UC Davis

3-Nitrooxypropanol (3-NOP) supplementation to cattle diets mitigates enteric CH₄ emissions and may also be economically beneficial at farm level. However, the wider rumen metabolic response to methanogenic inhibition by 3-NOP and the intermediary metabolite requires further exploration. Furthermore, supplementation potently decreases CH₄ emissions from cattle. The reduction of utilizes H₂ and yields , the latter of which may also inhibit rumen methanogens, although a different mode of action than for 3-NOP and its derivative was hypothesized. Our objective was to explore potential responses of the fermentative and methanogenic metabolism in the rumen to 3-NOP, and their metabolic derivatives using a dynamic mechanistic modeling approach. An extant mechanistic rumen fermentation model with state variables for carbohydrate substrates, bacteria and protozoa, gaseous and dissolved fermentation end products and methanogens was extended with a state variable of either 3-NOP or . Both new models were further extended with a state variable, with exerting methanogenic inhibition, although the modes of action of 3-NOP-derived and -derived are different. Feed composition and intake rate (twice daily feeding regime), and supplement inclusion were used as model inputs. Model parameters were estimated to experimental data collected from the literature. The extended 3-NOP and models both predicted a marked peak in H₂ emission shortly after feeding, the magnitude of which increased with higher doses of supplement inclusion. The H₂ emission rate appeared positively related to decreased acetate proportions and increased propionate and butyrate proportions. A decreased CH₄ emission rate was associated with 3-NOP and supplementation. Omission of the state variable from the 3-NOP model did not change the overall dynamics of H₂ and CH₄ emission and other metabolites. However, omitting the state variable from the model did substantially change the dynamics of H₂ and CH₄ emissions indicated by a decrease in both H₂ and CH₄ emission after feeding. Simulations do not point to a strong relationship between methanogenic inhibition and the rate of and formation upon 3-NOP supplementation, whereas the metabolic response to supplementation may largely depend on methanogenic inhibition by .