Exploring the combination of Asparagopsis taxiformis and phloroglucinol to decrease rumen methanogenesis and redirect hydrogen production in goats

Many strategies for mitigating enteric methane (CH₄) emissions in ruminants have focused on suppressing the activity of rumen methanogens, but this often leads to excess dihydrogen (H₂) accumulation in the rumen, which is subsequently expelled and represents a potential energy loss. We hypothesized that phloroglucinol could act as a H₂ acceptor when rumen methanogenesis is inhibited and be potentially transformed into beneficial compounds for the animal. Eight adult goats were randomly assigned to a replicated 4 × 4 Latin square design with a 2 × 2 factorial arrangement of treatments: two levels of Asparagopsis taxiformis as CH₄ inhibitor [0 vs. 5 g/kg on a dry matter (DM) basis; AT- and AT+, respectively] and two levels of phloroglucinol as alternative H₂ acceptor (0 vs. 20 g/kg DM, PG- and PG+, respectively). Therefore, four dietary treatments were considered: i) basal diet (AT-PG-); ii) A. taxiformis alone (AT+PG-); iii) phloroglucinol alone (AT-PG+); and iv) the combination of A. taxiformis and phloroglucinol (AT+PG+). Animals were fed a maintenance diet with a 70:30 forage-to-concentrate ratio. After 10 d of adaptation to the diet, enteric gas emissions were measured in respiration chambers during 3 d prior to rumen content sampling on d 14. Dietary supplementation with A. taxiformis decreased CH₄ production (-33.9 %) and increased H₂ emissions (+3465 %), along with greater rumen propionate concentration. In contrast, phloroglucinol supplementation alone did not impact CH₄ emissions or the rumen concentration of the main microbial groups but substantially increased acetate molar proportion (+10.2 %) which could act as an alternative H₂ acceptor. Moreover, when A. taxiformis was combined with phloroglucinol, it resulted in a decrease in H₂ emissions (-68.1 %). However, this decrease in H₂ emissions was not fully explained by the increase in the acetate as phloroglucinol led to an increase in acetate both when methanogenesis was inhibited and when it was not. These findings suggest that the rumen fermentation of phloroglucinol may capture some of the additional H₂ arising from the inhibition of methanogenesis by A. taxiformis through pathways other than acetate formation. Moreover, H₂ emissions were not eliminated and most of the decrease occurred during the post-prandial stage, suggesting that the efficiency of H₂ redirection could be further improved.