Evaluation of the influence of prenatal transportation stress on GnRH-stimulated luteinizing hormone and testosterone secretion in sexually mature Brahman bulls1,2

Abstract

This study examined the relationship of prenatal transportation stress (PNS) with exogenous GnRH-induced LH and testosterone secretion in sexually mature Brahman bulls. Brahman cows (n = 96; 48 were stressed by transportation at 5 stages of gestation and 48 were controls) produced a calf crop of 85 calves. All bulls (n = 46) from this calf crop were electroejaculated every 2 wk beginning at a scrotal circumference of 24 cm until sexual maturity (SM; i.e., 500 million sperm/ejaculate). The initial 11 control and 12 PNS bulls to reach SM were selected for the experiment. Within 7-21 d after reaching SM, bulls were fitted with jugular cannulas, from which blood samples were collected at 15-min intervals for 6 h prior to exogenous GnRH administration (10 ng/kg BW; i.v.) and for 6 h after GnRH. Serum concentrations of LH, testosterone, and cortisol were determined by RIA. Age and body weight did not differ ( > 0.1) between PNS and control bulls at the time of the experiment. All bulls responded similarly to exogenous GnRH, indicating no influence of PNS on LH or testosterone response to GnRH. More ( < 0.01) PNS (9 of 11) than control (3 of 12) bulls exhibited an endogenous pre-GnRH LH pulse, and more ( = 0.02) PNS (9 of 11) than control bulls (4 of 12) exhibited a pre-GnRH testosterone response to LH. The average concentration of testosterone during the 60 min (time -60, -45, -30, -15, and 0 min relative to GnRH) immediately preceding GnRH, tended to be greater ( = 0.07) in PNS (1.46 +/- 0.30 ng/mL) than control (0.68 +/- 0.28 ng/mL) bulls. During that time span serum cortisol was lower ( < 0.01) in PNS (4.00 +/- 0.91 ng/mL) than control (7.8 +/- 0.87 ng/mL) bulls. A treatment by time interaction ( = 0.03) affected testosterone concentrations from time -240 to 360 min relative to GnRH. Results from this study indicate that PNS did not affect pituitary responsiveness to GnRH or testicular responsiveness to GnRH-induced LH secretion.