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. We therefore studied the acclimatory capacities of the Antarctic fish Notothenia rossii after 4-6 weeks of acclimation to 7°C, hypercapnia (0.2 kPa CO2) and the combination of both. We analysed routine metabolic rate (RMR) during acute thermal challenge and after acclimation, extra- and intracellular acid-base status, mitochondrial as well as enzymatic capacities and lipid composition. Our results showed partially compensated RMR after warm acclimation and no effect of increased PCO2 on the RMR. Hypercapnic acclimation led to a general overcompensation of extracellular pH. Intracellular pH displayed a slight acidosis in liver after warm normocapnic/hypercapnic acclimation, whereas white muscle remained well buffered under hypercapnia. Mitochondrial state III respiration in liver was unaffected by temperature acclimation, but depressed in the hypercapnia acclimated animals, which went along with reduced rates of proton leak. The activities of the mitochondrial enzymes citrate synthase and cytochrome c oxidase increased during hypercapnia acclimation in red and white muscle, but not in liver and heart. Furthermore, there was a trend towards an enrichment of poly-unsaturated fatty acids in liver mitochondria towards the warm hypercapnic conditions. We conclude that N. rossii possesses basic acclimatory capacities towards ocean warming and acidification. However, these capacities are confined within strict limits, becoming obvious in metabolically more active organs like heart and liver that show less plasticity than muscle and ultimately define animal survival.