 +/- 0.1 ng/ml, for treated and control heifers, respectively; P<
0.05) and estradiol concentrations (25.9 +/- 4.3 & 4.3 +/- 0.4 pg/ml,
for treated and control heifers, respectively; P<0.05) were higher com
pared with those of the controls. No LH pulses were detected in FSH-tr
eated cows, and mean LH concentrations were significantly lower than t
hose in the controls (0.3 +/- 0.1 and 0.8 +/- 0.1, respectively; P<0.0
5). This suppression of LH was associated with an increase in estradio
l (9.5 +/- 1.4 pg/ml; P<0.05 compared with controls) but not in proges
terone concentrations (2.1 +/- 0.2 ng/ml; P>0.05 compared to controls)
. Both superovulatory protocols increased the ovulation rate (21.6 +/-
3.9 and 23.0 +/- 4.2, for eCG and FSH groups, respectively; P>0.05).
These data demonstrate that super-ovulatory treatments decrease LH pul
se frequency during the follicular phase of the treatment cycle. This
could be explained by increased steroid secretion in the eCG-treated h
eifers but not in FSH-treated animals.