Biochemistry of exercise-induced metabolic acidosis
One article on PainSci cites Robergs 2004: A Deep Dive into Delayed-Onset Muscle Soreness
original abstract †Abstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.
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.
related content
- “From Time Magazine to NBC Commentators: Why is everyone still so confused about lactate (and exercise physiology)?,” Matthew L Goodwin, LetsRun.com.
- “Lactic Acid Is Not Muscles' Foe, It's Fuel,” Gina Kolata, NYTimes.com.
- “Nothing ‘evil' and no ‘conundrum' about muscle lactate production,” Robergs, Experimental Physiology, 2012.
- “Biochemistry of exercise-induced metabolic acidosis,” Robergs et al, American Journal of Physiology, 2004.
This page is part of the PainScience BIBLIOGRAPHY, which contains plain language summaries of thousands of scientific papers & others sources. It’s like a highly specialized blog. A few highlights:
- Inciting events associated with lumbar disc herniation. Suri 2010 Spine J.
- Prediction of an extruded fragment in lumbar disc patients from clinical presentations. Pople 1994 Spine (Phila Pa 1976).
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- Effectiveness and cost-effectiveness of universal school-based mindfulness training compared with normal school provision in reducing risk of mental health problems and promoting well-being in adolescence: the MYRIAD cluster randomised controlled trial. Kuyken 2022 Evid Based Ment Health.
- Is there a relationship between throbbing pain and arterial pulsations? Mirza 2012 J Neurosci.