Defects in mitochondrial ATP synthesis in dystrophin-deficient mdx skeletal muscles may be caused by complex I insufficiency.

There was a strong trend toward increased CS total activity of the diaphragm compared to TA in both control and mdx muscle (20%; p = 0.07), however there were no significant differences in any of the other CS measures between muscles (CS before , CS after and CS before :CS after all p >0.05).

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While CS total activity was unchanged in dystrophic mitochondria compared to controls in both TA and diaphragm, thus indicating comparable CS expression and mitochondrial content, it was interesting to observe highly significant reductions in the absolute (CS after ) and functional CS activity (CS before ) of extracted MS.

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