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Postpartum acyclicity in suckled beef cows: a review
Authors:Yavas Y  Walton J S
Affiliation:Department of Animal and Poultry Science University of Guelph, Ontario, Canada.
Abstract:Prolonged postpartum acyclicity in suckled beef cows is a source of economic loss to beef cattle producers. Duration of postpartum acyclicity is influenced by suckling status, nutritional status, calving season, age, and several other factors. Although uterine involution begins and ovarian follicular waves resume soon after parturition, dominant follicles of these waves fail to ovulate, due to a failure to undergo terminal maturation. As a result, postpartum anovulatory dominant follicles are smaller than the ovulatory follicles in cyclic cows. Failure of postpartum dominant follicles to undergo terminal maturation is due to absence of appropriate LH pulses, a prerequisite for follicular terminal maturation prior to ovulation. Absence of LH pulses early post partum is primarily due to depletion of anterior pituitary LH stores, although GnRH pulses are also absent during this period due to suckling. Following replenishment of LH stores between Days 15 and 30 post partum, absence of LH pulses is due to continued sensitivity of the hypothalamic GnRH pulse-generator to the negative feedback effect of ovarian estradiol-17beta, which results in absence of GnRH pulses. This negative feedback effect of estradiol-17beta is modulated by suckling which stimulates release of endogenous opioid peptides from the hypothalamus. As the postpartum interval increases, sensitivity of the GnRH pulse-generator to the negative feedback effect of ovarian estradiol-17beta decreases. This is followed by an increasing frequency of GnRH discharges and LH pulses, terminal follicular maturation, ovulation, and continued cyclicity. The first ovulation post partum is usually followed by a short cycle due to premature luteolysis because of premature release of PGF2alpha from the uterine endometrium, which is possibly intensified by the suckling-induced oxytocin release from the posterior pituitary. A model for the postpartum ovulatory acyclicity and for the resumption of cyclicity is presented.
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