Establishment and maintenance of pregnancy is difficult in lactating dairy cows exposed to heat stress because of reductions in estrous detection rate and the proportion of inseminated cows that maintain pregnancy. The most common approach to ameliorate heat stress in developed countries has been to alter the cow's environment through provision of shade, fans, sprinklers, and so on. Nonetheless, seasonal variation in reproductive function persists. Increased understanding of bovine reproductive function and its alteration by heat stress has led to additional strategies for reducing deleterious consequences of heat stress on reproduction. These include hormonally induced timed artificial insemination, which can reduce losses in reproductive efficiency caused by poor detection of estrus, and embryo transfer, which can increase pregnancy rate by allowing embryos to bypass the period when they are most sensitive to elevated temperature (i.e., in the first 1 to 2 d after breeding). Other efforts are directed toward developing methods to protect the embryo from harmful actions of elevated temperature. Approaches being studied include manipulation of embryonic synthesis of heat shock proteins and use of antioxidants to reduce free radical damage associated with heat stress. It may also be possible to reduce the magnitude of hyperthermia caused by heat stress. This might be possible physiologically, for example by feeding of agents that affect thermoregulatory systems, or genetically by selecting for specific traits conferring thermal resistance. Finally, the development of bovine somatotropin as a lactational promotant means that it may be possible to extend lactations beyond 305 d and voluntarily discontinue inseminations during periods of heat stress.

In three experiments, we tested the efficacy of timed artificial insemination (AI) and beta-carotene supplementation for improvement of reproduction and milk yield. Experiments 1 and 2 were conducted during hot months, and Experiment 3 was conducted during cooler months. Cows were fed rations supplemented with beta-carotene at 0 or 400 mg/d per cow for > or = 15 d before the first AI. Cows were inseminated at each observed estrus after 70 d (Experiment 1) or at 50 d postpartum (Experiments 2 and 3) or were included in a timed AI program [d 0 (i.e., approximately 40 or 60 d postpartum), 8 micrograms of GnRH agonist; d 7, 25 mg of PGF2 alpha; d 9, 8 micrograms of GnRH agonist; d 10, AI] for first breeding. Pregnancy rate at first AI was similar among groups, but the percentage of cows that were pregnant by 90 d postpartum was greater for cows in the timed AI group in Experiments 1 (16.6% vs. 9.8%) and 2 (34.3% vs. 14.3%) but not in Experiment 3 (24.1% vs. 28.7%). Overall, beta-carotene had no effect on reproductive function. For cows fed supplemental beta-carotene for > or = 90 d, however, pregnancy rate at 120 d postpartum was increased in Experiment 1 (35.4% vs. 21.1%). In all experiments, beta-carotene increased cumulative milk yield on the last test day by 6 to 11%. In conclusion, timed AI can improve pregnancy rates during periods of heat stress. Supplemental beta-carotene may increase pregnancy rates for cows in the summer and can increase milk yield.

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Experiments were conducted with in vitro-produced bovine embryos to determine whether 1) increased culture temperatures (i.e., heat shock) adversely affected embryonic development, 2) embryos become more resistant to heat shock as they advance in development, and 3) selective antioxidant molecules alleviate heat shock effects on embryonic development. Development of 2-cell embryos to > or = 16-cell stage on d 5 after in vitro fertilization was not affected by a heat shock of 40 degrees C for 3 h, but 41 or 42 degrees C for 3 h decreased (P = .004) development. In a separate experiment, development of 2-cell embryos was decreased (P = .01) by exposure to 41 degrees C for 3 h but not for 1 h. In contrast, development of morulae to blastocysts was not affected by heat shock of 41 degrees C for 1 or 3 h. Medium supplementation with 50 nM glutathione or 50 mM taurine before heat shock did not reduce the effects of heat shock (41 degrees C for 3 h) on 2-cell embryos. Likewise, addition of glutathione ester, a more membrane-permeable analog of glutathione, did not protect 2-cell embryos from heat shock. In conclusion, early bovine embryos are susceptible to disruption in development caused by heat shock. As embryos progress in development, they acquire resistance to heat shock. Glutathione, taurine, and glutathione ester were not effective in alleviating the effects of heat shock on development of 2-cell embryos. Consequently, molecules have yet to be identified that can protect early-stage bovine embryos from the adverse effects of heat shock.

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