NUTRITIONAL FACTORS

Nutritional factors play a crucial role in regulating reproductive function in cattle and are a key determinant of delayed ovulation [47]. Nutritional disturbances, including energy deficiency or micronutrient imbalance, modulate endocrine function, ovarian steroid metabolism, and gonadotropic activity, thereby inhibiting normal ovulation [48].

Negative energy balance (NEB) is a primary cause of delayed ovulation, particularly in dairy cows during early lactation [49]. NEB lowers blood levels of glucose, insulin, and Insulin-like growth factor-1 (IGF-1), which in turn reduces ovarian sensitivity to gonadotropin stimulation [50]. Circulating IGF-1 concentrations below approximately 80–100 ng/mL are associated with reduced follicular growth and higher risk of delayed ovulation, as low IGF-1 inhibits granulosa cell proliferation and decreases LH receptor expression in the dominant follicle [51]. Consequently, the preovulatory follicle may fail to respond optimally to the LH surge, leading to delayed ovulation or the formation of persistent follicles [52].

Excessive lipid mobilization during NEB produces non-esterified fatty acids (NEFA) and β-hydroxybutyrate (BHB). Plasma NEFA levels >0.4–0.6 mmol/L and BHB >1.2–1.4 mmol/L during early lactation indicate subclinical ketosis, which is toxic to ovarian cells and impairs steroidogenesis [53]. In mid-lactation cows, NEB is generally less severe, but ongoing high milk production with inadequate dietary energy can still elevate NEFA and BHB, contributing to delayed ovulation.

Factor category | Sub-factor | Mechanism / Impact on ovulation | References
Nutrition | Negative Energy Balance (NEB) | Reduced glucose, insulin, and IGF-1 → decreased ovarian sensitivity to gonadotropins → impaired dominant follicle maturation → delayed ovulation or persistent follicles. Elevated non-esterified fatty acids (NEFA) (>0.4–0.6 mmol/L) and BHB (>1.2–1.4 mmol/L) cause follicular toxicity. | [50, 53]
 | Micronutrients (Se and Vit E) | Antioxidant deficiency → oxidative stress → impaired granulosa cell function and steroidogenesis → disrupted LH surge → delayed ovulation. | [55, 56]
 | Vitamin A | Impaired granulosa cell differentiation and post-ovulatory progesterone synthesis → affected oocyte maturation → prolonged follicular phase. | [57]
 | Body Condition Score (BCS) | Low BCS: suppressed GnRH/LH activity → delayed follicle response; High BCS: insulin resistance and systemic inflammation → follicle asynchrony → delayed ovulation. | [58–60]
Environment and Management | Heat stress | Elevated cortisol → decreased GnRH/LH pulsatility → impaired steroidogenesis and oocyte maturation → delayed ovulation or persistent follicles. | [62–65]
 | Mistimed estrus detection & insemination | Follicle-LH surge asynchrony → delayed or missed ovulation → reduced conception. | [66–68]
 | High production intensity | Increased metabolic demand → NEB and metabolic stress → impaired follicular steroidogenesis and endocrine function → delayed ovulation. | [70–72]
 | Housing / confinement stress | Restricted movement, poor ventilation, and heat retention → endocrine disruption → follicle growth delays → delayed ovulation. | [73]
Animal-related factors | Parity | Primiparous cows: higher NEB and immature metabolic capacity → lower GnRH/LH pulsatility → increased risk of delayed ovulation. | [76–78]
 | Breed | High-yielding dairy breeds more susceptible than beef or indigenous breeds due to higher metabolic demands and variability in LH receptor expression → altered follicular dynamics. | [78, 79]
 | Postpartum period | NEB + incomplete uterine involution → subclinical inflammation → suppressed GnRH/LH → delayed ovulation. | [82–84]
Endocrine and metabolic disorders | Hypothyroidism | Low T3/T4 → reduced IGF-1 → slow follicle growth → weakened LH surge → delayed ovulation. | [86–88]
 | Hyperprolactinemia | High prolactin → suppressed GnRH/LH pulsatility → impaired granulosa cell response → delayed ovulation. | [90–93]
 | Insulin resistance and metabolic stress | Disrupted insulin signaling → impaired steroidogenesis → poor oocyte quality → persistent follicles → delayed ovulation. | [94–99]
Infection and inflammation | Subclinical endometritis | Increased IL-1β, IL-6, TNF-α → suppressed GnRH/LH → delayed follicle maturation → persistent follicles. | [102–105]
 | Viral infections (infectious bovine rhinotracheitis and bovine viral diarrhea) | Ovarian damage + altered hormone profile → impaired follicle development → delayed ovulation. | [107–110]
 | Systemic inflammation | Elevated cortisol and cytokines → decreased GnRH/LH and granulosa cell apoptosis → impaired oocyte maturation → delayed ovulation. | [112–115]

Micronutrients play a crucial role in maintaining optimal reproductive function [54]. Selenium and vitamin E act as antioxidants, protecting ovarian tissue from oxidative stress and supporting enzymes in steroidogenesis [55]. Dietary selenium is supplied via forages, cereal grains, and premixes at 0.1–0.3 mg Se/kg dry matter, while vitamin E is commonly given at 500–1,000 IU/day during the periparturient period. Deficiencies impair follicular maturation and estradiol production, disrupting the positive feedback necessary to trigger the LH surge [56]. Vitamin A, primarily from β-carotene in green forages or supplemented at 50,000–100,000 IU/day, supports granulosa cell differentiation, follicle development, and post-ovulatory progesterone synthesis; deficiency prolongs the follicular phase and inhibits oocyte maturation [57].

Body condition score (BCS) provides an integrated measure of energy status [58]. Low BCS suppresses GnRH and LH activity, prolonging the time to ovulation, whereas excessively high BCS can induce insulin resistance and systemic inflammation, thereby negatively affecting ovarian function and oocyte quality [59]. Changes in BCS during the transition period are particularly informative: cows losing >0.5 BCS units in the first 4–6 weeks postpartum experience greater metabolic stress and hormonal imbalance, increasing delayed ovulation risk compared with cows maintaining a stable BCS, even if their absolute BCS is adequate [60].