Biological responses to heat stress in livestock: From thermoregulation to cellular and epigenetic adaptation.

Climate change driven increases in ambient temperature have positioned heat stress (HS) as a major biological constraint on livestock productivity and welfare. Excessive thermal load disrupts thermoregulatory balance, reduces feed intake and digestive efficiency, and perturbs immune and endocrine function, culminating in impaired energy metabolism and systemic dysfunction. Reproductive processes show pronounced thermal sensitivity, as HS alters hypothalamic-pituitary-gonadal axis signaling, compromises gametogenesis, reduces embryo viability, and suppresses fertility. Productive traits, including milk yield, growth rate, egg production, and carcass quality, decline as cumulative heat load exceeds adaptive capacity. Emerging evidence identifies the gut-brain axis as a critical mediator of HS pathology, where heat-induced vascular redistribution, epithelial hypoxia, and microbiome dysbiosis amplify inflammatory and metabolic stress. At the cellular level, HS triggers mitochondrial dysfunction, oxidative imbalance, activation of heat shock responses, immune dysregulation, and epigenetic remodeling with potential long-term consequences. Current mitigation strategies encompass nutritional and phytogenic modulation of stress pathways, genetic selection for thermo-tolerance, microclimate control, and precision livestock farming (PLF) technologies for real-time detection of thermal strain. However, partial understanding of molecular thresholds, epigenetic plasticity, and integrative system responses limits effective translation. Addressing these gaps through mechanistically driven and interdisciplinary research is essential for enhancing thermal resilience and sustaining livestock production under ongoing climate warming.