Osteoarthritis (OA) is a chronic–degenerative joint disease defined by pain, joint stiffness, and a progressive loss of function with considerable impact on the quality of life. Skeletal muscle atrophy has been connected to the functional impairment caused by the OA disease. However the aetiology of muscle weakness and how it relates to OA onset and progression is somewhat unclear. In a recent study, we aimed to address OA development post injury and how these factors contributed to skeletal muscle weakness. Animal models of OA are important as they provide a versatile and widely used tool for analysing molecular mechanisms underlying the OA pathology. The surgical model of destabilization of the medial meniscus (DMM), has become a gold standard for studying the onset and progression of OA. The DMM model mimics clinical meniscal injury, a known predisposing factor for the development of human OA, and permits the study of structural and biological changes over the course of the disease. In our study, Tibialis anterior (TA) muscle function was assessed in situ at 1, 4 and 8 weeks post-surgery whereas cartilage damage and joint inflammation were assessed by histologic scoring. Acute joint injury induced by DMM surgery led to a lasting impairment in TA muscle function. This impairment in TA muscle function occurred in the absence of any deterioration in muscle morphology and was evident in the early-mid stages of DMM OA disease progression prior to the onset of severe cartilage destruction. Previous studies have demonstrated a loss of fast twitch myosin heavy chain (MyHC) isoforms in muscles of OA guinea pigs. Here we show a decrease in fast twitch SERCA1 expression in the absence of muscle fibre atrophy, which is recognized as one of the contributors to muscle weakness in OA and following joint injury.