Full Article: Acidosis - Biochemistry of Exercise-Induced Metabolic Acidosis
Synopsis: 80+ Years of Fundamental Bio-Chemistry Errors in Mainstream Medical Literature
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A Brief Synopsis:
80+ Years of Fundamental Bio-Chemistry Errors in Maintream Medical Literature
Introduction
Acidosis if often misrepresented in mainstream North American medical, educational and scientific literature. Caution must be taken when reviewing such definitions and articles. The followng articles will clarify the significant and contrasting bio-chemistry differences between metabolic acidosis and lactic acidosis:
"The terms "lactate" or "lactic acid" need to be removed from any association with the cause of acidosis or the training that is used to delay the onset of acidosis." - Robert A. Robergs et al. - Exercise Physiology Laboratories, Department of Physical Performance and Development.
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Metabolic Acidosis - Medical Errors / Misinformation
The "Lactic Acid Concept" for causing Acidosis / Metabolic Acidosis:
"The lactic acidosis explanation of metabolic acidosis is not supported by fundamental biochemistry, has no research base of support, and remains a negative trait of all clinical, basic, and applied science fields and professions that still accept this construct.
The most important reason to discard the lactic acidosis concept is that it is invalid. It has no biochemical justification and, to no surprise, no research support. We have been criticized for our stance on the need to change how to teach and interpret metabolic acidosis."
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Metabolic Acidosis - What are they trying to hide?
What is the cause of Acidosis? ... THE FACTS:
This is the crucial question that all physiologists must be able to answer. There are several examples of why the correct cause of metabolic acidosis needs to be accepted, communicated in education, and used in research interpretation and publication.
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Scientific validity.:
The most important reason to discard the lactic acidosis concept is that it is invalid. It has no biochemical justification and, to no surprise, no research support. We have been criticized for our stance on the need to change how to teach and interpret metabolic acidosis.
As such, the concept of a lactic acidosis remains evidence of 1920s academic and scientific inertia and a summary equation that does not represent cause and effect ... and out of simple convenience and apathy, still remains today.
We would hope that the academics and professionals from the basic and applied fields that continue to accept the lactic acidosis construct immediately change the way they teach and interpret this topic.
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Education:
Education is a powerful force that can induce change or reinforce error. Rather than continuing to reinforce error, educators need to recognize their power in reshaping how students and academics alike explain and discuss all matters pertaining to metabolic acidosis and skeletal muscle proton buffering. The correct teaching of metabolic acidosis is crucial for the promotion and acceptance of the correct understanding of exercise-induced metabolic acidosis.
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Sports Physiology, Coaching, and Training:
An acceptance of the true biochemistry of metabolic acidosis means that terms and descriptions used throughout sports physiology and coaching need to be changed. The terms "lactate" or "lactic acid" need to be removed from any association with the cause of acidosis or the training that is used to delay the onset of acidosis.
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Research of Strategies to Retard Exercise-Induced Metabolic Acidosis:
If it is assumed that lactate production causes acidosis, then it is a logical extension to hypothesize that reducing lactate production for a given cellular ATP demand should retard acidosis. If decreasing the rate of lactate production is accomplished by stimulating increased mitochondrial respiration [such as through dichloracetate infusion/ingestion (18)], such a strategy might also increase mitochondrial proton uptake and decrease/delay acidosis.
However, as is clear from the biochemistry, for a given rate of mitochondrial respiration, decreasing lactate production will decrease proton buffering and removal from skeletal muscle and increase the rate of onset and worsen the severity of acidosis.
On the basis of the biochemistry of muscle metabolism, the best way to decrease metabolic acidosis is to decrease nonmitochondrial ATP turnover by stimulating mitochondrial respiration. For a given ATP demand, any effort to decrease lactate production without increasing mitochondrial respiration will worsen metabolic acidosis.
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No Biochemical Support for Lactic Acidosis Causing Metabolic Acidosis
There is no biochemical support for the construct of a lactic acidosis. Metabolic acidosis is caused by an increased reliance on nonmitochondrial ATP turnover. Lactate production is essential for muscle to produce cytosolic NAD+ to support continued ATP regeneration from glycolysis.
The production of lactate also consumes two protons and, by definition, retards acidosis. Lactate also facilitates proton removal from muscle. Although muscle or blood lactate accumulation are good indirect indicators of increased proton release and the potential for decreased cellular and blood pH, such relationships should not be interpreted as cause and effect.
The aforementioned interpretations of the biochemistry of lactate production and acidosis are also supported by research evidence. As such, research evidence also disproves the concept of a lactic acidosis. Quantifying nonmitochondrial ATP turnover during intense cycle ergometry exercise and assuming this value to be identical to proton release, reveals a near perfect stoichiometry to known components of proton consumption within contracting skeletal muscle.
Conversely, research data of muscle lactate production and proton release yield a lactate-to-proton stoichiometry approximating 1:3 (33:103 mmol H+/kg wet wt; Figs. 16 and 17).
Educating students on the correct biochemical cause of acidosis is extremely important for reasons of academic credibility and scientific validity. In addition, the past incorrect interpretations of lactic acidosis have yielded questionable research applications and data interpretations, with the indirect calculation of the muscle proton buffering unit of slyke {[(Δlactate + Δpyruvate)/ΔpH] ∼ (ΔH+/ΔpH)} being the best example of this error.
It is strongly recommended that all educators and researchers incorporate the application of the correct cause of acidosis into their professional practice
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Unquestioned Mainstream Acceptance Since the 1920's
The unquestioned acceptance of a lactic acidosis is a hallmark of almost all of the basic and applied science research of muscle metabolism since the 1920s.
Although the biochemistry of exercise-induced metabolic acidosis is unquestionable, there is considerable research support and therefore validation of nonmitochondrial ATP turnover as the cause of acidosis. For example, several researchers have denoted that the assumption that "lactic acid" is the source of H+ is inaccurate.
Gevers (10, 11) first drew attention to the very important possibility that protons might be generated in significant quantity in muscle by metabolic processes other than the lactate dehydrogenase reaction. He suggested that the major source of protons was the turnover of ATP produced via glycolysis. This important concept, quite contrary to the general concept of that time that "lactic acid" is the end product of glycolysis, aroused little interest for six years.
It was not until 1983 that Hochachka and Mommsen (16) rediscovered and wrote an extensive review on this topic. Hochachka et al. supported Gevers' idea that metabolic acidosis resulting from glycolysis is primarily due to ATP hydrolysis by myosin ATPase that yields ADP, Pi, and H+. According to these authors, only ADP and Pi are recycled via glycolysis to produce ATP, leaving H+ behind to accumulate within the cytosol.
In other words, the glycolytic generation of ATP and ATPase-catalyzed hydrolysis of ATP are, to some extent, coupled (Fig. 11). Busa and Nuccitelli (4) also commented on this topic in an invited opinion in 1984. These authors essentially reaffirmed the writings of Gevers (10, 11) and Hochachka and Mommsen (16).
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As stated by Busa and Nuccitelli (4):
"ATP hydrolysis, not lactate accumulation, is the dominant source
of the intracellular acid load accompanying anaerobiosis."
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"When evaluating past research for evidence in support of the nonmitochondrial ATP turnover cause of metabolic acidosis, the stoichiometry is far more impressive. These data are presented in Fig. 17. When the main consumers of protons are combined, there is a near equality between proton release (ATP-NM and glycolysis) and proton consumption."
- Robert A. Robergs, et al.
- Exercise Physiology Laboratories, Department of Physical Performance and Development
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- by Robert A. Robergs et al. - Exercise Physiology Laboratories,
Department of Physical Performance and Development.
Full Article: Acidosis - Biochemistry of Exercise-Induced Metabolic Acidosis
Synopsis: 80+ Years of Fundamental Bio-Chemistry Errors in Mainstream Medical Literature
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