Flight muscle mitochondria are seasonally plastic in a migratory songbird

Abstract

Birds metabolically remodel their flight muscle prior to migration to meet the high energetic demands of migratory flight. The degree of plasticity mediated by changes in mitochondrial function is poorly understood but could be explained by two non-mutually exclusive hypotheses: variation in mitochondrial quantity or individual mitochondrial function. For each hypothesis, we predicted higher mitochondrial abundance and predict higher substrate oxidative capacity and reduced reactive oxygen species formation during migration, respectively. We evaluated both hypotheses using yellow-rumped warblers (Setophaga coronata) captured during their autumn migration at Long Point, Ontario, Canada. Half of the birds were sampled in the migratory phenotype and the remaining birds were transferred to a short day photoperiod (9L:15D) and sampled in a non-migratory phenotype. We measured mitochondrial abundance via citrate synthase maximal activity in the pectoralis major flight muscle. We investigated mitochondrial function via high-resolution fluororespirometry on isolated pectoralis mitochondria. We measured O2 consumption and H2O2 formation rates from oxidation of lipid and carbohydrate substrates. We also measured oxygen consumption specific to electron transport system protein complexes using complex-specific substrates and inhibitors. Citrate synthase activity and mitochondrial respiration for each substrate and complexes II, III and IV was higher in the migratory phenotype, yet H2O2 formation rates were similar between phenotypes. These data suggest that pectoralis mitochondrial abundance and oxidative capacity are elevated during migration without increasing reactive oxygen species formation. Our findings support both hypotheses and indicate that mitochondrial function mediates seasonal metabolic plasticity in the pectoralis flight muscle of migratory songbirds.