Corticosteroids may cause myopathy of both skeletal and respiratory muscles. This is of specific clinical importance in patients with chronic obstructive pulmonary disease (COPD), who already have impaired respiratory muscle function. After treatment with fluorinated steroids, side-effects occur more frequently and are worse compared to treatment with non-fluorinated steroids. Acute myopathy and atrophy are caused by short-term high-dose corticosteroid administration, resulting in rhabdomyolysis, diffuse muscle weakness and severe dyspnoea. In contrast, chronic myopathy occurs after prolonged treatment with corticosteroids, and results in proximal muscle weakness and type IIb fibre atrophy. The pathophysiology of steroid myopathy is unknown, but reduction in protein synthesis and increased glycogen accumulation may play a major role. Animal models have demonstrated weakening of the diaphragm and a decrease in body and diaphragm mass after corticosteroid administration. In humans, a reduction in respiratory and peripheral muscle strength, an elevation of urinary creatine excretion and selective type IIb fibre atrophy may be observed. Treatment of corticosteroid-induced myopathy consists of tapering the dose of steroids or switching to non-fluorinated steroids.