Heat stress impacts productivity and methane emissions in dairy cattle

Abstract

Climate change, driven by rising greenhouse gas (GHG) accumulation in the atmosphere, poses major challenges to livestock production systems, particularly through increased intensity of heat stress (HS). Dairy cattle are highly vulnerable to HS due to high metabolic heat production associated with lactation. This review synthesizes current knowledge on the physiological, metabolic, and microbial responses of dairy cows to HS and examines the implications on milk production and enteric methane emissions. Heat stress disrupts feed intake, rumen motility, and saliva-mediated buffering, contributing to reduced ruminal pH and altered fermentation patterns. Endocrine responses include acute elevations in cortisol, prolactin, and insulin, which support thermoregulation but contribute to reduced nutrient availability for milk synthesis. Consequences for productivity depend on physiological stage; while early- and late-lactation cows partially recover from HS, mid-lactation cows experience persistent production losses driven by accelerated mammary epithelial cell apoptosis and reduced mammary persistence. Heat stress also influences methane emissions. Although total daily methane production generally declines due to reduced feed intake, methane corrected by feed intake and by milk yield increase. Altered rumen function, extended ruminal retention time, can increase methane corrected by intake, whereas impaired mammary gland function and reduced milk output increase methane corrected by milk yield. Current methane mitigation strategies, including methanogenesis inhibitors, seaweed supplementation, and ionophores, must be evaluated within the context of HS, as altered rumen physiology may modify their effectiveness. Further controlled research is needed to elucidate the interactive effects of HS on rumen microbiology, fermentation, and methane emissions.