Oxidative stress is associated with muscle fatigue and weakness in skeletal muscle of ischemic heart disease patients. Recently, it was found that endurance training elevates protective heat shock proteins and antioxidant enzymes in skeletal muscle in healthy subjects and antioxidant enzymes in heart failure patients. However, it is unknown whether coronary ischemia and mild infarct without heart failure contributes to impairment of stress proteins, and if exercise training reverses those effects. We tested the hypothesis that exercise training would reverse alterations in muscle TNF-, oxidative stress, HSP70, superoxide dismutase (Mn-SOD, Cu,Zn-SOD), glutathione peroxidase (GPX), and catalase (CAT) due to chronic coronary occlusion of the left circumflex (CCO). Yucatan swine were divided into three groups (n=6 each): sedentary with CCO (SCO); 12 weeks of treadmill exercise training following CCO (ECO); and sham surgery controls (SHAM). Forelimb muscle mass/body mass decreased by 27% with SCO, but recovered with ECO. Exercise training reduced muscle TNF- and oxidative stress (4-hydroxynonenal adducts) caused by CCO. HSP70 levels decreased with CCO (-45%), but were higher with exercise training (+348%). Mn-SOD activity, Mn-SOD protein expression, and Cu,Zn-SOD activity levels were higher in ECO than SCO by 72%, 82%, and 112%, respectively. GPX activity was 177% greater in ECO than in SCO. CAT trended higher (P=0.059) in ECO when compared to SCO. These data indicate that exercise training following the onset of coronary artery occlusion results in recovery of critical stress proteins and reduced oxidative stress.