Effects of supplementing rumen-protected niacin on fiber composition and metabolism of skeletal muscle in dairy cows during early lactation.

Nicotinic acid (NA) has been shown to induce muscle fiber switching toward oxidative type I fibers and a muscle metabolic phenotype that favors fatty acid (FA) utilization in growing rats, pigs, and lambs. The hypothesis of the present study was that supplementation of NA in cows during the periparturient phase also induces muscle fiber switching from type II to type I fibers in skeletal muscle and increases the capacity of the muscle to use free FA, which may help to reduce nonesterified fatty acid (NEFA) flow to the liver, liver triglyceride (TG) accumulation, and ketogenesis. Thirty multiparous Holstein dairy cows were allocated to 2 groups and fed a total mixed ration without (control group) or with ∼55 g of rumen-protected NA per cow per day (NA group) from 21 d before expected calving until 3 wk postpartum (p.p.). Blood samples were collected on d -21, -14, -7, 7, 14, 21, 35, and 63 relative to parturition for analysis of TG, NEFA, and β-hydroxybutyrate. Muscle and liver biopsies were collected on d 7 and 21 for gene expression analysis and to determine muscle fiber composition in the musculus semitendinosus, semimembranosus, and longissimus lumborum by immunohistochemistry, and liver TG concentrations. Supplementation of NA did not affect the proportions of type I (oxidative) or the type II:type I ratio in the 3 muscles considered. A slight shift from glycolytic IIx fibers toward oxidative-glycolytic fast-twitch IIa fibers was found in the semitendinosus, and a tendency in the longissimus lumborum, but not in the semimembranosus. The transcript levels of the genes encoding the muscle fiber type isoforms and involved in FA uptake and oxidation, carnitine transport, tricarboxylic acid cycle, oxidative phosphorylation, and glucose utilization were largely unaffected by NA supplementation in all 3 muscles. Supplementation of NA had no effect on plasma TG and NEFA concentrations, liver TG concentrations, and hepatic expression of genes involved in hepatic FA utilization and lipogenesis. However, it reduced plasma β-hydroxybutyrate concentrations in wk 2 and 3 p.p. by 18 and 26% and reduced hepatic gene expression of fibroblast growth factor 21, a stress hormone involved in the regulation of ketogenesis, by 74 and 56%. In conclusion, a high dosage of rumen-protected NA reduced plasma β-hydroxybutyrate concentrations in cows during early lactation, but failed to cause an alteration in muscle fiber composition and muscle metabolic phenotype.