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- Anderson 2006 Am J Physiol Cell Physiol + (Mitochondrial dysfunction is implicated in … Mitochondrial dysfunction is implicated in a number of skeletal muscle pathologies, most notably aging-induced atrophy and loss of type II myofibers. Although oxygen-derived free radicals are thought to be a primary cause of mitochondrial dysfunction, the underlying factors governing mitochondrial superoxide production in different skeletal myofiber types is unknown. Using a novel in situ approach to measure H<sub>2</sub>O<sub>2</sub> production (indicator of superoxide formation) in permeabilized rat skeletal muscle fiber bundles, we found that mitochondrial free radical leak H<sub>2</sub>O<sub>2</sub> produced/O<sub>2</sub> consumed) is two- to threefold higher (''p'' < 0.05) in white (WG, primarily type IIB fibers) than in red (RG, type IIA) gastrocnemius or soleus (type I) myofibers during basal respiration supported by Complex I (pyruvate + malate) or Complex II (succinate) substrates. In the presence of respiratory inhibitors, maximal rates of superoxide produced at both Complex I and Complex III are markedly higher in RG and WG than in soleus muscle despite approximately 50 % less mitochondrial content in WG myofibers. Duplicate experiments conducted with +/-exogenous superoxide dismutase revealed striking differences in the topology and/or dismutation of superoxide in WG vs. soleus and RG muscle. When normalized for mitochondrial content, overall H<sub>2</sub>O<sub>2</sub> scavenging capacity is lower in RG and WG fibers, whereas glutathione peroxidase activity, which is largely responsible for H<sub>2</sub>O<sub>2</sub> removal in mitochondria, is similar in all three muscle types. These findings suggest that type II myofibers, particularly type IIB, possess unique properties that potentiate mitochondrial superoxide production and/or release, providing a potential mechanism for the heterogeneous development of mitochondrial dysfunction in skeletal muscle. superoxide production and/or release, providing a potential mechanism for the heterogeneous development of mitochondrial dysfunction in skeletal muscle.)
