Recent findings indicate that elevated levels of glucocorticoids (GC), governed by the expression of 11-Hydroxysteroid dehydrogenase type 1 (11-HSD1) and glucocorticoid receptors (GR), in visceral adipose tissue and skeletal muscle lead to increased insulin resistance and the metabolic syndrome. Paradoxically, evidence indicates that aerobic exercise attenuates the development of the metabolic syndrome even though it stimulates acute increases in circulating GC levels. To investigate the hypothesis that training alters peripheral GC action to maintain insulin sensitivity, young male hamsters were randomly divided into sedentary (S) and trained (T) groups (n= 8 in each). Group T had 24hr access to running wheels over four weeks of study. In muscle, T hamsters had lower 11-HSD1 protein expression (19.2±1.40 vs 22.2±0.96 OD, P<0.05), similar 11-HSD1 enzyme activity (0.9±0.27% vs 1.1±0.26) and lower GR protein expression (9.7±1.86 vs 15.1±1.78 OD, P<0.01) than S hamsters. In liver, 11-HSD1 protein expression tended to be lower in T compared with S (19.2±0.56 vs 21.4±1.05, P= 0.07), while both enzyme activity and GR protein expression were similar. In contrast, visceral adipose tissue contained ~2.7-fold higher 11-HSD1 enzyme activity in T compared with S (12.9±3.3 vs 4.8±1.5 % conversion, P<0.05), but was considerably smaller in mass (0.24±0.02 vs 0.71±0.06 g). Thus, the intracellular adaptation of GC regulators to exercise is tissue specific resulting in decreases in GC action in skeletal muscle and increases in action in visceral fat. These adaptations may have important implications in explaining the protective effects of aerobic exercise on insulin resistance and other symptoms of the metabolic syndrome.