Hristov, A. N., Hanigan, M., Cole, A., Todd, R., McAllister T. A., Ndegwa, P. and Rotz, A. 2011. Review: Ammonia emissions from dairy farms and beef feedlots. Can. J. Anim. Sci. 91: 1–35. Ammonia emitted from animal feeding operations is an environmental and human health hazard, contributing to eutrophication of surface waters and nitrate contamination of ground waters, soil acidity, and fine particulate matter formation. It may also contribute to global warming through nitrous oxide formation. Along with these societal concerns, ammonia emission is a net loss of manure fertilizer value to the producer. A significant portion of cattle manure nitrogen, primarily from urinary urea, is converted to ammonium and eventually lost to the atmosphere as ammonia. Determining ammonia emissions from cattle operations is complicated by the multifaceted nature of the factors regulating ammonia volatilization, such as manure management, ambient temperature, wind speed, and manure composition and pH. Approaches to quantify ammonia emissions include micrometeorological methods, mass balance accounting and enclosures. Each method has its advantages, disadvantages and appropriate application. It is also of interest to determine the ammonia emitting potential of manure (AEP) independent of environmental factors. The ratio of nitrogen to non-volatile minerals (phosphorus, potassium, ash) or nitrogen isotopes ratio in manure has been suggested as a useful indicator of AEP. Existing data on ammonia emission factors and flux rates are extremely variable. For dairy farms, emission factors from 0.82 to 250 g ammonia per cow per day have been reported, with an average of 59 g per cow per day (n=31). Ammonia flux rates for dairy farms averaged 1.03 g m⁻²h⁻¹(n=24). Ammonia losses are significantly greater from beef feedlots, where emission factors average 119 g per animal per day (n=9) with values as high as 280 g per animal per day. Ammonia flux rate for beef feedlots averaged 0.174 g m⁻²h⁻¹(n=12). Using nitrogen mass balance approaches, daily ammonia nitrogen losses of 25 to 50% of the nitrogen excreted in manure have been estimated for dairy cows and feedlot cattle. Practices to mitigate ammonia emissions include reducing excreted N (particularly urinary N), acidifying ammonia sources, or binding ammonium to a substrate. Reducing crude protein concentration in cattle diets and ruminal protein degradability are powerful tools for reducing N excretion, AEP, and whole-farm ammonia emissions. Reducing dietary protein can also benefit the producer by reducing feed cost. These interventions, however, have to be balanced with the risk of lost production. Manure treatment techniques that reduce volatile N species (e.g., urease inhibition, pH reduction, nitrification-denitrification) are also effective for mitigating ammonia emissions. Another option for reducing ammonia emissions is capture and treatment of released ammonia. Examples in the latter category include biofilters, permeable and impermeable covers, and manure incorporation into the soil for crop or pasture production. Process-level simulation of ammonia formation and emission provides a useful tool for estimating emissions over a wide range of production practices and evaluating the potential benefits of mitigation strategies. Reducing ammonia emissions from dairy and beef cattle operations is critical to achieving environmentally sustainable animal production that will benefit producers and society at large.

Understanding the regulatory effects of individual amino acids (AA) on milk protein synthesis rates is important for improving protein and AA require

The objective of this study was to evaluate local molecular adaptations proposed to regulate protein synthesis in the mammary glands. It was hypothesized that AA and energy-yielding substrates independently regulate AA metabolism and protein synthesis in mammary glands by a combination of systemic and local mechanisms. Six primiparous mid-lactation Holstein cows with ruminal cannulas were randomly assigned to 4 treatment sequences in a replicated incomplete 4 x 4 Latin square design experiment. Treatments were abomasal infusions of casein and starch in a 2 x 2 factorial arrangement. All animals received the same basal diet (17.6% crude protein and 6.61 MJ of net energy for lactation/kg of DM) throughout the study. Cows were restricted to 70% of ad libitum intake and abomasally infused for 36 h with water, casein (0.86 kg/d), starch (2 kg/d), or a combination (2 kg/d starch+0.86 kg/d casein) using peristaltic pumps. Milk yields and composition were assessed throughout the study. Arterial and venous plasma samples were collected every 20 min during the last 8h of infusion to assess mammary uptake. Mammary biopsy samples were collected at the end of each infusion and assessed for the phosphorylation state of selected intracellular signaling molecules that regulate protein synthesis. Animals infused with casein had increased arterial concentrations of AA, increased mammary extraction of AA from plasma, either no change or a trend for reduced mammary AA clearance rates, and no change in milk protein yield. Animals infused with starch had increased milk and milk protein yields, increased mammary plasma flow, reduced arterial concentrations of AA, and increased mammary clearance rates and net uptake of some AA. Infusions of starch increased plasma concentrations of glucose, insulin, and insulin-like growth factor-I. Starch infusions increased phosphorylation of ribosomal protein S6 and endothelial nitric oxide synthase, consistent with changes in milk protein yields and plasma flow, respectively. Phosphorylation of the mammalian target of rapamycin was increased in response to starch only when casein was also infused. Thus, cell signaling molecules involved in the regulation of protein synthesis differentially responded to these nutritional stimuli. The hypothesized independent effects of casein and starch on animal metabolism and cell signaling were not observed, presumably because of the lack of a milk protein response to infused casein.

Extensive proliferation and death of cells in the mammary gland occur during pregnancy and lactation. In this study, a mechanistic model was developed that yielded a single equation to describe the pattern of mammary growth of mammals throughout pregnancy and lactation. The model contains a single pool, which is the cell population of the mammary gland; one influx, representing cell proliferation; and one efflux, representing cell death. The parameters of the equation lend themselves to direct physiological interpretation. The model fitted data on mammary gland DNA adequately and can be related to current knowledge on factors and inhibitors of mammary gland growth. A unique definition of the parameters of the model can be difficult because of the high degree of variation among animals, an improper number of observations, or timing, as indicated by analyses of simulated data. The model can also be applied to the study of the entire lactation curve. The widely applied gamma equation and the equation that was developed in this study were compared using weekly production data from dairy cows. The new model performed well, particularly when a sharp peak in milk production occurred. The model has the advantage of providing, for the first time, a simple biological description of the lactation curve that can be used to discriminate changes in lactational performance that are associated with experimental treatments.

Most prediction schemes of milk protein secretion overestimate milk protein yield from dairy cows at high protein intakes, thereby overestimating milk protein yield response to protein supplementation. This study was conducted to determine factors contributing to such an overestimation. Using published studies, a database was constructed that was limited to amino acid (AA) infusion studies, as then only the digestible amino acid of dietary origin needed to be estimated, whereas the amount infused was known exactly, thereby reducing the dependence on estimated values. Although milk protein yield was positively related with total energy supply, and both digestible duodenal supply and infused AA, in this database there was no relationship between milk protein yield response above control treatments and the nutrient status of the cows (energy or protein). Total milk protein yield was defined as a function of individual AA supply, using a segmented-linear and a logistic model to obtain estimates of the efficiency of conversion of AA into milk protein. Except for Lys and Met supply, the segmented-linear model yielded lower root mean square error and better correlation, but both models were similar in their reliability. For both models, the estimated efficiency of conversion of AA to milk differed among AA. Estimations of the ideal profile of AA for lactating dairy cows were similar between models, with requirements for Lys and Met in line with 2001 National Research Council recommendations. The major difference is that the segmented-linear model yields a constant efficiency of conversion of an AA until requirements are met, with zero efficiency beyond this point. The logistic model allows for an estimation of the decreasing marginal efficiency of conversion of AA as the supply approaches the requirements. The use of variable efficiency factors should improve our ability to predict protein yield in response to supplemental protein.

In current dairy production systems, an average of 25% of dietary N is captured in milk, with the remainder being excreted in urine and feces. About 60% of total N losses occur postabsorption. Splanchnic tissues extract a fixed proportion of total inflow of each essential AA (EAA). Those EAA removed by splanchnic tissues and not incorporated into protein are subjected to catabolism, with the resulting N converted to urea. Splanchnic affinity varies among individual EAA, from several fold lower than mammary glands' affinity for the branched-chain AA to similar or higher affinity for Phe, Met, His, and Arg. On average, 85% of absorbed EAA appear in peripheral circulation, indicating that first-pass removal is not the main source of loss. Essential AA in excess of the needs of the mammary glands return to general circulation. High splanchnic blood flow dictates that a large proportion of EAA that return to general circulation flow through splanchnic tissues. In association with this constant recycling, EAA are removed and catabolized by splanchnic tissues. This results in splanchnic catabolism equaling or surpassing the use of many EAA for milk protein synthesis. Recent studies have demonstrated that EAA, energy substrates, and hormones activate signaling pathways that in turn regulate local blood flow, tissue extraction of EAA, and rates of milk protein synthesis. These recent findings would allow manipulation of dairy diets to maximize mammary uptake of EAA and reduce catabolism by splanchnic tissues. Dairy cattle nutrient requirement systems consider EAA requirements in aggregate as metabolizable protein (MP) and assume a fixed efficiency of MP use for milk protein. Lysine and Met sufficiency is only considered after MP requirements have been met. By doing so, requirement systems limit the scope of diet manipulation to achieve improved gross N efficiency. Therefore, this review focuses on understanding the dynamics of EAA metabolism in mammary and splanchnic tissues that would lead to improved requirement prediction systems. Inclusion of variable individual EAA efficiencies derived from splanchnic and mammary responses to nutrient and hormonal signals should help reduce dietary protein levels. Supplementing reduced crude protein diets with individual EAA should increase gross N efficiency to more than 30%, reducing N excretion by the US dairy industry by 92,000 t annually.