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From the Department of Physiology,* The University of Melbourne, Victoria; and the Department of Medicine, Austin and Repatriation Medical Centre, The University of Melbourne, Heidelberg, Victoria, Australia
Limited knowledge exists regarding the efficacy of insulin-like growth factor I (IGF-I) administration as a therapeutic intervention for muscular dystrophies, although findings from other muscle pathology models suggest clinical potential. The diaphragm muscles of mdx mice (a model for Duchenne muscular dystrophy) were examined after 8 weeks of IGF-I administration (1 mg/kg s.c.) to test the hypothesis that IGF-I would improve the functional properties of dystrophic skeletal muscles. Force per cross-sectional area was 
49% greater in the muscles of treated mdx mice (149.6 ± 9.6 kN/m2) compared with untreated mice (100.1 ± 4.6 kN/m2, P < 0.05), and maintenance of force over repeated maximal contraction was enhanced 30% in muscles of treated mice (P < 0.05). Diaphragm muscles from treated mice comprised fibers with 36% elevated activity of the oxidative enzyme succinate dehydrogenase, and 23% reduction in the proportion of fast IId/x muscle fibers with concomitant increase in the proportion of type IIa fibers compared with untreated mice (P < 0.05). The data demonstrate that IGF-I administration can enhance the fatigue resistance of respiratory muscles in an animal model of dystrophin deficiency, in conjunction with enhancing energenic enzyme activity. As respiratory function is a mortality predictor in Duchenne muscular dystrophy patients, further evaluation of IGF-I intervention is recommended.
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