Upon activation of secretion pancreatic acinar cells require sufficient amount of energy. It is not known which metabolic pathways supply mitochondrial adaptive capacity of acinar cells in active functional state. Basal and FCCP-stimulated respiration of rat pancreatic acini was measured with Clark electrode. Mitochondrial adaptive capacity was assessed by maximal uncoupled respiration rate and optimal FCCP concentration. Upon acetylcholine or cholecystokinin stimulation, basal respiration rate increased in presence of glucose (by 16 or 25 %, respectively) or combinations of glucose with pyruvate (by 36 і 37 %,) or glutamine (21 or 29 %), but not with monomethyl-succinate or dimethyl-α-ketoglutarate. Maximal uncoupled respiration rate increased only upon the oxidation of pyruvate with glucose; acetylcholine increased it from 2.32 r.u. to 3.62 r.u. and cholecystokinin - to 3.19 r.u. The optimal FCCP concentration increased only after stimulation with cholecystokinin - from 1.17 to 1.33 μM. Thus, primary agonists increase adaptive capacity of pancreatic acinar cells’ mitochondria via intensification of pyruvate oxidation, but not other tested substrates.