Thermal sensitivity of respiration and ROS emission of muscle mitochondria in deer mice.

Abstract

The impacts of heat exposure on mitochondrial physiology are poorly understood in most mammals. We examined the thermal effects on muscle mitochondrial function in deer mice (Peromyscus maniculatus), a species in which running endurance is impaired when heat exposure increases body temperature beyond 40 °C. Mitochondrial physiology was examined at 37, 40, and 42 °C using both permeabilized fibres and isolated mitochondria from the gastrocnemius muscle. Hot temperatures increased leak respiration, reduced the coupling efficiency of oxidative phosphorylation, and increased reactive oxygen species (ROS) emission. These results suggest that heat exposure reduces mitochondrial efficiency, which could contribute to impairments in running performance, and may also induce oxidative stress. Thermal effects on mitochondrial function may thus represent a potential vulnerability during heat exposure in mammals.