Research shows that mitochondrial function and insulin resistance go hand in hand. As mitochondrial oxidative capacity is decreased, individuals are more likely to become insulin resistant and to develop type 2 diabetes. Exercise is known to increase mitochondrial oxidative capacity, helping these individuals enhance their insulin sensitivity. There are many genetic risk factors that are known to predispose individuals to type 2 diabetes and other metabolic disorders, some of which may limit the beneficial effects of exercise. I hypothesized that Single Nucleotide Polymorphisms (SNPs) associated with high BMI and type 2 diabetes and located in or near genes that regulate mitochondrial function will mediate the insulin sensitizing effects of exercise.