Abstract

Oxidative stress, the production of free radicals and reactive oxygen species, can be a result of prolonged and high intensity exercise and may lead to skeletal muscle fatigue and dysfunction, and decreased exercise performance. Manganese superoxide dismutase (MnSOD), a naturally existing mitochondrial antioxidant enzyme, provides the first line of defense against oxidative stress caused by superoxide anions. Transgenic mice overexpressing MnSOD have been studied within the context of disease pathology, but skeletal muscle function and exercise capacity in these mice have not been characterized. Therefore, the objective of this study was to investigate if grip strength, maximal exercise capacity, and exercise endurance differ between transgenic mice that overexpress MnSOD in the mitochondrial matrix (SOD2) and their wild‐type (WT) littermates. Female SOD2 and WT mice (8–10 mo old) performed 3 consecutive forelimb grip strength tests, with 1‐min rest between trials. Next, these mice performed a maximal exercise capacity test, which consisted of a 10‐min warm up at 10–12.5 m•min−1 and 5–10° incline, followed by 2‐min stages of increasing treadmill speed by 3 m•min−1 every stage; treadmill remained at 10° incline and mice ran to exhaustion. Then, 48 hours after the completion of the maximal exercise capacity test, all mice performed an exercise endurance test, consisting of a 10‐min warm up at 10–12.5 m•min−1 and 5–10° incline, followed by a run to exhaustion at a constant treadmill speed of 22 m•min−1 and incline of 10°. Grip strength, maximal exercise capacity, and exercise endurance were not different between SOD2 and WT mice, respectively (p>0.05, all). These findings suggest that overexpression of MnSOD in the mitochondrial matrix does not alter grip strength, treadmill exercise capacity, or endurance in mice.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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