In addition, even one exercise session of moderate intensity can lower blood glucose levels in people with diabetes, and can effect the breakdown and synthesis of glycogen in muscles. Exercise also has other important effects on skeletal muscles, including increasing the rate of gene transcription and increasing the ability to synthesize muscle proteins. These changes lead to increased function of the muscle, and probably are part of the reason why exercise is so beneficial for one's health. Despite these important responses to exercise, very little is known about the underlying molecular processes that enable exercise to have these effects. The Goodyear lab is working to define the cellular signaling mechanisms that occur within individual cells during exercise and muscle contraction.
Exercise has insulin-like effects in that it stimulates skeletal muscle uptake of glucose.
Dr. Goodyear and colleagues have shown that the effect of both exercise and insulin results from the movement of glucose transporters to the surface of the muscle cells. Despite these similar effects, Dr. Goodyear's group has determined that insulin causes glucose transporters to move via a signaling pathway that is distinctly different from the pathway which occurs when exercise is providing the stimulus. In cultured cells, the MAP kinase pathways are thought to be critical in regulating numerous cell processes, including gene transcription, protein synthesis and glycogen metabolism. Dr. Goodyear has shown that exercise stimulates all three of the MAP kinase pathways, suggesting that signaling through these cascades may mediate changes in skeletal muscle growth and metabolism that occur with exercise. Phosphatidylinositol 3-kinase Activity in Rat Skeletal Muscle.