Flight muscle mitochondria are robust against endurance flight damage in blackpoll warblers Setophaga striata

Abstract

Migratory birds are physiologically challenged by intense exercise while fasting during flights that may last hours to days. Exercise-induced oxidative stress could compromise flight performance by inducing mitochondrial dysfunction in the flight muscle. Endurance flight is partially fuelled by the catabolism of lean tissues, but how this catabolism is partitioned between different organs and muscles has not been previously studied under controlled conditions. We hypothesized that simulated migratory flight would result in dysfunction of flight muscle mitochondria, and selective catabolism of lean tissues. We predicted that simulated migratory flight would cause reduced mitochondrial oxidative phosphorylation capacity while increasing emission of reactive oxygen species (ROS) and that lean tissue mass catabolism would preferentially occur in digestive organs not needed in flight. We measured mitochondrial function, muscle morphology and the wet masses of organs and muscles following 8-hour wind tunnel flights in blackpoll warblers Setophaga striata, which use multi-day nonstop flights as part of their migration strategy. In contrast to our predictions, we found that simulated migratory flight did not alter mitochondrial fatty acid oxidation capacity or ROS emission. However, flight and fasting increased whole-animal lean mass catabolism and were associated with reductions in the masses of liver, gizzard and proventriculus, but masses of tissues in the flight apparatus (pectoralis, heart, lungs) were unaffected. Pectoralis muscle fiber morphology was also unchanged over the tested flight duration. Our findings indicate that mitochondrial function in blackpoll warblers is robust against damage induced by simulated migratory flight, and energy deprivation is sufficient for organ catabolism.