Heat stress affects the fertility and reproductive livestock performance by compromising the physiology reproductive tract, through hormonal imbalance, decreased oocyte quality and poor semen quality, and decreased embryo development and survival. Heat stress decreases the secretion of luteinizing hormone and estradiol resulting in reduced length and intensity of estrus expression, increased incidence of anoestrus and silent heat in farm animals. Oocytes exposed to thermal stress lose its competence for fertilization and development into the blastocyst stage, which results in decreased fertility because of the production of poor quality oocytes and embryos. Furthermore, low progesterone secretion limits the endometrial functions, and subsequently embryo development. In addition, the increased secretion of endometrial prostaglandin F2 alpha during heat stress threatens the maintenance of pregnancy. In general, the percentage of conception rate was found to be reduced by 4.6% for each unit increase in temperature humidity index (THI) above 70, and heat stress during pregnancy further slows down the growth of the foetus and results in lower birth weight. In tropical and subtropical regions, during hot days, the testicular temperature may increase and impair both the spermatogenic cycle and semen quality, which culminates in decreased bull fertility. The effects of heat stress on livestock can be minimized via adapting suitable scientific strategies comprising physical modifications of the environment, nutritional management and genetic development of breeds that are less sensitive to heat stress. In addition, the summer infertility may be countered through advanced reproductive technologies involving hormonal treatments, timed artificial insemination and embryo transfer, which may enhance the chances for establishing pregnancy in farm animals.
Part of the book: Theriogenology