In dairy cows inseminated during the hot months of the year, there is a decrease in fertility. Different factors contribute to this situation; the most important are a consequence of increased temperature and humidity that result in a decreased expression of overt estrus and a reduction in appetite and dry matter intake. Heat stress reduces the degree of dominance of the selected follicle and this can be seen as reduced steroidogenic capacity of its theca and granulosa cells and a fall in blood estradiol concentrations. Plasma progesterone levels can be increased or decreased depending on whether the heat stress is acute or chronic, and on the metabolic state of the animal. These endocrine changes reduce follicular activity and alter the ovulatory mechanism, leading to a decrease in oocyte and embryo quality. The uterine environment is also modified, reducing the likelihood of embryo implantation. Systems activated by heat stress can influence reproduction at the hypothalamus, pituitary gland or gonads. However, the major impact is thought to be within the brain or at the pituitary gland. Measurement of plasma concentrations of the gonadotrophins provides a good indication of the effects at these higher levels, since the pulsatile secretion of luteinizing hormone (LH) is a reflection of the secretion of gonadotropin-releasing hormone (GnRH) from the hypothalamus. Both the secretion and actions of GnRH are influenced by the feedback actions of gonadal sex steroids and inhibin. Recent studies suggest that the use of gonadotropins to induce follicular development and ovulation can decrease the severity of seasonal postpartum infertility in dairy cows.
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