Linking Mitochondrial Function In Skeletal Muscle To Disease
Sponsored by the APS Environmental & Exercise Physiology Section

It was not so long ago that our understanding of the function of mitochondria in cells – as the site of oxidative metabolism and provider of energy – seemed to be fairly complete.  Perhaps feeling a bit underappreciated, mitochondria in recent years have begun to reveal more and more of their inner secrets and the many important ways they impact cell function.   In skeletal muscle for example, research in the field of diabetes has suggested that inherited or acquired defects in mitochondrial function may play a role in the etiology of insulin resistance and type II diabetes.  Indeed, recent studies have documented that mitochondrial content and overall electron transport chain (ETC) activity are severely depressed in skeletal muscle of obese and obese/diabetic patients.  Mitochondria also represent the primary site of superoxide anion production, the parent molecule of reactive oxygen species (ROS).  Although ROS are known to activate specific signaling pathways as well as inflict damage to lipids, protein and DNA, the mechanisms regulating superoxide formation in mitochondria remain unknown.  Lastly, mitochondria have assumed front and center stage as the initiators/mediators of programmed cell death or apoptosis.  In skeletal muscle, localized mitochondrial dysfunction within specific regions along the length of myofibers has been hypothesized to be responsible for the programmed cell death of myofibers during the aging process.  The purpose of this symposium is to provide an integrated and comprehensive update on the central role mitochondrial function in skeletal muscle may play in the etiology/pathology of disease.