The elevated arterial lactate concentration in shock was investigated by measuring lactate production and clearance rate using a constant infusion of 14C-labeled lactate. In addition, the pathways of lactate metabolism were characterized by determining the percentage of lactate under-going oxidation and the percentage of the total carbon dioxide production which was derived from lactate. These measurements were performed on 16 normal dogs and on 23 dogs in a state of shock. Shock was induced by hemorrhage in ten, by controlled cardiac tamponade in seven and by endotoxin injection in six. In all of the dogs in a state of shock, there was a statistically significant increase in both the arterial lactate concentration and lactate turnover, while the lactate clearance decreased significantly. The percentage of the arterial lactate which underwent oxidation remained normal. The percentage of the total carbon dioxide production which was derived from lactate increased significantly, p less than 0.05, from 4.7 per cent in the normal dogs to 22.7 per cent in the dogs in a state of shock. Since both oxygen uptake and carbon dioxide production remain unchanged in shock, these data are consistent with an increased metabolism of substrates which from pyruvate and lactate as intermediary metabolites, that is, carbohydrates and certain amino acids, with a concomitant decrease in the metabolism of substrates which do not form pyruvate, that is, free fatty acids. In both the normal and shocked dogs, the arterial lactate concentration rose as the lactate production rate increased. Therefore, the elevated arterial lactate in shock was due to an increase in the lactate production and not to a lack of oxygen.