Inhibited Methanogenesis in the Rumen of Cattle: Microbial Metabolism in Response to Supplemental 3-Nitrooxypropanol and Nitrate

3-Nitrooxypropanol (3-NOP) supplementation to cattle diets mitigates enteric CH(4) emissions and may also be economically beneficial at farm level. However, the wider rumen metabolic response to methanogenic inhibition by 3-NOP and the [Formula: see text] intermediary metabolite requires further exploration. Furthermore, [Formula: see text] supplementation potently decreases CH(4) emissions from cattle. The reduction of [Formula: see text] utilizes H(2) and yields [Formula: see text] , the latter of which may also inhibit rumen methanogens, although a different mode of action than for 3-NOP and its [Formula: see text] derivative was hypothesized. Our objective was to explore potential responses of the fermentative and methanogenic metabolism in the rumen to 3-NOP, [Formula: see text] 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 [Formula: see text]. Both new models were further extended with a [Formula: see text] state variable, with [Formula: see text] exerting methanogenic inhibition, although the modes of action of 3-NOP-derived and [Formula: see text]-derived [Formula: see text] 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 [Formula: see text] models both predicted a marked peak in H(2) emission shortly after feeding, the magnitude of which increased with higher doses of supplement inclusion. The H(2) emission rate appeared positively related to decreased acetate proportions and increased propionate and butyrate proportions. A decreased CH(4) emission rate was associated with 3-NOP and [Formula: see text] supplementation. Omission of the [Formula: see text] state variable from the 3-NOP model did not change the overall dynamics of H(2) and CH(4) emission and other metabolites. However, omitting the [Formula: see text] state variable from the [Formula: see text] model did substantially change the dynamics of H(2) and CH(4) emissions indicated by a decrease in both H(2) and CH(4) emission after feeding. Simulations do not point to a strong relationship between methanogenic inhibition and the rate of [Formula: see text] and [Formula: see text] formation upon 3-NOP supplementation, whereas the metabolic response to [Formula: see text] supplementation may largely depend on methanogenic inhibition by [Formula: see text].