Why the study?
Does voluntary exercise accelerate structural remodeling in the hearts of dystrophin-deficient mice?
Does voluntary exercise accelerate structural remodeling in the hearts of dystrophin-deficient mice?
Voluntary exercise may accelerate the progression of ventricular dilation and fibrosis in young dystrophin-deficient mice, suggesting caution in exercise recommendations for patients with dystrophin deficiency.
Voluntary exercise may accelerate adverse remodeling in mdx mice; leaves open effects on human dystrophin-deficient cardiomyopathy and warrants prospective study.
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.
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Costas et al. (2010) studied this question.
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