Biochemistry of exercise-induced metabolic acidosis.

  title={Biochemistry of exercise-induced metabolic acidosis.},
  author={Robert Andrew Robergs and Farzenah Ghiasvand and Daryl L. Parker},
  journal={American journal of physiology. Regulatory, integrative and comparative physiology},
  volume={287 3},
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… 
Letters to the Editor
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Lactic acidosis in vivo: testing the link between lactate generation and H+ accumulation in ischemic mouse muscle.
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The Aerobic Energy Production and the Lactic Acid Excretion are both Impeded in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome
It is found that in severe ME, both the oxidative phosphorylation and the lactic acid excretion are impaired, and the combination of these two is responsible for the main characteristic of ME, the abnormally delayed muscle recovery after doing trivial things.
Lactate: Friend or Foe


Exercise-Induced Metabolic Acidosis : Where do the Protons come from ?
Researchers, clinicians, and sports coaches need to recognize the true causes of acidosis so that more valid approaches can be developed to diminish the detrimental effects of Acidosis on their subject/patient/client populations.
Regulation of lactic acid production during exercise.
It is proposed that the achievement of increased aerobic energy formation under conditions of limiting O2 availability requires increases of ADP, Pi, and NADH and that the increases in ADP (and therefore AMP via the adenylate kinase equilibrium) and Pi will stimulate glycolysis, and the resulting increase in cytosolic NADH will shift the lactate dehydrogenase equilibrium toward increased lactate production.
The Origin of the Acidosis in Hyperlactataemia
  • J. Zilva
  • Biology
    Annals of clinical biochemistry
  • 1978
It is suggested that only by understanding these important biochemical facts can the clinician found his diagnosis and treatment on a firm, rational basis.
Muscular exercise, lactic acid, and the supply and utilisation of oxygen
It has been shown that any substances other than lactic acid and oxygen are directly concerned in the recovery process in muscle, so the above relationship can be put in terms of these substances.
Acid-base regulation during exercise and recovery in humans.
It is concluded that arterial acidosis is the consistent arterial pH reaction for moderate-, heavy-, and very-heavy-intensity cycle ergometer exercise in humans and that this Acidosis is blunted but not eliminated by the ventilatory response.
Contribution of tissue acidosis to ischemic injury in the perfused rat heart.
It is suggested that the primary cause of the decreased peak systolic pressure with either acidosis or ischemia is not a result of a defect of energy metabolism, but is due to alteration of the calcium cycle of the heart.
Quantification of anaerobic energy production during intense exercise.
  • J. Bangsbo
  • Education
    Medicine and science in sports and exercise
  • 1998
Estimated pulmonary oxygen deficit based on an energy demand extrapolated from a linear relationship between exercise intensity and oxygen uptake at submaximal exercise does not appear to represent the anaerobic energy production during whole body exercise.
Relationship between intracellular pH and metabolite concentrations during metabolic inhibition in isolated ferret heart.
The results suggest that the acidosis produced by cyanide (without inhibition of glycolysis) is largely due to lactic acid production.
Factors influencing hydrogen ion concentration in muscle after intense exercise.
To assess the importance of factors influencing the resolution of exercise-associated acidosis, measurements of acid-base variables were made in nine healthy subjects after 30 s of maximal exercise
Effects of lactic acid accumulation and ATP decrease on muscle tension and relaxation.
The main findings in the present study were that tension decline in unpoisoned muscle is closely related to decrease in muscle pH and increase in ADP but not to ATP content per se and that slowing of relaxation rate is closely connected to decrease to muscle pHbut not to muscle content of ATP or creatine phosphate.