Meeting Abstract
Reactive oxygen species (ROS) are produced largely by mitochondria in skeletal muscle as a natural by-product of aerobic metabolism and have the potential to elicit oxidative stress. The blue crab, Callinectes sapidus, is a high-performance swimming crab, with an ability to undergo anaerobic burst swimming during predator-prey interactions, as well as aerobic endurance swimming during extended daily or seasonal migrations. The locomotor muscles that power these two types of swimming represent extreme ends of the aerobic spectrum. The aerobic (dark) muscles that power endurance swimming have a mitochondrial volume density (MVD) that is 25 times higher than the anaerobic (light) fibers that power burst swimming. We tested the hypothesis in juvenile and adult crabs that the much higher MVD in dark muscle leads to oxidative damage that may necessitate greater rates of turnover of intracellular components. Juveniles had greater protein carbonylation in both dark and light muscle, and greater lipid peroxidation in dark muscle than in adults. There was no difference in oxidative stress markers between muscle types. Surprisingly, relative protein translation rates were not different between muscle types, and dark muscle in juveniles had a lower translation rate than in adults. Ubiquitin was greater in light muscle of juveniles than in adults while calpain was not different between life stages. Calpain was significantly greater in light relative to dark muscle in adults. These results indicate that the extreme difference in MVD between muscle types does not lead to a proportional difference in oxidative stress or protein turnover, suggesting mechanisms exist to limit net ROS production in dark muscle.
