In Sprague-Dawley rats, daily intraperitoneal injections of pargyline, a monoamine oxidase inhibitor, produces a myopathy with grouped lesions, excess connective tissue, and sarcoplasmic fluorescence by the Falck-Hillarp technique. The myopathy is prevented by prior denervation and appears to be slightly accentuated by prior aortic ligation. A possible mechanism is thought to be an intraneuronal or intrafibrillar, or both, accumulation of catecholamines, resulting in the release of excessive acetylcholine or other substances at the myoneural junction. The experiments support the possibility of a relationship between Duchenne muscular dystrophy and biogenic arnine metabolism by showing that pargyline produces a myopathy with the histopathologic: characteristics of Duchenne muscular dystrophy.