The aim of this study was to elucidate the mechanism(s) involved in stress-induced subfertility by examining the effect of 4 h transport on surge and pulsatile LH secretion in intact ewes and ovariectomized ewes treated with steroids to induce an artificial follicular phase (model ewes). Transport caused a greater delay in the onset of the LH surge in nine intact ewes than it did in ten ovariectomized ewes (intact: 41.0 ± 0.9 h versus 48.3 ± 0.8 h, P < 0.02; ovariectomized model: 40.8 ± 0.6 h versus 42.6 ± 0.5 h, P < 0.02). Disruption of the hypothalamus–pituitary endocrine balance in intact ewes may have reduced gonadotrophin stimulation of follicular oestradiol production which had an additional effect on the LH surge mechanism. In the ovariectomized model ewes, this effect was masked by the exogenous supply of oestradiol. However, in these model ewes, there was a greater suppression of maximum LH surge concentrations (intact controls: 29 ± 4 ng ml−1 versus intact transported 22 ± 5 ng ml−1, P < 0.02; ovariectomized model controls: 35 ± 7 ng ml−1 versus model transported 15 ± 2 ng ml−1, P < 0.02). Subsequent exposure to progesterone for 12 days resulted in the resumption of a normal LH profile in the next follicular phase, indicating that acute stress leads to a temporary endocrine lesion. In four intact ewes transported in the mid-follicular phase, there was a suppression of LH pulse amplitude (0.9 ± 0.3 versus 0.3 ± 0.02 ng ml−1, P < 0.05) but a statistically significant effect on pulse frequency was not observed (2.0 ± 0.4 versus 1.7 ±0.6 pulses per 2 h). In conclusion, activation of the hypothalamus–pituitary–adrenal axis by transport in the follicular phase of intact ewes interrupts surge secretion of LH, possibly by interference with LH pulsatility and, hence, follicular oestradiol production. This disruption of gonadotrophin secretion will have a major impact on fertility.
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