Voluntary exercise induces structural remodeling in the hearts of dystrophin-deficient mice.

In this exploratory study, we test the hypothesis that voluntary exercise affects the progression of dystrophic changes in the left ventricle of the heart. Wild-type (C57BL/10ScSn) and dystrophin-deficient (mdx) mice, aged 7 weeks, were divided into sedentary and exercise-treated groups and tested for differences in cardiac histomorphometry. Exercised mdx mice were found to exhibit significantly enlarged ventricles and thinner lateral ventricular walls than sedentary mdx mice (P < 0.05). Trichrome staining indicated the presence of fibrotic lesions in the left ventricular myocardium in 20% of the exercised mdx group. Fibrotic lesions were not found in control or sedentary mdx mice. No histomorphometric differences were found between treatment groups in wild-type mice. Our findings suggest voluntary exercise may accelerate the progression of ventricular dilation and fibrosis in young mdx mice. The effects of exercise on cardiac remodeling should be considered during the treatment of cardiac disease in dystrophin-deficient patients.

The chondrogenic response to exercise in the proximal femur of normal and mdx mice.

BACKGROUND: Submaximal exercise is used in the management of muscular dystrophy. The effects of mechanical stimulation on skeletal development are well understood, although its effects on cartilage growth have yet to be investigated in the dystrophic condition. The objective of this study was to investigate the chondrogenic response to voluntary exercise in dystrophin-deficient mice. METHODS: Control and dystrophin-deficient (mdx) mice were divided into sedentary and exercise-treated groups and tested for chondral histomorphometric differences at the proximal femur. RESULTS: Control mice ran 7 km/week further than mdx mice on average, but this difference was not statistically significant (P > 0.05). However, exercised control mice exhibited significantly enlarged femur head diameter, articular cartilage thickness, articular cartilage tissue area, and area of calcified cartilage relative to sedentary controls and exercised mdx mice (P < 0.05). No differences were found between other treatment groups. CONCLUSIONS: Mdx mice exhibit a reduced chondrogenic response to increased mechanical stimulation relative to controls. However, no significant reduction in articular dimensions was found, indicating loss of chondral tissue may not be a clinical concern with dystrophinopathy.