Ongoing ocean warming and acidification have been found to particularly affect polar marine ecosystems. However, few data exist about the ability of Antarctic fish to respond to environmental change. While whole animal and transcriptomic data on the effects of ocean acidification and warming exist for fish, the acclimation capacities of the subcellular, organelle levels have been poorly studied in this respect. Diffusion of CO2 into the bloodstream and into the intracellular milieu in aquatic water breathing organisms leads to an acidification of body fluids. Fish can regulate extracellular and intracellular pH by actively accumulating bicarbonate to compensate for the acidification of the extracellular and intracellular milieu. However, chronically elevated bicarbonate levels may interfere with a variety of metabolic processes. For example, bicarbonate is known to strongly interact with mitochondrial metabolism, among others it competitively inhibits citrate oxidation, ultimately influencing ETS capacities. We therefore studied the capacities for mitochondrial acclimation towards elevated PCO2 and bicarbonate levels in fish that were incubated at different water PCO2. We studied ETS capacities in permeabilised heart fibres in fish-MiR06, modified to contain different levels of [HCO3-], and enzymatic activies of citrate synthase and cytochrome c oxidase. We found a strong influence of bicarbonate on mitochondrial metabolism and a compensatory increase of mitochondrial capacities after hypercapnia acclimation. Our findings illustrate the importance of adjusting bicarbonate levels to represent intracellular conditions in fish and other aquatic organisms.