Acclimation to warm temperatures has important implications for mitochondrial function in Atlantic salmon (Salmo salar)

In fish. the capacity of thermal acclimation to preserve cardiac mitochondrial function under future warming scenarios is important to understand given the central roles that cardiac energy metabolism and performance play in this taxa's thermal tolerance. We acclimated Atlantic salmon to 12 and 20 degrees C (for >2 months), and investigated the effects of acute and chronic warming on cardiac mitochondrial respiration and reactive oxygen species (ROS) production (release rate) using high-resolution fluorespirometry. Further, we compared the sensitivity of mitochondrial respiration to nitric oxide (i.e. the NO IC50), and assessed the mitochondrial response to anoxiareoxygenation (AR). Acute exposure to 20 degrees C increased maximal mitochondrial respiration by similar to 55%; however, the mitochondria's complex I respiratory control ratio was 17% lower and ROS production was increased by >= 60%. Acclimation to 20 degrees C: (1) preserved mitochondrial coupling and aerobic capacity; (2) decreased the mitochondria's ROS production by similar to 30%; (3) increased the mitochondria's NO IC50 by similar to 23%; and (4) improved mitochondrial membrane integrity at 20 degrees C. AR did not affect mitochondrial function at 12 degrees C, but acute exposure to 20 degrees C and AR depressed maximal mitochondrial respiration (by similar to 9%) and coupling (by similar to 16%) without impacting ROS production. Finally, warm acclimation did not improve the capacity of mitochondria to recover from AR, indicating that there was no 'cross-tolerance' between these challenges. Our findings provide compelling evidence that thermal plasticity of cardiac mitochondrial function contributes to the Atlantic salmon's capability to survive at >= 20 degrees C for prolonged periods, but call into question whether this plasticity may allow them to withstand high temperatures when combined with other stressors.