Glucocorticoids cause insulin resistance in skeletal muscle. The aims of the present study were to investigate the effects of contraction on glucose uptake, insulin signaling, and regulation of glycogen synthesis in skeletal muscles from rats treated with the glucocorticoid analogue dexamethasone (1 mg ^. kg^{-1 .} day^-1 i^.p. for 12 days). Insulin resistance in dexamethasone-treated rats was confirmed by reduced insulin-stimulated glucose uptake ( 35 %), glycogen synthesis ( 70 %), glycogen synthase activation ( 80 %), and protein kinase B (PKB) Ser⁴⁷³ phosphorylation ( 40 %). Chronic dexamethasone treatment did not impair glucose uptake during contraction in soleus or epitrochlearis. In epitrochlearis (but not in soleus) the presence of insulin during contraction enhanced glucose uptake to similar level in control and dexamethasone-treated rats. Contraction also increased glycogen synthase fractional activity and dephosphorylated glycogen synthase at Ser⁶⁴⁵, Ser⁶⁴⁹, Ser⁶⁵³, Ser⁶⁵⁷ normally in muscles from dexamethasone treated rats. After contraction, insulin-stimulated glycogen synthesis was completely restored in epitrochlearis and improved in soleus from dexamethasone-treated rats. Contraction did not increase insulin-stimulated PKB Ser⁴⁷³ or glycogen synthase-3 (GSK-3) phosphorylation. Instead, contraction increased GSK-3 Ser⁹ phosphorylation in epitrochlearis (but not in soleus) in muscles from control and dexamethasone-treated rats. In conclusion, contraction stimulates glucose uptake normally in dexamethasone-induced insulin resistant muscles. After contraction, insulins ability to stimulate glycogen synthesis was completely restored in epitrochlearis and improved in soleus from dexamethasone-treated rats.