Lactic acid and its influence on acidosis

[Caleb]

Hi,

I got my Science of Sports Training a few days ago, and have just started reading it.

On p. 14, it says this regarding acidosis:

Speed-endurance work such as all-out efforts lasting 15-50 seconds lead to increased acidity of body fluids. Even a single all-out effort of about 35 seconds can raise blood lactate concentration to over 14 mmol/l and impair the function of the central nervous system. *snipped* During a single workout, exercises that raise blood lactate should not be done before practicing technical and tactical skills as well as working on speed or strength.

Execess lactic acid taxes the body's abilities to restore the proper acid and alkaline balance. Sodium is taken from the body fluids and phosphorus is taken up from bones, which causes their demineralization and loss of calcium, and this is detrimental to muscle and nerve function (McArdle, Katch, and Katch, 1991).

I'm trying to understand these paragraphs, do they imply that it is the lactic acid that is directly responsible for acidosis, or is just correlated with it?

I've been looking this up, and found this recent paper on the subject: R. Robergs, F. Ghiasvand, D. Parker (2004). "Biochemistry of exercise-induced metabolic acidosis". Am J Physiol Regul Integr Comp Physiol 287 (3): R502–16. http://ajpregu.physiology.org/cgi/conte ... 287/3/R502

To quote the abstract (emphasis is mine):

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 Pi, 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.

[Caleb]

Interestingly enough, a review of the aforementioned paper (http://ajpregu.physiology.org/cgi/conte ... 289/3/R891) concludes the opposite:

In conclusion, it is useful and instructive to accurately follow the path of protons in metabolic pathways. We agree with the data as summarized by others (18, 27, 28) that lactic acid is not produced in muscle and that it is not present in meaningful concentrations. There is merit in providing a useful summary of the underlying biochemical reactions involved in energy production within muscle and in identifying the correct species of metabolic substrates and products. However, failure to apply the entirety of physicochemical principles leads to the incorrect and misleading conclusion that lactate– is unrelated to the metabolic acidosis of exercise. We do contend, therefore, that the accumulation of lactate– within skeletal muscle directly contributes to intracellular acidosis, by virtue of the fact that it is a strong acid anion that fundamentally alters the behavior of water. With respect to acid-base balance, it is inappropriate to consider each biochemical reaction independently, and it is similarly inappropriate to try to link them temporally or in biochemical sequence. Acid-base balance changes instantaneously; therefore, a more complete understanding of the acidosis of exercise considers the simultaneous biochemical, transport, and proton buffering reactions, as well as their instantaneous and simultaneous physicochemical interactions with water, at any point in time.