Lactate and shock state: the metabolic viewLevy, BrunoCurrent Opinion in Critical Care: August 2006 - Volume 12 - Issue 4 - p 315–321 doi: 10.1097/01.ccx.0000235208.77450.15 Pharmacology, metabolism and nutrition Buy Abstract Author InformationAuthors Article MetricsMetrics Purpose of review The conventional view in severe sepsis or septic shock is that most of the lactate that accumulates in the circulation is due to cellular hypoxia and the onset of anaerobic glycolysis. A number of papers have suggested that lactate formation during sepsis is not due to hypoxia. I discuss this hypothesis and outline the recent advances in the understanding of lactate metabolism in shock. Recent findings Numerous experimental data have demonstrated that stimulation of aerobic glycolysis – that is, glycolysis not attributable to oxygen deficiency – and glycogenolysis occurs not only in resting, well-oxygenated skeletal muscles but also during experimental haemorrhagic shock and experimental sepsis, and is closely linked to stimulation of sarcolemmal Na+/K+-ATPase under epinephrine stimulation. A human study of hyperkinetic septic shock demonstrated that skeletal muscle is a leading source of lactate production by exaggerated aerobic glycolysis through Na+/K+-ATPase stimulation. Summary There is increasing evidence that sepsis is accompanied by a hypermetabolic state, with enhanced glycolysis and hyperlactataemia. This should not be rigorously interpreted as an indication of hypoxia. It now appears, at least in the hyperkinetic state, that increased lactate production and concentration as a result of hypoxia are often the exception rather than the rule. Service de Réanimation Médicale, CHU Brabois, 54500 Vandoeuvre les Nancy, Nancy, France Correspondence to Professor Bruno Levy, Service de Réanimation Médicale, CHU Brabois, 54500 Vandoeuvre les Nancy, France Tel: +33 3 8385 1494; fax: +33 3 8385 1911; e-mail: email@example.com © 2006 Lippincott Williams & Wilkins, Inc.