Muscle wasting is observed in numerous chronic diseases as well as during an acute illness or inflammatory insult, leading to a significant decline in function and increased mortality. Wasting results from an imbalance of protein synthesis and degradation with microRNAs (miRNAs) a key regulator, controlling post-transcriptional gene expression. miRNAs 424-5p, 542-3p and 542-5p are raised in patients who waste and their targets have been established. Furthermore, miR-675 and its’ host gene H19 are also implicated. This thesis explores the in vitro and in vivo use of locked nucleic acid (LNA) and 2’-O-methyl phosphorothioate (2’OM) oligonucleotides to block the action of miRNAs 322-5p (murine 424-5p), 542-3p, and 542-5p, as well as to further establish the role of miR-675 and H19. Both the LNAs and 2’OMs successfully blocked the action of their target miRNAs in C2C12 mouse myoblasts, restoring miRNA target gene expression and increasing protein synthesis. The oligos were overexpressed in the tibialis anterior (TA) of mice, with a control oligo in the opposite TA, in a model of acute muscle wasting using elderly mice which were subsequently infected with Respiratory Syncytial Virus (RSV). Whilst the LNA to miR-322-5p appeared to be toxic, with high uptake leading to smaller muscles, the 2’OM against miR-322-5p enhanced muscle fibre size by increasing expression of the known miRNA targets, UBTF and POLR1A. An LNA to block the sequestration of H19 and the Lethal (Let)-7 miRNAs resulted in a decrease in the levels of inflammatory cytokines and muscle transcription factors MEF2C and NFATc3 in vitro and supressed the inflammatory response in RSV infected mice. Over expression of miR-675-3p and -5p in vitro also knocked down the expression of MEF2C, implying this may be a novel target. The data supports the development of therapies aimed at targeting miRNAs implicated in muscle wasting.