Parasites can affect host behaviour and many physiological traits. Changes to host aerobic metabolism are likely responsible for these parasite induced performance alterations. Whole organism metabolic rate is underpinned by cellular energy metabolism driv en most prominently by the mitochondria. However, few studies have explored how mitochondrial enzymatic activities are linked to parasite infection despite being a putative site for metabolic disruptions. Our previous work suggest ed a link between parasite intensity and mitochondrial enzymatic activities in a variety of metabolic pathways including the tricarboxylic acid cycle, oxidative phosphorylation, and lipid oxidation in key organs of wild caught pumpkinseed sunfish ( Lepomis gibbosus infected with trematode and cestode worms . Here, we expand on these results and assess the link between enzymatic activity and parasite infection across multiple populations of L. gibbosus which differ in the prevalence of these parasite s . We measured enzyme activities in several metabolic pathways (TCA cycle, OXPHOS, lipid oxidation and anaerobic glycolysis) in key organs. We found enzymatic activities differed across lakes. Compared to an uninfected l ake, fish from lakes with high parasite prevalence had higher citrate synthase (CS) and carnitine palmitoy ltransferase (CPT) activity in their hearts higher CPT and cytochrome c oxidase (CCO) activity in the ir gills and higher activities of all tested enzymes in the spleen . For the brain, fish from high prevalence lakes had a higher CCO activity but a lower ETS activity. These results suggest that parasite exposure is related to altered energy metabolism at a cellular level mirroring results observed at the whole organism level