Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/12162
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dc.contributor.authorGarcia-Alvarez, Mercedesen
dc.contributor.authorMarik, Paulen
dc.contributor.authorBellomo, Rinaldoen
dc.date.accessioned2015-05-16T01:48:48Z
dc.date.available2015-05-16T01:48:48Z
dc.date.issued2013-11-29en
dc.identifier.citationThe Lancet. Diabetes & Endocrinology 2013; 2(4): 339-47en
dc.identifier.govdoc24703052en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/12162en
dc.description.abstractAn increased blood lactate concentration is common during physiological (exercise) and pathophysiological stress (stress hyperlactataemia). In disease states, there is overwhelming evidence that stress hyperlactataemia is a strong independent predictor of mortality. However, the source, biochemistry, and physiology of exercise-induced and disease-associated stress hyperlactataemia are controversial. The dominant paradigm suggests that an increased lactate concentration is secondary to anaerobic glycolysis induced by tissue hypoperfusion, hypoxia, or both. However, in the past two decades, much evidence has shown that stress hyperlactataemia is actually due to increased aerobic lactate production, with or without decreased lactate clearance. Moreover, this lactate production is associated with and is probably secondary to adrenergic stimulation. Increased lactate production seems to be an evolutionarily preserved protective mechanism, which facilitates bioenergetic efficiency in muscle and other organs and provides necessary substrate for gluconeogenesis. Finally, lactate appears to act like a hormone that modifies the expression of various proteins, which themselves increase the efficiency of energy utilisation and metabolism. Clinicians need to be aware of these advances in our understanding of stress hyperlactataemia to approach patient management according to logical principles. We discuss the new insights and controversies about stress hyperlactataemia.en
dc.language.isoenen
dc.subject.otherExercise.physiologyen
dc.subject.otherHumansen
dc.subject.otherLactic Acid.blood.metabolismen
dc.subject.otherOxidation-Reductionen
dc.subject.otherStress, Physiological.physiologyen
dc.titleStress hyperlactataemia: present understanding and controversy.en
dc.typeJournal Articleen
dc.identifier.journaltitleThe lancet. Diabetes & endocrinologyen
dc.identifier.affiliationDepartment of Anaesthesiology, Hospital de Sant Pau, Barcelona, Spain; Department of Intensive Care Medicine, Austin Hospital, Melbourne, Australia.en
dc.identifier.affiliationDivision of Pulmonary and Critical Care Medicine, Eastern Virginia Medical School, Norfolk, VA, USA.en
dc.identifier.affiliationDepartment of Intensive Care Medicine, Austin Hospital, Melbourne, Australia; Australian and New Zealand Intensive Care Research Centre, Melbourne, Australia. Electronic address: rinaldo.bellomo@austin.org.au.en
dc.identifier.doi10.1016/S2213-8587(13)70154-2en
dc.description.pages339-47en
dc.relation.urlhttp://www.ncbi.nlm.nih.gov/pubmed/24703052en
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