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Skeletal muscle catabolism in amyotrophic lateral sclerosis and chronic spinal muscular atrophy

Muscular Dystrophy Association (Dr. Corbett), and the Department of Neurology, Medicine, and Pediatrics (Dr. Griggs), University of Rochester School of Medicine and Dentistry, and the Departments of Neurology and Pediatrics and the Center for Brain Research (Dr. Moxley), University of Rochester School of Medicine and Dentistry, Rochester, NY.

ALS and chronic spinal muscular atrophy are characterized by wasting of skeletal muscle, suggesting accelerated catabolism or reduced synthesis of muscle protein. We studied seven patients with ALS and three with chronic spinal muscular atrophy using 24-hour urinary 3-methylhistidine excretion as a measure of the rate of muscle catabolism and 24-hour urinary creatinine excretion as an index of muscle mass. The ratio of 3-methylhistidine to creatinine excretion was significantly and similarly higher in both groups of patients than in controls (p < 0.0005), implying a state of accelerated skeletal muscle protein catabolism in these diseases.

Address correspondence and reprint requests to Dr. Moxley, Department of Neurology. University of Rochester School of Medicine and Dentistry. 601 Elmwood Avenue, P.O. Box 673, Rochester. NY 14642.

This research was supported by research grants from the Muscular Dystrophy Association. Inc., the National ALS Foundation, the Waasdorp Foundation, US Public Health Service Grant No. RR 00044 from the Division of Research Resources of the National Institutes of Health, and by grant from the National Institute of Arthritis, Metabolism, and Digestive Diseases No. AM 22048.

Accepted for publication October 12, 1981.

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