Abstract
Migration, a bird's metabolic apex, depends primarily on the liver and muscle for fuel mobilization and endurance flight. In migratory redheaded buntings, adaptive increase in mitochondrial membrane (MM) proton gradient to drive ATP synthesis, measured by MM potential (MMP+) and reactive oxygen species (ROS) response, have been well characterized in the blood but not in the muscle or liver. We assessed MMP+, ROS, and apoptosis in the liver and pectoralis muscle of photosensitive nonmigratory (nMig.) male redheaded buntings photoinduced to migratory (Mig.) states. Relative expression levels of genes associated with energy (ACADM, PEPCK, GOT2, GLUT1, and CS), ROS modulation (SIRT1), mitochondrial free-radical scavengers (SOD1, PRX4, NOS2, GPX1, and GPX4), anti-apoptotic genes (NF-κβ), apoptotic (CASP7), and tissue damage using histology, during migration were assessed. The MMP+ decreased and the ROS concentration increased, due to the metabolic load on liver and pectoralis muscle tissues during Mig. However, percentage of apoptotic cells increased in liver but decreased in muscle, which is of functional significance to migratory passerines. During Mig., in muscle, SIRT1 increased, while an increase in anti-apoptotic NF-κβ aided immune pathway-mediated antioxidant activity and guarded against muscle oxidative damage during migration. Inter-organ differences in metabolism add to our current understanding of metabolic flexibility that supports successful migration in buntings.