UPREGULATION OF ANTIOXIDANT CAPACITY BY ENDURANCE TRAINING IN PIGS FOLLOWING CHRONIC CORONARY ARTERY OCCLUSION

Abstract

Growing evidence indicates that oxidative stress is associated with muscle fatigue and weakness in skeletal muscle of heart disease patients. Previously, our laboratory and others demonstrated that reactive oxygen species (ROS) and reactive nitrogen species (RNS) have the ability to inhibit key antioxidant enzymes in skeletal muscle, thus increasing susceptibility to oxidative stress. Endurance training has been shown to elevate skeletal muscle mantioxidant enzyme activities in healthy animal models. Chronic coronary artery occlusion in pigs was used to model heart disease and to test the following hypothesis: twelve weeks of treadmill endurance training will increase the antioxidant capacity in skeletal muscle in pigs with chronic coronary occlusion. Miniature Yucatan swine were divided into three groups: sedentary animals (n = 6) with coronary artery occlusion (SO); endurance trained animals (n = 6) with coronary occlusion (EO); and sedentary (n = 3) without coronary occlusion (CON). Skeletal muscle samples (triceps brachii) were extracted after a 12 week training period, and frozen in liquid nitrogen until analysis. Superoxide dismutase (total SOD, Mn-SOD isoform, and Cu, Zn-SOD isoform), glutathione peroxidase (GPX), and catalase (CAT) activities were measured. The quenching of ABTS+ radical was used as a marker of non-enzymatic antioxidant scavenging capacity (TASC). Total SOD, Mn-SOD, and Cu, Zn-SOD activities were significantly higher in EO than SO by 82.6%, 72.0%, and 112.0%, respectively. GPX activity was 176.6% greater in EO than in SO. CAT trended higher (P = 0.059) in EO when compared to SO. TASC was also significantly improved (12.7%) by exercise training over SO. All antioxidant measurements for EO were not different from CON, while SO values were lower than CON. These data indicate that endurance exercise training is critical for the protection of antioxidant capacity in pigs with chronic coronary occlusion. Grant support by NIH PO1-HL52490 and HL64931.