The overload-induced increase in muscle mass is accompanied by protein accretion, however the initiating events are poorly understood. Regulated in Development and DNA Damage 1 (REDD1), a repressor of the mechanistic target of rapamycin in complex 1 (mTORC1), blunts the elevation in protein synthesis induced by acute muscle contractions. Therefore, this study was designed to determine whether REDD1 alters the rate of the overload-induced increase in muscle mass. Wild type (WT) and REDD1 null mice underwent unilateral functional overload (OV) of the plantaris, while the contralateral sham leg served as a control. After 3 and 5 days of OV, puromycin incorporation was used as measurement of protein synthesis. The percent increase in plantaris wet weight and protein content was greater in REDD1 null mice after 3, 5, and 10 days OV. The overload-stimulated rate of protein synthesis in the plantaris was similar between genotypes after 3 days OV, but translational capacity was lower in REDD1 null mice indicating elevated translational efficiency. This was likely due to elevated absolute mTORC1 signaling (phosphorylation of p70S6K1 (Thr389) and 4E-BP1 (Ser65)). By 5 days of OV, the rate of protein synthesis in REDD1 null mice was lower than WT mice with no difference in absolute mTORC1 signaling. Additionally, markers of autophagy (LC3II/I ratio and p62 protein) were decreased to a greater absolute extent after 3 days OV in REDD1 null mice. These data suggest that loss of REDD1 augments the rate of the overload-induced increase in muscle mass by altering multiple protein balance pathways.