Oxygen and steroid concentrations in preovulatory follicles of lactating dairy cows exposed to acute heat stress

Maternal heat stress reduces oocyte competence for fertilization and post-fertilization development, but the mechanism is unknown. The present experiment investigated two potential mechanisms: (1) reduced oxygen delivery to the preovulatory follicle (due to increased thermoregulatory vascular perfusion of skin and respiratory tract); (2) reduced follicular steroid synthesis. These hypotheses were tested by measuring the fractional concentration of oxygen and concentrations of estradiol-17β and progesterone in follicular fluid of the preovulatory follicle of lactating Holstein cows. Estrous cycles were synchronized using GnRH on Day −9 and PGF2α on Day −2. On Day 0, all cows without a CL and with a large preovulatory follicle were assigned to control or heat stress treatments for 1 d (beginning at 1030 h). Between 4 and 6 h after treatment (1430–1630 h), follicular fluid was aspirated by transvaginal puncture, and fractional oxygen concentration in follicular fluid of the dominant follicle was determined with a fluorometric fiber-optic oxygen sensor. There was no significant effect of heat stress on follicular fluid PO2PO2 or concentrations of estradiol-17β or progesterone among cows that had follicular fluid steroid concentrations considered typical of a preovulatory follicle. Follicular oxygen concentration was 6.9 ± 0.4% for control cows and 7.3 ± 0.3% for heat-stressed cows. Oxygen concentration tended to be inversely correlated to follicular diameter (P = 0.09). In conclusion, it was unlikely that reduced oocyte competence due to acute heat stress was caused by reductions in follicular concentrations of oxygen, estradiol-17β, or progesterone.