BACKGROUND Lactacidemia is often seen under stress conditions including septic shock in the newborn. Under stress conditions, plasma catecholamine concentrations are increased and play an important role in lactate metabolism. Our previous study shows that perinatal feeding of omega-3 polyunsaturated fatty acid enriched diet (omega-3PUFA) attenuates lactacidemia of endotoxic shock in 10-day-old rats. In the omega-6 fatty acids series, decosapentanoic acid, two series prostaglandins and four series leukotrienes are synthesized through linoleic acids. As plasma lactate concentration correlates with the outcome of septic shock in the newborn, it is important to understand the effects of omega-3PUFA on lactate metabolism. Thus, we tested the hypothesis that perinatal feeding of omega-3 polyunsaturated fatty acid enriched diet (omega-3PUFA) alters responses to catecholamines and attenuates the stress-induced lactacidemia in 10-day-old rats. METHODS Ten-day-old rats which perinatally fed omega-3PUFA. Lactacidemia was induced by swimming for 5 min. Ten-day-old rats which perinatally fed omega-6PUFA were controls. Omega-6 fatty acids series are contained in animal fats and corn oil. Adrenergic blockers were used to assess roles of catecholamines in swimming-induced lactacidemia. RESULTS Swimming increased plasma lactate concentration less (P<0.05) in rats fed omega-3PUFA than rats fed omega-6PUFA. Swimming increased plasma concentrations of glucose and glucagon, cyclic adenosine monophosphate (cAMP) concentration and phosphoenolypruvate carboxykinase mRNA in the liver, and cAMP concentration in the hindlimb muscle more (P<0.05) in rats fed omega-3PUFA than in rats fed omega-6PUFA. Phentolamine and propranolol enhanced swim-induced lactacidemia in the omega-3PUFA group, while they decreased the lactacidemia in the omega-6PUFA group. Propranolol enhanced swimming-induced hyperglycemia in the omega-6PUFA group more than in the omega-3PUFA group. CONCLUSIONS Omega-3PUFA might increase beta-adrenergic response in the liver and increase gluconeogenesis in response to stress, resulting in decreased lactacidemia.