The Atlantic cod (Gadus morhua) is an economically important marine fish species exploited by both fishery and aquaculture, especially in the North Atlantic and Arctic oceans. Ongoing climate changes are happening faster in the high latitude oceans with a higher increase of temperature and a steeper decrease in water pH due to anthropogenic CO2 than in the temperate regions threatening the existence of the Atlantic cod in the areas of its maximum exploitation. In this study, we investigated the mitochondrial physiology of two life-stages of cod under the sea water temperatures and pCO2 conditions forecasted for the year 2100 in the North Atlantic (+ 5 °C, 1000 μatm CO2). In embryos, the metabolism during development showed to be sensitive to rising temperatures with a general increase in respiratory activity until 9 °C (5 °C over the natural range) and a drop in activity at 12 °C mainly caused by a dramatic decrease in Complex I activity, which was not compensated by Complex II. In the adults, already well known for their metabolic plasticity, mitochondria from liver and heart are not affected by either increasing temperature or pCO2. However, in heart mitochondria of animals that were reared under warm hypercapnia (10 °C + 1000 μatm CO2), we found OXPHOS to exploit already 100% of the ETS capacity. This suggests that a further increase in temperature or pCO2 might lead to a mismatch in the ATP demand/production and consequently decrease heart performances. The different mitochondrial plasticities of the two life-stages reflect the sensitivity range at population level and thus can provide a more realistic reading frame of the potential survival of the North Atlantic cod population under climate change.