Impaired fasting glucose (IFG) blunts the reversal of impaired glucose tolerance (IGT) after exercise training. Metabolic inflexibility has been implicated in the etiology of insulin resistance, however, the efficacy of exercise on peripheral and hepatic insulin sensitivity or substrate utilization in adults with IFG, IGT or IFG+IGT is unknown. Twenty-four older (66.7±0.8yr) obese (34.2±0.9kg/m²) adults were categorized as IFG (n=8), IGT (n=8), or IFG+IGT (n=8) according to a 75-gram oral glucose tolerance test (OGTT). Subjects underwent 12-weeks of exercise (60 min/d for 5 d/wk at ~85% HR_max) and were instructed to maintain a eucaloric diet. A euglycemic-hyperinsulinemic clamp (40 mU/m²/min) with [6,6-²H]-glucose was used to determine peripheral and hepatic insulin sensitivity. Non-oxidative glucose disposal and metabolic flexibility (insulin-stimulated respiratory quotient [RQ] minus fasting RQ) were also assessed. Glucose incremental area under the curve was calculated from the OGTT (iAUC_OGTT). Exercise increased clamp-derived peripheral and hepatic insulin sensitivity more in adults with IFG or IGT alone than IFG+IGT (P<0.05). Exercise reduced glucose iAUC_OGTT in IGT only (P<0.05), and the decrease in glucose iAUC_OGTT was inversely correlated with the increase in peripheral, but not hepatic, insulin sensitivity (P<0.01). Increased clamp-derived peripheral insulin sensitivity was also correlated with enhanced metabolic flexibility, reduced fasting RQ, and higher non-oxidative glucose disposal (P<0.05). Adults with IFG+IGT had smaller gains in clamp-derived peripheral insulin sensitivity and metabolic flexibility, which was related to blunted improvements in post-prandial glucose. Further work is required to assess the molecular mechanism(s) by which chronic hyperglycemia modifies insulin sensitivity following exercise training.