Abstract

In addition to the primary symptoms arising from inflammatory processes in the joints, muscle weakness and impaired work capacity are commonly reported by patients with rheumatoid arthritis (RA). Reduced muscle strength has always been more or less synonymous with decreased muscle mass. However, our data show that muscle weakness associated with RA is not only a result of atrophic muscles. Instead, intracellular (intrinsic) muscle dysfunction appears as important factors behind arthritis-induced muscle weakness. Our data suggests that the impaired capacity to produce force is the result of free radical (reactive oxygen/nitrogen species (ROS/RNS)) signaling altering the intracellular Ca2+ release and contractile proteins (myosin and actin) inside the skeletal muscle fibers. Here our latest data on the mechanisms behind arthritis-induced skeletal muscle weakness from animal studies and patients with RA will be presented. Altered contractile function induced by the RNS peroxynitrite (ONOO-) and the prospective of using antioxidant treatment to counteract muscle weakness in inflammatory conditions will be discussed.