The aim of this research was to investigate myogenic (i.e. growth) and proteolytic (i.e. breakdown) gene expression (GE) in skeletal muscle of young and old women. Myogenic (MyoD, MRF4, Myf5, myogenin, myostatin) and proteolytic (Atrogin-1, MuRF-1, FOXO3A) genes were examined in the basal state and after resistance exercise (RE). Six old women (OW: 85 ± 1 y) and eight young women (YW: 23 ± 1) performed 3 x 10 knee extensions at 70% of 1-repetition-maximum. Muscle biopsies were obtained from the vastus lateralis (i.e. thigh) before and 4 hours after RE.In the basal state, OW expressed higher levels (p<0.05) of MyoD, MRF4, myf5, myogenin, myostatin, FOXO3A and MuRF-1 compared to YW. Fiber type specific GE analysis in the OW showed that slow-twitch muscle fibers (MHC I) expressed higher levels (p<0.05) of myogenin and Atrogin-1, compared to fast-twitch (MHC Ila) fibers. In response to RE both YW and OW increased (p<0.05) mRNA levels of MyoD and MRF4, while a decrease (p<0.05) was observed for myostatin. MuRF-1 mRNA increased (p<0.05) in both age groups, while there was an age-specific induction (p<0.05) of Atrogin-1 after RE. Fiber type specific GE after RE in the old women showed that MHC Ila fibers did not induce myogenic GE. Robust increases (p<0.05) in MyoD, MRF4, and myogenin were only observed in the MHC I fibers. Both fiber types decreased (p<0.05) myostatin, and increased Atrogin-1 with RE. MuRF-1 mRNA levels increased specifically in MHC Ila fibers. In summary, skeletal muscle of OW expresses higher levels of mRNA for most selected genes at rest. With RE, aging skeletal muscle retains the ability to induce myogenic GE, although exclusive to MHC I fibers. After RE, proteolytic GE induction is greater in OW and most pronounced in MHC Ila fibers. Collectively, these data suggest that an imbalance exists in the regulation of the myogenic and proteolytic program in aging skeletal muscle. This research also provides the first evidence of intrinsic molecular differences between MHC I and MHC Ila fibers in OW, and may, in part, explain the MHC Ila atrophy apparent in sarcopenic muscle. / School of Physical Education, Sport, and Exercise Science