Management, nutrition, production, and genetics are the main reasons for the decline in fertility in the modern dairy cow. Selection for the single trait of milk production with little consideration for traits associated with reproduction in the modern dairy cow has produced an antagonistic relationship between milk yield and reproductive performance. The outcome is a multi-factorial syndrome of subfertility during lactation; thus, to achieve a better understanding and derive a solution, it is necessary to integrate a range of disciplines, including genetics, nutrition, immunology, molecular biology, endocrinology, metabolic and reproductive physiology, and animal welfare. The common theme underlying the process is a link between nutritional and metabolic inputs that support complex interactions between the gonadotropic and somatotropic axes. Multiple hormonal and metabolic signals from the liver, pancreas, muscle, and adipose tissues act on brain centers regulating feed intake, energy balance, and metabolism. Among these signals, glucose, fatty acids, insulin-like growth factor-I, insulin, growth hormone, ghrelin, leptin, and perhaps myostatin appear to play key roles. Many of these factors are affected by changes in the somatotropic axis that are a consequence of, or are needed to support, high milk production. Ovarian tissues also respond directly to metabolic inputs, with consequences for folliculogenesis, steroidogenesis, and the development of the oocyte and embryo. Little doubt exists that appropriate nutritional management before and after calving is essential for successful reproduction. Changes in body composition are related to the processes that lead to ovulation, estrus, and conception. However, better indicators of body composition and measures of critical metabolites are required to form precise nutritional management guidelines to optimize reproductive outcomes. The eventual solution to the reduction in fertility will be a new strategic direction for genetic selection that includes fertility-related traits. However, this will take time to be effective, so, in the short term, we need to gain a greater understanding of the interactions between nutrition and fertility to better manage the issue. A greater understanding of the phenomenon will also provide markers for more targeted genetic selection. This review highlights many fruitful directions for research, aimed at the development of strategies for nutritional management of reproduction in the high-producing subfertile dairy cow.

In mature male sheep, the level of nutrition acutely influences the secretion of reproductive hormones. The mechanism involved is not fully understood but findings in humans and laboratory rodents would suggest a major role for leptin that is secreted from adipose tissue and then travels via the circulation to the central nervous system. Before we can begin to test this hypothesis, we need to be able to measure leptin concentrations in blood plasma and cerebrospinal fluid. We have therefore developed a radioimmunoassay using antibodies raised against biologically active recombinant bovine-ovine leptin. Using this assay, we found that plasma concentrations of leptin were highly correlated to back-fat thickness and to the ratio of back-fat thickness to liveweight, in female and castrated male sheep. Plasma concentrations of leptin were higher in female sheep than in castrated or intact male sheep. Serial samples (every 5 min) suggested that the secretion of leptin in male sheep is episodic but it does not appear to show clear pulsatility, increases post-prandially, or a diurnal rhythm. Leptin concentrations in both plasma and cerebrospinal fluid increased within 5 days in male sheep fed a diet with a high content of energy and protein that also stimulates the secretion of LH pulses. These data suggest that in sheep, as in other species, leptin production is correlated with the mass of adipose tissue and that the hormone passes from the circulation to the cerebrospinal fluid and then to hypothalamic sites. There, it may affect appetite and perhaps GnRH secretion. The role of leptin in the link between nutrition and reproduction needs further investigation.

The objective of this study was to determine whether the physiological response to an intravenous glucose challenge would be affected by genetic strain or concentrate supplementation in grazing Holstein-Friesian cows in early lactation. North American (NA; n = 30) or New Zealand (NZ; n = 30) cows were randomly allocated to 1 of 3 feeding treatments. All cows were offered a generous pasture allowance, and 4 of the 6 groups received either 3 or 6 kg of dry matter (DM)/cow per day of concentrates. During wk 5 of lactation, all cows underwent an intravenous glucose challenge. Cows of NA origin produced more milk than NZ cows, but there was no significant strain effect on milk fat or protein yield. Milk yield and the yield of individual components increased with increasing level of concentrate eaten, but there were no significant strain x diet interactions. During wk 1 to 6, mean body weight and body condition score decreased in all treatments. Average body weight was greater in NA cows, but body condition score was greater for NZ cows. There was no strain or diet effect on the length of the postpartum anovulatory interval, with cows ovulating before 40 d postpartum on average. Glucose fractional turnover rate was greater in NZ cows compared with those of NA origin and in all cows receiving 6 kg of DM concentrates, indicating a less severe insulin resistance in those treatments. Consistent with this, the time taken to dispose of half the peak glucose concentration was less when 6 kg of DM concentrate was fed, and tended to be less in NZ than in NA cows. There was no effect of genetic strain on glucose area under the curve (AUC) at 60 or 120 min, but AUC at both time points was less in cows receiving 6 kg of DM concentrates per day. Neither genetic strain nor nutrition affected basal or peak insulin concentrations, insulin increment, or insulin AUC, and there were no strain x diet interactions for any of the glucose challenge response variables measured. In conclusion, differences in milk production between NA and NZ cows in early lactation can, at least in part, be explained by the greater degree of insulin resistance in the NA cows, and this insulin resistance can be overcome by supplementing grazing cows with 6 kg of DM concentrates.

Ghrelin is an endogenous ligand of the growth hormone secretagogue receptor, and a potent orexigenic agent in human and rodent studies. We hypothesized that ghrelin may play a role in the reduced grazing time in dairy cows receiving supplementary feeds. Fifty-eight Holstein-Friesian (HF) dairy cows of New Zealand (NZ; n = 28) and North American (NA; n = 30) ancestry were provided with unrestricted access to pasture and randomly allocated at calving to either 0, 3, or 6 kg of dry matter concentrates in a 2 x 3 factorial arrangement. Concentrates were offered in equal amounts at each milking. In peak lactation (75 and 79 +/- 19.7 d in milk), blood was sampled from all cows prior to the a.m. milking (i.e., baseline) and following 2 h of unrestricted access to fresh pasture after the a.m. milking on 2 consecutive weeks. Daily milk yield and fat, protein, and lactose concentrations were measured on the day of blood sampling. North American cows produced more milk and consumed numerically more pasture than did NZ cows, and NA cows had elevated plasma ghrelin concentrations pre- and postfeeding. A negative association between dry matter intake and postprandial ghrelin concentrations indicated that other controlling factors may be involved. Circulating ghrelin concentrations before feeding were not affected by concentrate supplementation, but increasing supplementation was associated with a linear decline in pasture intake and postprandial ghrelin concentrations. This negative association between concentrate supplementation and plasma ghrelin concentrations offers a potential neuroendocrine basis for the reduced pasture intake when supplements are offered to cows in grazing systems.

This study examined the effect of monopropylene glycol (MPG) supplementation on LH secretion, postpartum interval to first ovulation, and milk production in heifers calving with poor body condition score (BCS). Forty-seven heifers were allocated to 3 treatments: 1) heifers with high BCS (BCH; n = 13) that calved at a BCS of 3.4 (BCS scale of 1 to 5); 2) heifers with low BCS (BCL; n = 17) that calved at a BCS of 2.8; and 3) heifers with low BCS that calved at a BCS of 2.8 and were assigned to receive MPG supplementation (BCL + MPG; n = 17) and grazed pasture ad libitum. Monopropylene glycol was drenched (250 mL) twice daily for 16 wk after calving. Patterns of change in plasma LH were measured at 2 and 5 wk after calving. Pulsatile release of LH at 2 and 5 wk was greater in BCL + MPG and BCH cows compared with the BCL control cows. The BCL + MPG cows had lower NEFA concentrations than did the BCL cows during wk 1 to 6 after calving. At 12 wk postpartum, the proportion of cows cycling was 77, 82, and 28% for the BCH, BCL + MPG, and BCL treatments, respectively. Mean milk fat yield was greater for the BCH treatment during the first 12 wk postpartum compared with the BCL + MPG or BCL treatments, which did not differ from each other. Results of this study indicate that MPG supplementation reduced the interval from calving to first ovulation in heifers having poor body condition at calving.