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Mitochondrial Enzyme Defects in Normal and Low-Frequency-Stimulated Muscles of Young and Aging Rats

Dejan korjanc^a, Georg Dünstl^a and Dirk Pette^a

^a Department of Biology, University of Konstanz, Germany

Dirk Pette, Department of Biology, University of Konstanz, D-78457 Konstanz, Germany E-mail: dirk.pette{at}uni-konstanz.de.

Decision Editor: John A. Faulkner, PhD

The age-related increase in cytochrome c-oxidase-deficient (COX^-) muscle fibers has been suggested to be positively correlated with mitochondrial content (Müller-Höcker, Brain Pathol. 1992; 2:149–158). As a way to test this relationship, tibialis anterior muscles of young (15 weeks) and aging (101 weeks) Brown Norway rats were exposed to chronic low-frequency stimulation (CLFS) for 50 days, an experimental protocol known to induce marked increases in mitochondrial content. CLFS produced elevated activity levels of COX and succinate dehydrogenase (SDH) in most fibers of young and aging rats. Some fibers low or deficient in COX and a few fibers low or deficient both in COX and SDH (COX^-/SDH^-) were detected in unstimulated muscles of young and, more frequently, aging rats. According to their myosin complement, these fibers were immunohistochemically identified as type I fibers. CLFS increased their number in young muscles, but reduced it in aging muscles. Stimulated aging muscles contained some very small, most likely newly formed COX⁺ and SDH⁺ type I fibers. Thus, the fraction of COX^- fibers was reduced in aging muscle by enhanced contractile activity.

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