Jill M. Coenen-Schimke

TL;DR: It is demonstrated that age-related muscle mitochondrial dysfunction is related to reduced mtDNA and muscle functional changes that are common in the elderly, supporting the oxidative damage theory of aging.

TL;DR: The muscle mitochondrial response to 4 months of aerobic exercise training was similar in all age-groups, although the older people did not have an improvement in insulin sensitivity, and insulin sensitivity improved in younger people but not in middle-aged or older groups.

TL;DR: The current data supports that muscle mitochondrial dysfunction in type 2 diabetes is not an intrinsic defect, but instead a functional defect related to impaired response to insulin.

TL;DR: Despite being more insulin resistant, diabetic Indians had similar muscle OXPHOS capacity as nondiabetic Indians, demonstrating that diabetes per se does not cause mitochondrial dysfunction.

TL;DR: The hypothesis that MHC isoform protein composition and mRNA abundance would favor a fast-to-slow isoform shift with aging and in response to endurance exercise training is tested and suggests that the altered expression of M HC isoforms with aging is transcriptionally regulated.