Evaluation of hindgut buffers under high-starch diet conditions in lactating Holstein cows

Buffering of the rumen environment can alleviate some of the negative effects of acidosis, and the same may hold true in the hindgut. The objective of this study was to evaluate the potential for 2 dietary buffers at different dosages to mitigate excessive intestinal fermentation and systemic inflammation due to hindgut acidosis. Ten ruminally cannulated lactating cows were randomly assigned to a replicated 5 × 5 Latin square with a 7-d adaptation period, 14-d experimental periods, and 7-d washout periods between each experimental period. Daily treatments during experimental periods were abomasal infusion of water without feeding supplemental buffer (control; CON), abomasal infusion of corn starch without feeding supplemental buffer (IS), or abomasal infusion of starch with 150 g/d of buffer A (calcium carbonate, magnesium oxide, and crushed oyster shell blend; T1), 300 g/d of buffer A (T2), or 150 g/d of buffer B (magnesium oxide; T3). Daily abomasal starch infusions were 2 g/kg BW in period 1 and 4 g/kg BW in periods 2 to 5, and were split into 2 bolus infusions provided every 12 h during the 14-d experimental periods. Cows were fed a 30.9% starch TMR (on a DM basis), and 1 cow was removed from the study between periods 1 and 2. Although not intended, the high-starch TMR seemed to induce SARA, as evidenced by mean rumen pH of 5.8 to 6.0. Compared with CON, abomasal corn starch addition decreased fecal pH (6.80 vs. 6.37) and apparent total-tract starch digestibility (95.6% vs. 86.1%). Starch infusion did not increase serum acute phase proteins, and effects on fecal LPS and total fecal VFA concentrations were modest, suggesting that infused starch was only partially digested. Buffer additions increased fecal pH as expected (mean of 6.76 for T1, T2, and T3, respectively), but also increased fecal acetate (64.0 mM for IS compared with a mean of 74.5 mM for T1, T2, and T3, respectively) and total VFA concentration (81.5 mM for IS compared with a mean of 100.1 mM for T1, T2, and T3, respectively), suggesting that they may have increased hindgut fermentation. Additionally, the T2 treatment may have had an inflammatory effect, as evidenced by increased serum amyloid A compared with IS (71.5 vs. 22.0 µM, respectively). Despite increased fecal pH, the inclusion of different buffer formulations in a high-starch diet seemed to increase hindgut fermentation, as evidenced by increased VFA concentration. The buffers employed in this experiment did not alleviate the negative effects of abomasal starch infusions and, in the case of T2, may have presented a challenge.