Past and current nutritional models used to assess nutrient requirements of dairy cattle have attempted to ameliorate metabolic disease after calving through the cow’s ration during the three to four weeks preceding calving.

In spite of current evidence suggesting that nutrient supply and hormonal signals at specific windows during development may exert permanent changes in the metabolism of the offspring, the nutritional models used today assume that nutrient requirements for pregnancy are only relevant for the last three months of gestation and neglect any potential long-term effect of maternal nutrition on the offspring.

Nourishing the pregnant cow

Since the early ’90s, late-pregnant cows have been fed high-energy rations in the immediate pre-calving period to compensate for the assumed decrease in feed intake as calving approaches.

Supposedly, this minimizes body fat mobilization, reduces the likelihood of ketosis and fatty liver after calving, adapts the rumen microflora toward a highly nutrient-dense ration and fosters the growth of rumen papillae to minimize the risk of rumen acidosis during lactation through an improved absorption of volatile fatty acids from the rumen.

However, compensation for reduced feed intake and minimization of body fat mobilization do not seem to be attained by feeding high-energy diets before calving. Several studies have shown energy-dense diets fed prepartum do not physically limit the cow’s intake, resulting in the overconsumption of energy.

Furthermore, overfeeding energy to cows during the last 21 days of gestation triggers a robust up-regulation of lipogenic gene expression in adipose tissue, suggesting that insulin sensitivity may not be impaired by the hyperinsulinemic response to overfeeding energy. This may increase the cow’s odds of accumulating fat pre-calving when fed high-energy density diets.

Overfeeding energy to non-pregnant non-lactating cows drastically increases omental, mesenteric and perirenal adipose tissue of dairy cows without translating in detectable changes in the animal’s body condition.

In addition, cows that are moderately overfed during the prepartum period have an altered immune response and are more prone to liver lipidosis than those fed low-energy diets. Recent evidence supports feeding low-energy diets prepartum, as they result in increased dry matter intake postpartum, increased milk yield and alleviate negative energy balance.

The commonly recommended high-energy diets for the close-up period seem unnecessary, possibly even detrimental, since a much lower energy density will meet the energy requirements of the late-pregnant cow.

The average prepartum cow requires about 15 Mcal of NEl per day, and feeding a ration with an energy density of 1.60 Mcal of NEl per kg ration would readily provide more than 19 Mcal of NEl per day.

Feeding rations of approximately 13 percent crude protein is recommended. However, producers may want to feed a slightly higher percentage to a dry pen with a significant number of first-calving heifers.

The need for adapting the rumen microflora to a high-starch diet (typically fed after calving) by feeding increased amounts of grain to the close-up diet is debatable. In ruminant nutrition, it has been assumed that at least three weeks are needed for the rumen microflora to adapt to a dietary change.

However, the vast majority of organisms in the rumen are bacteria, which can double population in 20 minutes. Thus, three weeks seems an extremely long time to consolidate a change.

In fact, a recent study evaluated changes in the rumen microbial population when shifting steers from a prairie-based diet to a high-grain ration. Within a week of each step-up, the authors reported drastic changes in the rumen microbial population.

Lastly, the fourth objective (fostering growth of rumen papillae) could also be argued.

A study that compared a high-fiber diet versus the same diet plus additional 800 g per day of barley pre-calving reported that total mass of rumen papillae excised from the floor of the cranial sac was not affected by transition diets, but the number tended to be greater when barley was fed, and this was associated with a marked reduction in average width, which resulted in a reduced average surface area.

Thus, it would seem that there would be no need to “adapt” rumen papillae before calving by providing high-starch diets.

Feeding special diets pre-calving is necessary, however, to minimizing the incidence of hypocalcemia and udder edema. Dairy cows have between 2 and 4 g of calcium in their blood, half of which is in the ionized form.

On the first day of lactation, synthesis and secretion of colostrum imposes calcium losses equivalent to seven to 10 times the amount of calcium present in blood. The incidence of clinical hypocalcemia postpartum ranges from 3.5 percent in the U.S. and Australia to 6 percent in Europe, but the threat for dairy cattle lies in the subclinical cases, which are estimated at 50 percent.

Cows with milk fever are at increased risk of developing other periparturient problems, including dystocia, ketosis, displaced abomasum, uterine prolapse and retained placenta. Hypocalcemic cows have increased plasma concentrations of cortisol, reduced proportion of neutrophils with phagocytic activity and impaired mononuclear cell response to an antigen-activating stimulus.

This reduction of immune response has linked hypocalcemia to metritis and mastitis. Preventing or minimizing the incidence of hypocalcemia should be a priority when feeding prepartum dairy cattle.

Strategies to minimize hypocalcemia consist of either feeding anionic salts or low-calcium diets. If a low-calcium dry cow ration was not possible to make (due to available feeds), then a close-up diet, low in energy, containing anionic salts would be necessary.

Nourishing the calf

Throughout most of a lactating cow’s gestation, the embryo’s development is competing with milk production for nutrients. Nutrition is among the most influential intrauterine factors dictating placental and fetal growth.

In dairy cattle, there is little information about the potential effects of maternal metabolic status on subsequent metabolic function of the offspring. Nutrient requirements associated with early pregnancy are ignored and unknown.

However, embryonic metabolic activity is high, and it is a critical period for organogenesis and tissue hyperplasia, and fetal development is most vulnerable to maternal nutrition around the peri-implantation period and during rapid placental development.

The dam’s energy balance during gestation seems to affect the offspring. Although macronutrient requirements for embryonic growth are low in early pregnancy, it is likely the embryo is sensitive to micronutrient deficiencies, circulating concentrations of hormones and growth factors.

For example, methionine is a limiting amino acid in lactating and dry cows. It is instrumental in the regulation of translation and DNA methylation.

Perturbations in the methionine-homocysteine and folate cycles, associated with inadequate methyl donors (i.e., methionine, folic acid, vitamine B12, homocysteine) supply during development stages, may lead to hypomethylation of DNA and deregulation of the offspring’s gene expression and metabolism.

In dairy cattle, evidence suggests that calves whose dams were overfed during the last three weeks of gestation experienced a carryover effect on some of the calf’s metabolism measurements at birth and its phagocytic capacity of blood neutrophils after colostrum feeding. Consequently, a low-energy diet before calving should be recommended.

A protein deficiency of the dam during early pregnancy may compromise the reproductive performance of the offspring. Also, protein deficiencies at the end of the gestation seem to alter the hormonal content of the colostrum. This may compromise intestinal maturation and the immune passive transfer to the calf.

Linear decreases in protein intake during the last 100 days of gestation result in linearly impaired serum IgG concentrations in the calf although the concentration and amount consumed may not. This may have been caused by a moderate nutrient restriction during early to mid-pregnancy, which altered the jejunal proliferation and total intestinal vascularity of the fetus.

Lastly, the nutritional environment is not the only factor that can program or alter the calf’s metabolism. Late-gestation heat stress decreases birthweight, which reflects compromised fetal development in utero.

Fetal growth retardation under heat stress is independent of the nutritional status of the dam. Heat stress of the dam during the dry period compromises the offspring’s immune functions from birth through weaning. Under thermoneutral conditions, the fetus has a consistently higher body temperature relative to its dam.

This is mainly due to poor heat exchange with the dam and the fetus’s twofold greater metabolic rate in relation to its dam. These calves have greater insulin concentrations relative to calves born to cooled dams that consumed equal amounts of colostrum within the first four days.

A high-energy diet before calving does not seem to offer a plausible solution to compensate for the metabolic problems associated with calving. Feeding a low-energy diet before calving seems more effective.

Overfeeding energy decreases intake and predisposes the cow to metabolic problems. On the other hand, an inadequate nutrient supply to the fetus in terms of energy, protein and micronutrients can have a long-term negative impact on the offspring’s performance.

It can be expected that, in the near future, pregnant cows will be supplemented with specific amounts of micronutrients to ensure optimal fetal development and maximum expression of the genetic potential.