PATHOPHYSIOLOGY OF DELAYED OVULATION

Delayed ovulation in cattle occurs when oocyte release takes place later than the normal physiological timeframe, generally due to disturbances in endocrine regulation and ovarian activity [11]. Normally, ovulation is triggered by an LH surge that occurs in response to increased estradiol produced by the dominant follicle [31].

The mechanistic flow can be summarized as: cause → endocrine disruption → ovarian outcome → fertility consequence [32]. Primary triggers include stress, metabolic disorders, nutritional imbalances, and postpartum recovery delays, which disrupt pulsatile GnRH release from the hypothalamus. This leads to altered LH pulse frequency and amplitude, impairing the preovulatory LH surge and delaying oocyte maturation and follicle rupture [33, 34].

A delay in the LH surge can result in follicular persistence, where the dominant follicle remains unovulated despite large size and high steroidogenic activity [8]. Persistent follicles exhibit reduced estradiol production and impaired granulosa cell differentiation, decreasing responsiveness to gonadotropins and prolonging the follicular phase [35].

Oxidative stress further contributes by disrupting steroidogenesis and LH receptor signaling, suppressing the LH surge [36]. Low LH receptor expression in granulosa and theca cells or impaired luteotropic response compromises final follicle maturation [37].

Temporary versus recurrent delayed ovulation is mechanistically distinct: transient delays typically arise from postpartum recovery or acute stress, whereas recurrent delays are often due to chronic metabolic, endocrine, or inflammatory disorders [38].

Delayed ovulation is also linked to impaired corpus luteum (CL) function, particularly when CLs arise from persistent follicles [39]. These CLs produce less progesterone and have shortened functional lifespan, resulting in prolonged inter-estrus intervals, increased repeat breeding, and reduced conception rates [40, 41].

Neuroendocrine interactions via the hypothalamic-pituitary-adrenal (HPA) axis exacerbate delays [42]. Elevated cortisol from stress or metabolic challenges suppresses GnRH pulsatility, reduces LH production, and directly impairs ovarian steroidogenic enzymes and gonadotropin receptor expression [43, 44].

Figure 2 illustrates the integrated pathophysiological cascade leading to delayed ovulation.

Figure 2: Integrated pathophysiological mechanisms of delayed ovulation in cattle. The figure was prepared by the authors based on information synthesized from previous studies [8, 11, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44]. The graphical illustration was generated with the assistance of ChatGPT (OpenAI, San Francisco, CA, USA) and designed using Canva (Canva Pty Ltd., Sydney, Australia). The final figure was critically reviewed, refined, and validated by the authors to ensure scientific accuracy and consistency with the cited literature.