Alterations in mitochondrial functions are proposed as key processes in seasonal as well as evolutionary temperature adaptations of ectotherms. Cold exposure frequently induces mitochondrial proliferation to cope with the decelerating effects of low temperatures. In populations of cod (Gadus morhua) along a latitudinal cline differences at the functional level became evident mostly at cold temperature with higher mitochondrial capacities in the sub-Arctic population. In metabolically active tissues like liver, cold acclimation was found to comprise a shift between mitochondrial functions, indicated by increased activity ratios of the mitochondrial key-enzymes citrate synthase (CS) and cytochrome-c oxidase (COX). In all cases transcript levels and functional capacities were not tightly correlated with enzyme activities during thermal adaptation and thereafter, though transcriptional processes are clearly involved and seem to be important to establish the new steady state. However, cold exposure of isolated hepatocytes prepared from the common eelpout (Zoarces viviparus) resulted in increments in CS as well as COX capacities contrasting the situation in whole animal acclimation. This suggests that systemic signals coordinate the pattern of adaptation at the organismic level. As adenosine levels rose transiently during cold acclimation of eelpout in vivo, we tested its role as a regulatory signal during thermal acclimation. In isolated hepatocytes, adenosine had in fact a suppressing effect on COX activity and total RNA contents, but most striking was the activation of COX expression, found for both, mitochondrial and nuclear encoded subunits. Finally, a pattern of expression results which is similar to the one observed in vivo.