This 2013 review assesses the links between exercise, weight loss, and the function of skeletal muscle mitochondria. As outlined in a previous post on CrossFit.com, defects in skeletal muscle mitochondrial function are associated with (and may in fact contribute to the development of) insulin resistance observed in individuals suffering from obesity and Type 2 diabetes. In particular, the paper proposes a pathological pathway through which obesity and improper lipid regulation lead to fat accumulation within the liver and skeletal muscle. This fat accumulation then disrupts mitochondrial function in these tissues, thereby affecting their ability to process energetic fuels (i.e., lipids and glucose).
The authors provide evidence that these mitochondrial defects are reversible with weight loss and especially exercise training, which leads to substantial increases in skeletal muscle mitochondrial function and content in obese and diabetic subjects. These mitochondrial improvements often correlate with improvements in insulin sensitivity, though it is not precisely known whether changes in mitochondrial status directly cause changes in insulin sensitivity or are correlated through other yet undetermined factors.
The authors note that aging, like obesity and diabetes, is associated with impaired energy metabolism and decreased muscular mitochondria content and function. Exercise in the elderly has been shown to improve mitochondrial function, though the impact of these improvements on insulin sensitivity is not discussed.
In sum, the authors conclude the mitochondrial dysfunction frequently present in obese and diabetic individuals can be consistently reversed at least in part through exercise, though the implications for insulin resistance remain uncertain.