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Cited by 1,304Cardiovascular and exercise physiologyMuscle metabolism and nutritionExercise and Physiological Responses

The DOI matches its Crossref record; 66 of the 66 references it cites were found in a registry or an index.

Biochemistry of exercise-induced metabolic acidosis

Robergs, Robert A., Ghiasvand, Farzenah, Parker, Daryl·2004·American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
DOI 10.1152/ajpregu.00114.2004
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Abstract

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.

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Research works printed but not linked: 2

  1. Laski ME and Wesson DE. Lactic acidosis. In: Acid-Base and Electrolyte Disorders: A Companion to Brenner and Rector's The Kidney , edited by DuBose TD and Hamm LL. Philadelphia, PA: Saunders, 2002, p. 835–108
  2. 10.1152/ajpcell.1981.240.3.C121 · DOI

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Metadata

Authors
Robergs, R. A., Ghiasvand, F., & Parker, D.
Affiliations
University of New Mexico (US)
ORCID
Robergs, Robert A.
Venue
American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
Publisher
American Physiological Society
Published
2004-09
Volume
287
Issue
3
Pages
R502-R516
ISSN
  • 0363-6119 (ISSN-L)
  • 1522-1490
DOI
10.1152/ajpregu.00114.2004
OpenAlex
W2171756298
Cited by
1,304
References
66
Citations by year
2026: 58 · 2025: 60 · 2024: 71 · 2023: 75 · 2022: 82 · 2021: 82 · 2020: 71 · 2019: 54 · 2018: 81 · 2017: 62 · 2016: 53 · 2015: 51 · 2014: 70 · 2013: 63 · 2012: 58
FWCI
74.59
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Regulatory, Integrative and Comparative Physiology (publishedVersion)
  • PubMed (publishedVersion)
  • Faculty of Health
Topics
  • Health Sciences › Medicine › Physiology (medical) › Cardiovascular and exercise physiology
  • Health Sciences › Nursing › Nutrition and Dietetics › Muscle metabolism and nutrition
  • Health Sciences › Medicine › Physiology (medical) › Exercise and Physiological Responses
Keywords
lactic acidosis, lactic acid production, muscle fatigue, proton release, ATP regeneration, glycolysis, phosphagen system, mitochondrial respiration, oxidative phosphorylation, pyruvate accumulation, NAD+ regeneration, exercise performance
MeSH terms
Acidosis, Acidosis, Lactic, Animals, Buffers, Humans, Models, Biological, Protons, Exercise, Lactic Acid, History, 18th Century, History, 20th Century

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