The present study aimed to determine whether dietary supplementation with methanogen inhibitors during early life may lead to an imprint on the rumen microbial community and change the rumen function and performance of calves to 49-weeks of rearing. Twenty-four 4-day-old Friesian x Jersey cross calves were randomly assigned into a control and a treatment group. Treated calves were fed a combination of chloroform (CF) and 9,10-anthraquinone (AQ) in the solid diets during the first 12 weeks of rearing. Afterward, calves were grouped by treatments until week 14, and then managed as a single group on pasture. Solid diets and water were offered ad libitum. Methane measurements, and sample collections for rumen metabolite and microbial community composition were carried out at the end of weeks 2, 4, 6, 8, 10, 14, 24 and 49. Animal growth and dry matter intake (DMI) were regularly monitored over the duration of the experiment. Methane emissions decreased up to 90% whilst hydrogen emissions increased in treated compared to control calves, but only for up to 2 weeks after treatment cessation. The near complete methane inhibition did not affect calves’ DMI and growth. The acetate:propionate ratio decreased in treated compared to control calves during the first 14 weeks but was similar at weeks 24 and 49. The proportions of Methanobrevibacter and Methanosphaera decreased in treated compared to control calves during the first 14 weeks; however, at week 24 and 49 the archaea community was similar between groups. Bacterial proportions at the phylum level and the abundant bacterial genera were similar between treatment groups. In summary, methane inhibition increased hydrogen emissions, altered the methanogen community and changed the rumen metabolite profile without major effects on the bacterial community composition. This indicated that the main response of the bacterial community was not a change in composition but rather a change in metabolic pathways. Furthermore, once methane inhibition ceased the methanogen community, rumen metabolites and hydrogen emissions became similar between treatment groups, indicating that perhaps using the treatments tested in this study, it is not possible to imprint a low methane microbiota into the rumen in the solid feed of pre-weaned calves.

本研究旨在确定在生命早期添加产甲烷菌抑制剂是否可能对瘤胃微生物群落产生影响，并将犊牛的瘤胃功能和性能改变到饲养 49 周。将 24 头 4 天大的 Friesian x Jersey 交叉小牛随机分配到对照组和治疗组。在饲养的前 12 周，经过处理的小牛在固体日粮中饲喂氯仿 (CF) 和 9,10-蒽醌 (AQ) 的组合。之后，小牛按处理分组直到第 14 周，然后在牧场上作为一个单独的组进行管理。提供固体饮食和水随意. 在第 2、4、6、8、10、14、24 和 49 周结束时进行甲烷测量以及瘤胃代谢物和微生物群落组成的样品收集。实验的持续时间。与对照小牛相比，甲烷排放量减少了 90%，而氢排放量增加了，但仅在治疗停止后最多 2 周。几乎完全的甲烷抑制不影响犊牛的 DMI 和生长。在前 14 周内，与对照犊牛相比，治疗组中的醋酸盐:丙酸盐比率下降，但在第 24 周和 49 周时相似。甲烷短杆菌 和 甲烷球菌属在前 14 周内，与对照小牛相比，治疗后的小牛减少；然而，在第 24 周和第 49 周，各组之间的古细菌群落相似。处理组之间门水平的细菌比例和丰富的细菌属相似。总之，甲烷抑制增加了氢排放，改变了产甲烷菌群落并改变了瘤胃代谢物谱，而对细菌群落组成没有重大影响。这表明细菌群落的主要反应不是组成的变化，而是代谢途径的变化。此外，一旦甲烷抑制停止产甲烷菌群落，处理组之间的瘤胃代谢物和氢排放变得相似，这表明可能使用本研究中测试的处理，