Skeletal muscle insulin resistance is a hallmark feature of type 2 diabetes, and improvement of insulin action in this tissue is likely to have favorable effects on glycemic control for individuals with diabetes. Aerobic exercise training, which ischaracterized by a large number of contractions (often many thousand) performed with relatively low force development, has been studied extensively and is well recognized for its beneficial effects on skeletal muscle glucose metabolism. In contrast, the effects of resistance training, which typically consists of a small number of contractions (often fewer than 10–20) with relatively high force development on skeletal muscle glucose metabolism has not received as much attention. The conventional thinking has been that these types of training induce very different adaptations, but both types of training can improve insulin action and glucoregulation, although it is not clear if these methods of training achieve this same outcome by identical mechanisms. A body of literature exists indicating that resistance training can improve whole body carbohydrate metabolism and insulin action (i.e., activation of the insulin signaling cascade and glucose transporter system), and it has been suggested that these improvements are the result of increases in lean body mass. Miller et al. (9) evaluated the effects of strength training in young males after a 10-wk resistance training program and observed, posttraining compared with pretraining, that the glucose response during an oral glucose tolerance test was not altered, but that less insulin was required to achieve the same effect on plasma glucose concentration, suggesting that insulin sensitivity was improved. These investigators also reported that the decreased insulin response after the resistance training program was correlated (r = 0.89) with increased lean body mass, leading to the conclusion that because muscle mass was greater and because skeletal muscle is an important site for insulin-stimulated glucose disposal, that the greater muscle mass would be able to clear a greater amount of blood glucose. The high correlation between changes in lean body mass (which is assumed to be muscle) and the change in insulin during an oral glucose tolerance test sometimes has been misinterpreted to mean that the effects of resistance training on insulin sensitivity are largely or entirely attributable to an increase in muscle mass. What is assumed is that qualitative changes in muscle are irrelevant for the improved insulin action with resistance exercise training. However, a high correlation does not necessarily prove that a cause-and-effect relationship exists. It has been shown that the magnitude of increased insulin-stimulated glucose disposal outstrips the magnitude of changes in muscle mass found with typical resistance-training protocols (8), which argues strongly for changes in the quality of the muscle (as opposed solely to quantity of muscle) being important for improving skeletal muscle insulin sensitivity. The question, then, is what are the changes in the quality of the muscle that are important for enhancing insulin sensitivity in response to resistance exercise training?