Effects of evolved migration strategy, seasonal flexibility, and endurance flight on songbird mitochondrial bioenergetics
Abstract
Migratory birds make large-scale movements using flight twice per year, which are physiologically challenging due to high energetic costs and oxidative damage from reactive oxygen species (ROS). Muscle mitochondria play central roles in energy supply and ROS homeostasis during exercise, but the role of mitochondrial function in overcoming the demands of migratory flight is presently unclear. In this dissertation, I explore how mitochondrial function is modulated in three contexts relevant to avian migration: seasonal flexibility, endurance flight and evolved variation in migration strategy. For my first aim, I compared flight muscle mitochondrial respiration and ROS emission between a migratory and short-day photoperiod-induced non-migratory phenotype in yellow-rumped warblers (Setophaga coronata). I found that fatty acid-fuelled respiration was higher and ROS emission was lower in the migratory compared to the non-migratory phenotype, indicating that mitochondria are seasonally remodeled to support greater fatty acid oxidation and lower risk of oxidative stress during migration. For my second aim, I assessed mitochondrial respiration and ROS emission and lean tissue catabolism before and after up to eight hour endurance flight using a wind tunnel in blackpoll warblers (Setophaga striata). I found that endurance flight had little effect on flight muscle size, ultrastructure, mitochondrial respiration or ROS emission, but a modest reduction in the mass of liver, gizzard and proventriculus. These findings suggest that mitochondria are resilient against the damaging aspects of endurance flight and that the flight muscle may be preferentially protected to support endurance flight performance. For my third aim, I assessed pectoralis size, mitochondrial physiology, and mitochondrial abundance across 19 passerine species of varying migratory strategy. I found that long-distance migration was associated with lower pectoralis size and fatty acid oxidation capacity, while mitochondrial abundance and ROS emission were unaffected. Surprisingly, these data suggest that longer migration distance is associated with a lower oxidative capacity, which may reflect evolved reductions in energy expenditure during migration. Together, my findings indicate that mitochondrial metabolism is modulated by migratory songbirds to better meet the demands of migratory flight.