Diminished force production and mitochondrial respiratory deficits are strain-dependent myopathies of subacute limb ischemia

Skeletal muscle morphology and function are key predictors of clinical manifestation and outcomes in peripheral arterial disease. Our findings show that genetic background is a critical determinant of muscle functional deficits and mitochondrial respiration. Because of the range of peripheral arterial disease manifestations, BALB/c mice provide a useful model for studying the role of muscle and mitochondrial respiratory functional abnormalities in determining morbidity and mortality outcomes in genetically susceptible patients. Novel therapies that directly target the muscle tissue response to limb ischemia could be used alone or in conjunction with current revascularization therapies to reduce morbidity and mortality outcomes in claudicants or patients with critical limb ischemia.