The obese Zucker rat (OZR) is a model of metabolic syndrome, which has lower skeletal muscle size compared to the lean Zucker rat (LZR). Because satellite cells are essential for postnatal muscle growth, this study was designed to determine if reduced satellite cell proliferation contributes to the reduction of skeletal mass in the OZR compared with the LZR. Satellite cell proliferation, as determined by incorporation of a constant release of 5-bromo-2-deoxyuridine, was significantly attenuated in control soleus and plantaris muscles of the OZR compared to the LZR. To determine whether this attenuation of satellite cell activity could be rescued in OZR muscles, the soleus and the gastrocnemius muscles were denervated, placing a compensatory load on the plantaris muscle. There was a ~25% and ~30% increase in the plantaris muscle wet weight compared to the contra-lateral control muscle in the LZR and the OZR, respectively after 21-days of loading. The number of BrdU positive nuclei increased similarly in loaded plantaris muscles from LZR and OZR. Myogenin, MyoD and Akt protein expression, were lower in the control muscles of OZR compared to LZR, but they were all elevated to similar levels in the loaded plantaris muscles of OZR and LZR. These data indicate that metabolic syndrome may reduce satellite cell proliferation and this may be a factor that contributes to the reduced mass in control muscles of OZR; however, satellite cell proliferation can be restored with compensatory loading in OZR.