The Exercise and Lactate Lactic Acid

In industry, lactic acid fermentation is performed by lactic acid bacteria. These bacteria can also grow in the mouth; the acid they produce is responsible for the tooth decay known as caries. During power exercises such as sprinting, when the rate of demand for energy is high, lactate is produced faster than the ability of the tissues to remove it, so lactate concentration begins to rise. This is a beneficial process, since the regeneration of NAD+ ensures that energy production is maintained and exercise can continue. The increased lactate produced can be removed in a number of ways, including:

Oxidation to pyruvate by well-oxygenated muscle cells.

Pyruvate is then directly used to fuel the Krebs cycle. Conversion to glucose via gluconeogenesis in the liver and release back into the circulation; see the Cori cycle. If not released, the glucose can be used to build up the liver's glycogen stores if they are empty.

Contrary to popular belief, this increased concentration of lactate does not directly cause acidosis, nor is it responsible for delayed onset muscle soreness. This is because lactate itself is not capable of releasing a proton, and, second, the acidic form of lactate, lactic acid, "is not produced in muscle". 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.

Lactic acid is the root of lactose sugar, and they are directly related.

The effect of lactate on acidosis has been the topic of many recent conferences in the field of exercise physiology. Robergs et al. have accurately chased the proton movement that occurs during glycolysis. However, in doing so, they have suggested that [H+] is an independent variable that determines its own concentration. A recent review by Lindinger et al. has been written to rebut the stoichiometric approach used by Robergs et al. In using this stoichiometric process, Robergs et al. have ignored the causative factors (independent variables) of the concentration of hydrogen ions (denoted [H+]). These factors are strong ion difference [SID], PCO2, and weak acid buffers. Lactate is a strong anion, and causes a reduction in [SID], which causes an increase in [H+] to maintain electroneutrality. PCO2 also causes an increase in [H+]. During exercise, the intramuscular lactate concentration and PCO2 increase, causing an increase in [H+], and, thus, a decrease in pH.

During intense exercise, the respiratory chain cannot keep up with the amount of hydrogen atoms that join to form NADH. NAD+ is required to oxidize 3-phosphoglyceraldehyde in order to maintain the production of anaerobic energy during glycolysis. During anaerobic glycolysis, NAD+ “frees up” when extra nonoxidized hydrogens combine with a pyruvate molecule and then form lactate. If this does not occur, glycolysis comes to a stop. However, there is lactate being continually formed at rest and during moderate exercise. This occurs due to the metabolism of red blood cells that do not have mitochondria and limitations resulting from enzyme activity that occurs in muscle fibers that contain a high glycolytic capacity.

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