Exercise training decreases rat heart mitochondria free radical generation but does not prevent Ca -induced dysfunction

Starnes JW, Barnes BD, Olsen ME. Exercise training decreases rat heart mitochondria free radical generation but does not prevent Ca induced dysfunction. J Appl Physiol 102: 1793–1798, 2007. First published February 15, 2007; doi:10.1152/japplphysiol.00849.2006.—Exercise provides cardioprotection against ischemia-reperfusion injury, a process involving mitochondrial reactive oxygen species (ROS) generation and calcium overload. This study tested the hypotheses that isolated mitochondria from hearts of endurance-trained rats have decreased ROS production and improved tolerance against Ca induced dysfunction. Male Fischer 344 rats were either sedentary (Sed, n 8) or endurance exercise trained (ET, n 11) by running on a treadmill for 16 wk (5 days/wk, 60 min/day, 25 m/min, 6° grade). Mitochondrial oxidative phosphorylation measures were determined with glutamate-malate or succinate as substrates, and H2O2 production and permeability transition pore (PTP) opening were determined with succinate. All assays were carried out in the absence and presence of calcium. In response to 25 and 50 M CaCl2, Sed and ET displayed similar decreases in state 3 respiration, respiratory control ratio, and ADP:O ratio. Ca -induced PTP opening was also similar. However, H2O2 production by ET was lower than Sed (P 0.05) in the absence of calcium (323 12 vs. 362 11 pmol min 1 mg protein ) and the presence of 50 M CaCl2 (154 3 vs. 197 7 pmol min 1 mg protein ). Rotenone, which blocks electron flow from succinate to complex 1, reduced H2O2 production and eliminated differences between ET and Sed. Mitochondrial superoxide dismutase and glutathione peroxidase were not affected by exercise. Catalase activity was extremely low but increased 49% in ET (P 0.05). In conclusion, exercise reduces ROS production in myocardial mitochondria through adaptations specific to complex 1 but does not improve mitochondrial tolerance to calcium overload.