Heat stress as a multilevel disruptor of gamete function and early embryo development in cattle.

Elevated ambient temperatures disrupt fertility through coordinated effects on female and male gametes as well as early embryos. In females, heat stress alters hypothalamic-pituitary-ovarian signaling, reduces follicular perfusion, disrupts steroidogenesis, and induces oxidative and metabolic stress within the follicular microenvironment, resulting in compromised oocyte competence that can persist across multiple follicular waves. In males, elevated testicular temperature interferes with spermatogenesis in a stage-dependent manner, leading to delayed impairments in sperm chromatin integrity, motility, and fertilizing capacity that may not be detected by routine semen evaluation. Early embryos are particularly vulnerable to elevated temperature, with heat stress activating mitochondrial dysfunction, oxidative stress, apoptotic pathways, and impaired stress-response mechanisms before thermotolerance is acquired at later developmental stages. This review integrates systemic, cellular, and molecular evidence to describe how heat stress acts as a multilevel disruptor of reproduction in cattle, identifies key mechanisms underlying carryover effects on fertility, and highlights knowledge gaps critical for improving reproductive resilience under thermal stress.