Approximately 66% of the patients with rheumatoid arthritis (RA) have significant loss of cell mass (rheumatoid cachexia), mainly of skeletal muscle (rheumatoid sarcopenia). Sarcopenia is defined as muscle wasting associated with functional impairment. Patients with RA possess significant reduction in muscle strength, caused by muscle protein wasting, and loss of functionality. Various conditions leading to muscle wasting involve different pathways of intracellular signaling that trigger: (i) programmed cell death (apoptosis); (ii) increased protein degradation through autophagy, calcium-dependent proteases (calpains and caspases), and proteasome system; (iii) decreased satellite cell activation, responsible for muscle regeneration. This article aimed at reviewing these general mechanisms of sarcopenia and their involvement in RA. Greater knowledge of these mechanisms may lead to the development of innovative therapies to this important comorbidity.