Meeting Abstract
High-altitude environments provide fertile ground for investigating the mechanisms and evolution of mitochondrial physiology and animal performance. The cold and oxygen-depleted (‘hypoxic’) environment at high altitudes requires that endothermic animals sustain high rates of O2 consumption for thermogenesis and locomotion while facing a diminished O2 availability. I will present our work examining the ways in which high-altitude populations of deer mice (Peromyscus maniculatus) overcome these challenges and maintain respiratory performance through evolved changes in mitochondrial function. High-altitude mice have evolved an enhanced respiratory capacity (VO2max) in hypoxia compared to their low-altitude counterparts, in association with increases in mitochondrial quantity, quality, and O2 supply in the skeletal muscle. Increases in mitochondrial quantity arise from the combined effects of having greater abundances of oxidative muscle fibres and higher mitochondrial volume densities. Changes in mitochondrial quality, as reflected by changes in the capacity of mitochondria for supporting oxidative phosphorylation, also differentiate high- and low-altitude populations. Mitochondrial O2 supply is augmented in high-altitude populations by changes in the intracellular distribution of mitochondria, such that more mitochondria are situated in a subsarcolemmal location adjacent to the cell membrane, and by a greater capillarity of muscle fibres. Our results therefore suggest that several evolved changes in mitochondrial function and O2 supply contribute to respiratory performance at high altitudes. (Supported by NSERC of Canada)
