Type 2 diabetes is characterized by a decreased ability of insulin to facilitate glucose uptake into insulin sensitive tissue, i.e., skeletal muscle. The mechanism behind this is at the moment unresolved. It has been suggested that increased amount of lipids inside the skeletal muscle (intramuscular triglyceride, diacylglycerol and ceramides) will impair insulin action in skeletal muscle, but data are not consistent in the human literature. It has also been hypothesized that the impaired insulin sensitivity is due to a dysfunction in the mitochondria resulting in an impaired ability to oxidize lipids, but the majority of the literature is not supporting this hypothesis. Recently it has been suggested that the production of reactive oxygen species play an essential role in skeletal muscle insulin sensitivity. It is well accepted that physical activity (endurance, strength and high intensity training) improves insulin sensitivity in healthy humans and in patients with type 2 diabetes. Whether patients with type 2 diabetes have the same beneficial effects (same improvement) as control subjects, when it comes to regular physical activity in regard to mitochondrial function, is not established in the literature. This review will focus only on the effect of physical activity on skeletal muscle (mitochondrial function) in patients with type 2 diabetes.
World Journal of Diabetes, 2014, Vol 5, Issue 4, p. 482-92