Abstract

Mitochondrial function [e.g., respiration, respiratory coupling ratio (RCR) and reactive oxygen species (ROS) production] is negatively impacted by high temperatures, and may limit fish cardiac performance and upper thermal tolerance. Nevertheless, direct evidence of this is lacking, and testing at different levels of organization will be critical to establishing whether this construct has validity. We acclimated salmon to 10 and 20°C for >2 weeks and then: used strips from half of the ventricle to simultaneously measure muscle work and O2 consumption (and thus efficiency) at 20 and 26oC; and the other half to obtain myocardial homogenates and isolated mitochondria so that mitochondrial functional parameters could be measured at the same temperatures. State 4 respiration for isolated mitochondria and State 2 respiration for homogenates, and absolute ROS production during these states, were positively correlated with resting muscle O2 consumption in fish acclimated to both temperatures. In contrast, we were unable to consistently identify relationships between mitochondrial parameters and O2 consumption/efficiency while the muscle was working. For example, the P:O ratio (Complex I) and RCR (Complex I+II) for these preparations were not related to the absolute efficiency of shortening work. Further, while total CI+CII ROS production was negatively correlated with the efficiency of shortening work in 20oC acclimated salmon, this relationship was not evident for 10oC acclimated fish. These results: are consistent with previous data showing that warm acclimation improves cardiac mitochondrial function at high temperatures; but only provide a tenuous link between heart and mitochondrial performance in salmon under such conditions.

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