It is well established that peripheral insulin resistance is exacerbated by aging and sedentarism. On the other hand, long-term exercise training prevents the aging-induced decrease in insulin sensitivity. The training effects represented by improved insulin action in vivo are attributed largely to changes in muscular factors such as increased muscle volume, increased rate of blood flow in the exercising muscle, and changes in the post-insulin receptor mechanisms. However, little is known about the responses to short-term exercise training of muscular insulin signaling molecules such as insulin receptor, insulin receptor substrate-1 (IRS-1), phosphatidylinositol 3-kinase (PI 3-kinase), 3-phosphoinositidedependent protein kinase 1 (PDK-1), and Cbl. In the present study, we examined the effects of aging and short-term exercise training on the protein contents of insulin signaling molecules in rat skeletal muscle. Female Sprague-Dawley rats (7 and 27 wk old) were divided into 2 groups. One half of the rats in each group was kept sedentary (SED) and another half was trained (TR) by swimming exercise. Rats in the training group were swim-trained for 5 days. Dissection procedures to obtain gastrocnemius muscle were carried out approximately 16 h after the last bout of exercise. The contents of the gastrocnemius insulin signaling molecules were determined by Western blotting. Aging and exercise training did not affect the content of insulin receptor, PI 3-kinase, PDK-1, and Cbl, proteins in rat skeletal muscle. On the other hand, while the IRS-1 protein in sedentary rats was significantly decreased with aging (53 % at 27 wk of age relative to the abundance at 7 wk of age), it was not affected by aging in trained animals (TR-7wk: 92%, TR-27wk: 68%). These results suggest that the improvement in insulin sensitivity by training may be due, at least in part, to regulation on the IRS-1 protein content in skeletal muscle.

DESCENTE SPORTS SCIENCE Vol.25/THE DESCENTE AND ISHIMOTO MEMORIAL FOUNDATION FOR THE PROMOTION SPORTS SCIENCE