Antarctic fish species possess very low metabolic rates and poor metabolic plasticity, thus making them extremely vulnerable to changing environmental conditions. Mitochondria are a key element in shaping whole organism energy turnover and functional capacities. In our study, we compared two nototheniid fish, the Austral black cod (Notothenia angustata, New Zealand) and the Antarctic marbled rockcod (Notothenia rossii, Antarctic Peninsula) for their abilities of metabolic compensation for rising temperature and PCO2 at the intracellular level. We acclimated N. angustata to control conditions (PCO2 of 0.04 kPa) and to an ambient PCO2 of 0.2 kPa for 11 days, and kept N. rossii at a PCO2 of 0.04 kPa. We assessed permeabilized heart fibre oxygen consumption at various respiratory states (e.g. state III complex I/ II, state IV (leak), uncoupled/ ETS capacity, complex IV) in acutely hypercapnic (PCO2 of 2 kPa, corresponds to intracellular PCO2 under 0.2 kPa ambient hypercapnia) vs. normocapnic (PCO2 of 0.04 kPa) respiration media. In all respiratory states, acute exposure to the hypercapnic respiration medium resulted in reduced mitochondrial capacities, in the Austral and the Antarctic notothenioids Yet, overall heart fibre respiration was higher in the hypercapnia acclimated N. angustata than in their control group. This suggests that chronic acclimation of the fish to moderately elevated PCO2 levels might enhance mitochondrial aerobic capacities, involving e.g. changes in enzyme capacities or mitochondrial proliferation. Our data indicate that while acute high PCO2 levels of 2 kPa reduce mitochondrial oxidative capacities in Austral and Antarctic notothenioids, at least the Austral fish seem to be able to compensate for these acutely reduced metabolic capacities by hypercapnia acclimation.