Abstract
Heat stress causes a large decline in pregnancy success per insemination during warm times of the year. Improvements in fertility are possible by exploiting knowledge about how heat stress affects the reproductive process. The oocyte can be damaged by heat stress at the earliest stages of folliculogenesis and remains sensitive to heat stress in the peri-ovulatory period. Changes in oocyte quality due to heat stress are the result of altered patterns of folliculogenesis and, possibly, direct effects of elevated body temperature on the oocyte. While adverse effects of elevated temperature on the oocyte have been observed in vitro, local cooling of the ovary and protective effects of follicular fluid may limit these actions in vivo. Heat stress can also compromise fertilization rate. The first seven days of embryonic development are very susceptible to disruption by heat stress. During these seven days, the embryo undergoes a rapid change in sensitivity to heat stress from being very sensitive (2- to 4-cell stage) to largely resistant (by the morulae stage). Direct actions of elevated temperature on the embryo are likely to be an important mechanism for reduction in embryonic survival caused by heat stress. An effective way to avoid effects of heat stress on the oocyte, fertilization, and early embryo is to bypass the effects through embryo transfer because embryos are typically transferred into females after acquisition of thermal resistance. There may be some opportunity to mitigate effects of heat stress by feeding antioxidants or regulating the endocrine environment of the cow but neither approach has been reduced to practice. The best long-term solution to the problem of heat stress may be to increase genetic resistance of cows to heat stress. Thermotolerance genes exist within dairy breeds and additional genes can be introgressed from other breeds by traditional means or gene editing.