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Proton (H+) Load of Intense Exercise

Based on the results and implications of my 2004 manuscript that questioned the classic theory of a lactic acidosis, I computed the proton release or consumption from the reactions of the phosphagen and glycolytic energy systems.  I estimated the capacity of each reaction based on muscle metabolite accumulation data from prior research that applied methods based on highly intense exercise (where most blood flow would be occluded), or intense exercise with circulatory occlusion.  I completed this manuscript in about 2008, and have been trying to publish this on and off for almost 6 years!  Once again, I have nothing good to say about the past and current "climate" in editorial peer review on topics that are controversial, because so much bias is inherent in peer reviewers who cannot remove their own bias and ego from the peer review system.  This manuscript represents the best work of my career, and it is blocked from publication by a select group of researchers unable to question their own bias in their acceptance of the Stewart approach to a theoretical physico-chemical model of metabolic acidosis.

Note that the Stewart approach is just a theory, has never been adequately validated, and while it can explain the influence of changes in the concentrations of strong ions in blood to a developing systemic acidosis, it is flawed by the assumption that the pH of body fluids is a dependent variable - only influenced by external events.  Such an assumption ignores all the evidence and "reality" of how numerous (not all) chemical reactions directly alter proton release and consumption kinetics and thereby influence the pH of their immediate body fluid compartment.  The lactate dehydrogenase reaction is a classic example of this as shown left in the accompanied Figure and chemical reaction below.  The figure data represent the increase in solution pH as the LDH reaction proceeds, with the pH change eventually diminishing as NAD+ decreases in the reagent cocktail. Thus, as lactate is produced, a proton (H+) is consumed (a pH dependent process, which for muscle remains relatively stable at close to 1 H+ per lactate produced) across the physiological pH range).

pyuvate + NADH + H+ <---> lactate + NAD+ + H20

One of the main tenants of metabolic biochemistry is that cellular H+ kinetics are influenced by select individual chemical reactions.  Peter Stewart was simply wrong in his theoretical foundation of the physico-chemical approach to explaining systemic acidosis. Yes, changes in blood strong ions can alter pH, but this does not remove any role of classic Henderson derived acid-base chemistry altering H+ kinetics within a fluid compartment.  In reality, a mix of classic and physico-chemical influences need to be combined to more accurately profile systemic metabolic acidosis.

I am trying to do this but the bias in science on this topic is astoundingly incompetent and thwarts scientific progress in understanding acid-base biochemistry and related physiology.