Exercise and lactate
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. 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 which is then directly used to fuel the citric acid cycle and conversion to glucose via the Cori cycle in the liver through the process of gluconeogenesis.
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 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, aerobic metabolism cannot produce ATP quickly enough to supply the demands of the muscle. As a result, 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.[citations needed]
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 causitive factors (independent variables) of [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 and increase in [H+] to maintain electroneutrality. PCO2 also causes an increase in [H+]. During exercise, intramuscular [lactate] and PCO2 increase, causing an increase in [H+], and thus a decrease in pH. It is unclear as to why Robergs et al. have ignored these independent variables in their review. [SID], PCO2, and [weak acid buffer] have been measured during exercise by Jones et al. The reader interested in acid-base balance during exercise is recommended to consult work by Peter Stewart.
· 1 decade ago