ENVIRONMENTAL AND MANAGEMENT FACTORS

Environmental factors and husbandry management play a significant role in regulating cow reproductive function, particularly regarding follicle dynamics and the timing of ovulation [61]. One of the most influential environmental factors is heat stress, which occurs when ambient temperatures exceed a cow’s ability to maintain stable body temperature [62]. Heat stress is often quantified using the temperature–humidity index (THI), with values above 68–72 indicating the onset of heat stress and values >78 associated with severe heat stress and increased risk of delayed ovulation.

Heat stress triggers increased glucocorticoid production, particularly cortisol, which suppresses GnRH pulse frequency and LH release amplitude, weakening or delaying the LH surge required for ovulation [28, 63]. Additionally, heat stress disrupts granulosa cell steroidogenesis, reduces estradiol production, and impairs oocyte maturation [64]. Cows exposed to sustained temperature–humidity index above critical thresholds during the peri-estrus period exhibit a higher incidence of delayed ovulation and persistent follicles, reflecting combined endocrine and cellular effects of thermal stress [65].

From a management perspective, errors in estrus detection and insemination timing are significant contributors to delayed ovulation [66]. Misidentifying estrus phases can create a mismatch between peak follicle development and insemination timing. In synchronization programs, improper administration of prostaglandin or GnRH, or mistimed insemination, can disrupt preovulatory follicle development [67, 68]. Real-world examples include delayed or missed GnRH injection in Ovsynch protocols, insemination before the dominant follicle reaches ovulatory size, or failure to administer prostaglandin at recommended intervals. These errors prolong the follicular phase, inhibit the LH surge, and increase the risk of delayed or absent ovulation [69].

Production pressure, particularly in high-yielding dairy cows, also contributes to ovulatory disorders [2]. High-producing cows face elevated metabolic demands, predisposing them to NEB [70], which not only reduces nutritional adequacy but also acts as a metabolic stressor suppressing reproductive function [71]. Efficiency of ovarian tissue energy utilization decreases, and levels of IGF-1, insulin, and other metabolic hormones that support follicular response decline [72].

Housing systems further modulate these effects: cows in tie-stall systems often have restricted movement, reduced heat dissipation, and less overt estrus expression compared with free-stall systems, which provide better ventilation, cow comfort, and behavioral estrus expression. In beef cattle, lower production intensity generally reduces the risk of ovulatory disorders; however, management factors such as feeding inconsistencies, transport stress, high stocking density, or inadequate thermal comfort can still disrupt ovarian function [73].