In dairy cattle, the final weeks before parturition are physiologically challenging and an important determinant of subsequent production performance. External stressors should be carefully managed during this period to avoid adding strain on the animals. Late-gestation heat stress impairs productivity in the dam and exerts transgenerational effects on progeny. Physiological responses are complex and detriments to performance are multifaceted. Late-gestation heat stress blunts mammary gland involution in the first half of the dry period and impairs cell proliferation as calving approaches. Moreover, cows that were exposed to prepartum heat-stress exhibit reduced adipose tissue mobilization and a lower degree of insulin resistance during early lactation. Prepartum heat exposure also depresses immune function and evidence links this decrease to altered prolactin signaling under heat stress. Placental functions are also impaired as reflected in a higher cotyledon mass but lower maternal circulating estrone sulfate concentrations, potentially resulting in lower nutrient supply and reduced calf birth weight. In addition, calves born to heat-stressed dams show impaired immune function and therefore higher disease susceptibly. Novel evidence reported that intrauterine heat stress alters the methylation profile of liver and mammary DNA, which may also contribute to the poorer performance during adulthood of calves exposed to heat stress in utero. Understanding the contribution of all altered biological systems during late-gestation heat stress can be used as a basis for improving cow management during the dry period. This article provides a review of the impacts of late-gestation heat stress and of the emerging understanding of the biological mechanisms that underlie the observed impairments of performance.

中文翻译：

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奶牛妊娠后期热应激：对母牛和子代的影响

在奶牛中，分娩前的最后几周在生理上具有挑战性，并且是后续生产性能的重要决定因素。在此期间应仔细管理外部压力源，以避免给动物增加压力。妊娠后期的热应激会损害大坝的生产力并对后代产生跨代影响。生理反应是复杂的，对表现的损害是多方面的。妊娠后期的热应激会减弱干奶期前半段的乳腺退化，并在产犊临近时损害细胞增殖。此外，暴露于产前热应激的奶牛在泌乳早期表现出减少的脂肪组织动员和较低程度的胰岛素抵抗。产前热暴露也会抑制免疫功能，有证据表明这种降低与热应激下催乳素信号传导的改变有关。胎盘功能也受到损害，这反映在较高的子叶质量但较低的母体循环硫酸雌酮浓度，可能导致较低的营养供应和降低的犊牛出生体重。此外，热应激母牛所生的小牛显示出免疫功能受损，因此更容易患上疾病。新证据报告称，宫内热应激会改变肝脏和乳腺 DNA 的甲基化谱，这也可能导致暴露于宫内热应激的犊牛在成年期表现较差。了解所有改变的生物系统在妊娠后期热应激期间的贡献可用作改善干奶期奶牛管理的基础。本文综述了妊娠后期热应激的影响，以及对所观察到的性能损害背后的生物学机制的新理解。