Document Detail


Lactate metabolism: a new paradigm for the third millennium.
MedLine Citation:
PMID:  15131240     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
For much of the 20th century, lactate was largely considered a dead-end waste product of glycolysis due to hypoxia, the primary cause of the O2 debt following exercise, a major cause of muscle fatigue, and a key factor in acidosis-induced tissue damage. Since the 1970s, a 'lactate revolution' has occurred. At present, we are in the midst of a lactate shuttle era; the lactate paradigm has shifted. It now appears that increased lactate production and concentration as a result of anoxia or dysoxia are often the exception rather than the rule. Lactic acidosis is being re-evaluated as a factor in muscle fatigue. Lactate is an important intermediate in the process of wound repair and regeneration. The origin of elevated [lactate] in injury and sepsis is being re-investigated. There is essentially unanimous experimental support for a cell-to-cell lactate shuttle, along with mounting evidence for astrocyte-neuron, lactate-alanine, peroxisomal and spermatogenic lactate shuttles. The bulk of the evidence suggests that lactate is an important intermediary in numerous metabolic processes, a particularly mobile fuel for aerobic metabolism, and perhaps a mediator of redox state among various compartments both within and between cells. Lactate can no longer be considered the usual suspect for metabolic 'crimes', but is instead a central player in cellular, regional and whole body metabolism. Overall, the cell-to-cell lactate shuttle has expanded far beyond its initial conception as an explanation for lactate metabolism during muscle contractions and exercise to now subsume all of the other shuttles as a grand description of the role(s) of lactate in numerous metabolic processes and pathways.
Authors:
L B Gladden
Publication Detail:
Type:  Journal Article; Review     Date:  2004-05-06
Journal Detail:
Title:  The Journal of physiology     Volume:  558     ISSN:  0022-3751     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2004 Jul 
Date Detail:
Created Date:  2004-06-30     Completed Date:  2005-01-19     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  5-30     Citation Subset:  IM    
Affiliation:
Department of Health and Human Performance, 2050 Memorial Coliseum, Auburn University, Auburn, AL 36849-5323, USA. gladdlb@auburn.edu
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Acidosis, Lactic / metabolism*
Animals
Energy Metabolism / physiology*
Exercise / physiology*
Humans
Lactic Acid / metabolism*
Chemical
Reg. No./Substance:
50-21-5/Lactic Acid
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Development affects in vitro vascular tone and calcium sensitivity in ovine cerebral arteries.
Next Document:  Differential involvement of multidrug resistance-associated protein 1 and P-glycoprotein in tissue d...