Citizendium - a community developing a quality, comprehensive compendium of knowledge, online and free.
Click here to join and contribute
CZ thanks our previous donors. Donate here. Treasurer's Financial Report

Lactic fermentation

From Citizendium
Jump to: navigation, search
This article is developing and not approved.
Main Article
Related Articles  [?]
Bibliography  [?]
External Links  [?]
Citable Version  [?]
This editable Main Article is under development and subject to a disclaimer.

Lactic acid fermentation is a form of fermentation that occurs in animal cells in the absence of oxygen. Under these conditions, Glycolysis occurs normally, producing 2 molecules of ATP, 2 molecules of NADH and 2 molecules of pyruvate. However, the lack of O2 prevents the NADH from being recycled to NAD+ (which is required for glycolysis) through the electron transport chain. Instead, it transfers electrons to pyruvate:

pyruvate + NADH lactate + NAD+

Lactate then diffuses out of the cell and into the blood. Certain cells, such as cardiac muscle cells, are highly permeable to lactate. Lactate is converted into pyruvate and metabolised normally (ie: via the citric acid cycle). Since these cells are highly oxygenated, it is unlikely that lactate would accumulate (as is the case in oxygen-starved muscle cells). This also allows circulating glucose to be available to muscle cells.

Any excess lactate is taken up by the liver, converted to pyruvate and then to glucose. This, along with the production of lactate from glucose in muscle cells constitutes the Cori cycle.

Phosphofructokinase (PFK), which catalyses an irreversible step in glycolysis, is inhibited by a low pH and this prevents the formation of excess lactate and/or lactic acidosis (sudden drop in blood pH).

Lactic fermentation and exercise

Lactic fermentation is much faster than the Krebs cycle or oxidative phosphorylation, and is therefore the preferred pathway for energy generation in muscle cells under strenuous exercise. During intense exercise, such as sprinting type activities, when the rate of demand for energy is high, lactate is produced faster than the ability of the tissues to remove it and lactate concentration begins to rise. Contrary to popular belief, this increased concentration of lactate does not directly cause acidosis, nor is it responsible for muscle pain or "burning".[1] This is because lactate itself is not capable of releasing a proton, and secondly, the acidic form of lactate (lactic acid) cannot be formed under normal circumstances in human tissues. Analysis of the glycolytic pathway in humans indicates that there are not enough hydrogen ions present in the glycolytic intermediates to produce lactic or any other acid.

The acidosis that is associated with increases in lactate concentration during heavy exercise arises from a separate reaction. When ATP is hydrolysed, a hydrogen ion is released. ATP-derived hydrogen ions are primarily responsible for the decrease in pH. During intense exercise, oxidative metabolism (aerobic) cannot produce ATP quickly enough to supply the demands of the muscle. As a result, glycolysis (i.e. anaerobic metabolism) becomes the dominant energy producing pathway as it can form ATP at high rates. Due to the large amounts of ATP being produced and hydrolysed in a short period of time, the buffering systems of the tissues are overcome, causing pH to fall and creating a state of acidosis. This may be one factor, among many, that contributes to the acute muscular discomfort experienced shortly after intense exercise.

Although it is not firmly established, it is possible that lactate may contribute to an acidotic effect via the strong ion difference, however this has not been well investigated in exercise physiology research and so its contribution is still uncertain.


  1. Robergs R, Ghiasvand F, Parker D (2004). "Biochemistry of exercise-induced metabolic acidosis.". Am J Physiol Regul Integr Comp Physiol 287 (3): R502-16. PMID 15308499.

See also