A single exercise bout stimulates skeletal muscle glucose transport (GT) in the absence or presence of insulin. It has been suggested that the Kallikrein-Kinin System (KKS) may contribute to exercise effects on both insulin-independent and insulin-dependent glucose transport. Plasma kininogen, a key KKS component, is a protein substrate for the enzyme kallikrein and the source of the peptide bradykinin. PURPOSE:: To determine if the post-exercise (PEX) increase in insulin-dependent or insulin-independent GT is reduced in rats deficient in plasma kininogen vs. normal rats. METHODS:: Male Brown Norway (BN) and Brown Norway Katholiek (BNK; plasma kininogen deficient) rats were studied. BN and BNK rats were assigned to exercise (4 × 30 minute swim) or sedentary (SED) groups. Rats were anesthetized immediately (0hPEX) or 3 hours (3hPEX) after exercise. For 0hPEX and 0hSED rats, one epitrochlearis muscle per rat was used for AMPK phosphorylation and muscle glycogen analyses. The contralateral muscle was incubated with [H]-3-O-methylglucose (3MG) for GT assay. For 3hPEX and 3hSED rats, one muscle from each rat was incubated without insulin, and the contralateral muscle was incubated with 60µU/ml insulin and both muscles were incubated with 3MG for GT measurement. RESULTS:: For 0hPEX vs. 0hSED, both BN and BNK rats had greater insulin-independent GT and AMPK phosphorylation with reduced glycogen post-exercise. No genotype effects were found 0hPEX. There was a significant main effect of exercise (3hPEX > 3hSED) and no interaction between exercise and genotype for basal or insulin-stimulated GT. CONCLUSION:: Plasma kininogen deficiency did not alter insulin-independent GT, AMPK phosphorylation or glycogen depletion 0hPEX or insulin-dependent GT 3hPEX suggesting that normal plasma kininogen is not essential for these important exercise effects.