Effect of resistance exercise on insulin sensitivity of skeletal muscle

Insulin resistance(IR) is the common pathophysiological basis of many metabolic diseases. IR is characterized by decreased glucose uptake in skeletal muscle and adipose tissue, especially in skeletal muscle. Skeletal muscle is the main target tissue of glucose uptake under insulin stimulation. Glucose uptake by skeletal muscle is complex, and it is controlled by many pathways. The PI3 K/AKt/GSK-1 signaling pathway is not only the main pathway for insulin signal transduction but also an important mechanism for regulating blood glucose. From the binding of insulin to its receptors on the surface of target cells to the transportation of glucose from extracellular fluid to skeletal muscle, a series of signal transduction processes is completed, any of which potentially affects the physiological effects of insulin and leads to IR. Resistance exercise(RT) can reduce skeletal muscle IR and effectively improve blood glucose control and glycosylated hemoglobin level in patients with type 2 diabetes mellitus(T2 DM). However, the exact mechanism by which RT improves skeletal muscle IR remains unclear. Therefore, this paper discusses the above problems by tracking the progress of the literature to deepen the correlation between RT and skeletal muscle insulin sensitivity and provide further evidence for the application of exercise therapy in IR. In conclusion, RT mainly improves insulin sensitivity of skeletal muscle by increasing muscle mass, microvascular blood flow, and glucose transporter-4 expression in skeletal muscle, as well as by reducing lipid accumulation and inflammation in skeletal muscle. Thus, it is potentially useful in the prevention and treatment of T2 DM.