Genetic improvement of dairy cows has markedly increased milk yield over the last three decades. Increased production has been associated with reduced conception rates (66% in 1951 versus 40 to 50% since 1975). Because conception rate in dairy heifers has remained higher, the metabolic demands of higher production may be related to the decline in reproductive performance in cows. During early lactation, increasing dietary intake fails to keep pace with rising milk production. The resultant negative energy balance and rate of mobilization of body reserves appear directly related to the postpartum interval to first ovulation and lower conception rate. Delays in the onset of normal ovarian activity, thus limiting the number of estrous cycles before breeding, may account for the observed decrease in fertility. Negative energy balance probably acts similarly to undernutrition and may manifest in delayed ovarian activity by impinging on pulsatile secretion of LH. Lower availability of glucose and insulin may also decrease LH pulsatility or limit ovarian responsiveness to gonadotropins. Alternatively, release of endogenous opioids in association with increasing feed intake or other lactational hormone responses may provide neural or pituitary inhibition of the pulsatile LH production that is requisite for ovarian follicular development.

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Dairy cows suffer from an intense energy deficit at parturition due to the onset of copious milk synthesis and depressed appetite. Despite this deficit, maternal metabolism is almost completely devoted to the support of mammary metabolism. Evidence from rodents suggests that, during periods of nutritional insufficiency, a reduction in plasma leptin serves to co-ordinate energy metabolism. As an initial step to determine if leptin plays this role in periparturient dairy cows, changes in the plasma concentration of leptin were measured during the period from 35 days before to 56 days after parturition. The plasma concentration of leptin was reduced by 50% after parturition and remained depressed during lactation despite a gradual improvement in energy balance; corresponding changes occurred in the abundance of leptin mRNA in white adipose tissue. To determine whether negative energy balance caused this reduction in circulating leptin, cows were either milked or not milked after parturition. Absence of milk removal eliminated the energy deficit of early lactation, and doubled the plasma concentration of leptin. The plasma concentration of leptin was positively correlated with plasma concentrations of insulin and glucose, and negatively correlated with plasma concentrations of growth hormone and non-esterified fatty acids. In conclusion, the energy deficit of periparturient cows causes a sustained reduction in plasma leptin. This reduction could benefit early lactating dairy cows by promoting a faster increase in feed intake and by diverting energy from non-vital functions such as reproduction.

Milk production and dry matter intake of dairy cows are stimulated in response to increased intake of dietary protein, but, unfortunately, decreased fertility is often associated with this nutritional strategy. Ruminally degradable protein or ruminally undegradable protein in excess of requirement can contribute to reduced fertility in lactating cows. Dietary protein nutrition or utilization and the associated effects on ovarian or uterine physiology have been monitored with urea nitrogen in plasma or milk; concentrations above 19 mg/dl have been associated with altered uterine pH and reduced fertility in dairy cows. The uterine pH changed dynamically and inversely with plasma urea nitrogen, signaling possible changes in the uterine milieu. Mechanisms for reduced fertility include exacerbation of negative energy balance and reduced plasma progesterone concentrations when cows were fed rations that were high in ruminally degradable intake protein. Alternatively, changes in uterine secretions that are associated with high protein intake and elevated plasma urea nitrogen might be detrimental to embryos. Bovine endometrial cells in culture respond directly to increasing urea concentrations with alteration in pH gradient but respond most notably with increased secretion of prostaglandin F2 alpha (PGF2 alpha). Increased uterine luminal PGF2 alpha interferes with embryo development and survival in cows, thus providing a plausible link between elevated plasma urea nitrogen concentrations and decreased fertility. Poor fertility in high producing dairy cows reflects the combined effects of a uterine environment that is dependent on progesterone and rendered suboptimum by the antecedent effects of negative energy balance or postpartum health problems and that is further compromised by the effects of urea resulting from intake of high dietary protein.