Document Detail


Biochemistry of exercise-induced metabolic acidosis.
MedLine Citation:
PMID:  15308499     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The development of acidosis during intense exercise has traditionally been explained by the increased production of lactic acid, causing the release of a proton and the formation of the acid salt sodium lactate. On the basis of this explanation, if the rate of lactate production is high enough, the cellular proton buffering capacity can be exceeded, resulting in a decrease in cellular pH. These biochemical events have been termed lactic acidosis. The lactic acidosis of exercise has been a classic explanation of the biochemistry of acidosis for more than 80 years. This belief has led to the interpretation that lactate production causes acidosis and, in turn, that increased lactate production is one of the several causes of muscle fatigue during intense exercise. This review presents clear evidence that there is no biochemical support for lactate production causing acidosis. Lactate production retards, not causes, acidosis. Similarly, there is a wealth of research evidence to show that acidosis is caused by reactions other than lactate production. Every time ATP is broken down to ADP and P(i), a proton is released. When the ATP demand of muscle contraction is met by mitochondrial respiration, there is no proton accumulation in the cell, as protons are used by the mitochondria for oxidative phosphorylation and to maintain the proton gradient in the intermembranous space. It is only when the exercise intensity increases beyond steady state that there is a need for greater reliance on ATP regeneration from glycolysis and the phosphagen system. The ATP that is supplied from these nonmitochondrial sources and is eventually used to fuel muscle contraction increases proton release and causes the acidosis of intense exercise. Lactate production increases under these cellular conditions to prevent pyruvate accumulation and supply the NAD(+) needed for phase 2 of glycolysis. Thus increased lactate production coincides with cellular acidosis and remains a good indirect marker for cell metabolic conditions that induce metabolic acidosis. If muscle did not produce lactate, acidosis and muscle fatigue would occur more quickly and exercise performance would be severely impaired.
Authors:
Robert A Robergs; Farzenah Ghiasvand; Daryl Parker
Related Documents :
8275049 - Physiological responses to specific maximal exercise tests for cross-country skiing.
2920719 - Influence of cold exposure on blood lactate response during incremental exercise.
1541729 - Kinetics of amino acid extraction by lactating mammary glands in control and sometribov...
19650379 - Specific circuit training in young judokas: effects of rest duration.
10994919 - Effect of training status and relative exercise intensity on physiological responses in...
21200339 - Intermittent-sprint performance and muscle glycogen following 30 h sleep deprivation.
24666729 - Perceptual effects and efficacy of intermittent or continuous blood flow restriction re...
6703499 - Neutrophil chemotactic activity and histamine in atopic and nonatopic subjects after ex...
15357319 - Comparative study of lung cytologic features in normal rhesus (macaca mulatta), cynomol...
Publication Detail:
Type:  Biography; Historical Article; Journal Article; Portraits; Review    
Journal Detail:
Title:  American journal of physiology. Regulatory, integrative and comparative physiology     Volume:  287     ISSN:  0363-6119     ISO Abbreviation:  Am. J. Physiol. Regul. Integr. Comp. Physiol.     Publication Date:  2004 Sep 
Date Detail:
Created Date:  2004-08-13     Completed Date:  2004-09-10     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  100901230     Medline TA:  Am J Physiol Regul Integr Comp Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  R502-16     Citation Subset:  IM    
Affiliation:
Exercise Science Program, Department of Physical Performance and Development, Johnson Center, Rm. B143, The University of New Mexico, Albuquerque, NM 87131-1258, USA. rrobergs@unm.edu
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Acidosis / etiology*
Acidosis, Lactic / etiology,  history
Animals
Buffers
Exercise / physiology*
History, 18th Century
History, 20th Century
Humans
Lactic Acid / biosynthesis
Models, Biological
Protons
Chemical
Reg. No./Substance:
0/Buffers; 0/Protons; 50-21-5/Lactic Acid
Personal Name Subject
Personal Name Subject:
Carl Wilhelm Scheele; Archibald V Hill; Otto Meyerhof
Comments/Corrections
Comment In:
Am J Physiol Regul Integr Comp Physiol. 2006 Jul;291(1):R235-7; author reply R238-9   [PMID:  16760335 ]
Am J Physiol Regul Integr Comp Physiol. 2005 Sep;289(3):R902-3; author reply R904-910   [PMID:  16105825 ]
Am J Physiol Regul Integr Comp Physiol. 2005 Sep;289(3):R895-901; author reply R904-910   [PMID:  16105824 ]
Am J Physiol Regul Integr Comp Physiol. 2005 Sep;289(3):R891-4; author reply R904-910   [PMID:  16105823 ]

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


Previous Document:  Role of tubular secretion and carbonic anhydrase in vertebrate renal sulfate excretion.
Next Document:  Membrane lipids and sodium pumps of cattle and crocodiles: an experimental test of the membrane pace...