Duchenne’s Muscular Dystrophy (DMD) is a recessive hereditary myopathy linked to the chromosome X, caused by a mutation in the dystrophin gene, which strengthens and stabilizes the sarcolemma during the stress of muscular contraction and, when absent, the sarcollema ruptures and allows calcium to enter, which causes the muscle fiber to necrotize. The object of the present study was to perform the morphologic analysis of the anterior tibial and the gastrocnemius muscles with (w/pa) or without (n/pa) physical activity for five weeks. We used 72 mice, divided in 12 experimental groups – 6 of them mdx and 6 control groups (C57/10J) aged 4, 7, and 10 weeks. The samples were collected, processed and stained with hematoxylin-eosin. They were analyzed by light microscopy, selected and photomicrographed. On the cross-sections of control animals aged 4, 7 and 10 weeks w/pa and n/pa, polygonal muscle fibers of many different sizes, ellipse-shaped and with several peripheral nucleuses were observed. In the mdx mice w/pa aged 4, 7 and 10 weeks, the muscle fibers showed different shapes, sizes and stain affinities, rounded edges, anuclear or centered nucleuses; hyalines and myofibrillas were highly contracted. Muscular regeneration and nectrotic areas with inflammatory infiltrates were identified in the mdx animals aged 4, 7 and 10 weeks w/pa, as well as in animals aged 10 weeks n/pa. With the progression of the disease in the animals submitted to physical activity, there was evidence of failure in the regeneration and muscular degeneration, intensified and characterized by the gradual replacement of the striated skeletal muscle tissue by fibroadipose connective tissue.