Temperature acclimation of mitochondria function from the hearts of a temperate wrasse (Notolabrus celidotus).

Understanding how mitochondrial function alters with acclimation may provide insight to the limits these organelles place on temperate fish hearts facing seasonal temperature fluctuations. This investigation determined if compromised cardiac mitochondrial function contributed to heart failure (HF) in the New Zealand wrasse Notolabrus celidotus acclimated at their mean summer and winter ocean temperatures. To test this hypothesis, fish were acclimated to cold (CA, 15°C) and warm (WA, 21°C) temperatures. The temperature of HF was determined by Doppler sonography and mitochondrial function in permeabilised cardiac fibres was tested using high resolution respirometry. Heat stress mediated HF occurred at a THF of 26.7±0.4°C for CA fish, and at 28.2±0.6°C for WA fish. Biochemical analyses also revealed that WA fish had elevated resting plasma lactate indicating an increased dependence on anaerobic pathways. When cardiac fibres were tested with increasing temperatures, apparent breakpoints in the respiratory control ratio (RCR-I) with substrates supporting complex I (CI) oxygen flux occurred below the THF for both acclimated groups. While WA cardiac mitochondria were less sensitive to increasing temperature for respirational flux supported by CI, Complex II, and chemically uncoupled flux, CA fish maintained higher RCRs at higher temperatures. We conclude that while acclimation to summer temperatures does alter cardiac mitochondrial function in N. celidotus, these changes need not be beneficial in terms of oxidative phosphorylation efficiency and may come at an energetic cost, which would be detrimental in the face of further habitat warming.