Muscle-specific MicroRNAs Are Not Altered In Human Muscle Following Ingestion Of Leucine-enriched Essential Amino Acids

Abstract

Introduction: Essential amino acid (EAA) ingestion results in a significant increase in mixed muscle protein synthesis in humans. The muscle-specific microRNAs (miR-1, -133a, and -206) have been postulated to participate in the regulation of skeletal muscle size by inhibiting translation of specific target mRNAs. Our laboratory has recently shown that miR-1 expression decreased immediately following the combined anabolic stimulus of resistance exercise and EAA ingestion. PURPOSE: We hypothesized that expression of miR-1, -133a, and -206 would be decreased immediately following ingestion of leucine-enriched EAA in young healthy humans. METHODS: Five young subjects (2 men, 3 women, 31±2 yr) ingested leucine-enriched (35%) EAA (10g) following an overnight fast. Muscle biopsies were sampled before and 1 and 2h following EAA ingestion. Standard laboratory procedures were utilized to isolate RNA. This was followed by real-time PCR using commercially available kits (mirVana) and primers in order to determine the expression of miR-1, -133a, and -206. RESULTS: The expression levels of miR-1, -133a, and -206 were unaltered following EAA ingestion as compared to baseline. CONCLUSION: We conclude that the muscle-specific microRNAs (miR-1, -133a, and -206) are not associated with the acute increase in human skeletal muscle protein synthesis during the first couple of hours following essential amino acid ingestion. Therefore, it appears that the changes we detected in microRNA expression following resistance exercise and EAA ingestion were likely due to muscle contraction rather than increased amino acid availability. However, future studies are needed to determine the individual effect of resistance exercise on microRNA expression and whether increased amino acid availability post-exercise is a contributing factor. Supported by ACSM Research Endowment Grant (MJD), P30 AG-024832 (MJD) and NIH/NIAMS grant RO1 AR049877 (BBR)