Lactate (a.k.a. Lactic acid) Is Not The Source

Lactate is not lactic acid; lactate is proton consuming. Acidosis is a condition that tends to lower ph levels (increases acidosis). An acid may be proton donating, or may be defined as a molecular substance that releases positive hydrogen ions in a neutral, aqueous solution.  Lactate buffers against acidosis. In an experimental study conducted by Smith et al. (1993) when lactate was decreased and there was a greater rate of non-mitochondrial ATP hydrolysis, ph levels dropped- increased acidity.

Lactic acid is not produced during exercise or present in any physiological system (Robergs et al., 2017). Early research indicates a positive association between acidosis and lactate levels; no experimental research is indicative of this claim. Sum of lactate and pyruvate to ph demonstrates a strong positive association (r = 0.912) between the variables. This association has been misinterpreted as causation. This demonstrates the third variable problem, as it is referred to in research methodology.  Past research cited to indicate lactate causes acidosis is based entirely on correlations; “no experimental evidence has ever been shown to reveal a cause-effect relationship between lactate production and acidosis” (Robergs et al., 2004, p.R504).

“False Belief 1: Metabolism of Pyruvate produces lactic acid” Venkatesh, 2017

Video- Does Lactic Acid Really Cause Muscle Soreness?

Video- Refuting lactate myths

Key points Biochemistry of metabolic acidosis:

There is no biochemical support for lactate causing acidosis

Lactate doesn’t cause the muscle burn

Lactate slows acidosis

If muscle doesn’t produce lactate, acidosis and fatigue will occur quicker

Lactate is product of glycolysis, and is used by skeletal, cardiac and smooth muscle

Lactate is produced during aerobic and anaerobic conditions

“Metabolic acidosis is caused by an increased reliance on nonmitochondrial ATP turnover. Lactate production is essential…to support continued ATP regeneration from glycolysis. The production of lactate also consumes two protons and, by definition, retards acidosis. Lactate also facilitates proton removal from muscle. Although muscle or blood lactate accumulation are good indirect indicators of increased proton release and the potential for decreased cellular and blood pH, such relationships should not be interpreted as cause and effect” (Robergs et al.,2004, p.R514).

The intent of this article is to provide some key points relevant to an appropriate understanding of lactate’s role in metabolism. It is easy to understand why lactate myths are widespread; they permeate textbooks, college lectures and popular media. There is a large body of scientific literature that refutes lactate miconceptions. In a future article I will provide a lengthy discussion regarding other misconeptions associated with lactate.

Addendum (12-12-18)

Abstract – Mann, 2007:

Background. Lactate or, as it was customarily known, ‘lactic acid’ was one of the first molecules to attract the attention of early exercise scientists, mainly because blood lactate concentration could be measured and was shown to increase with increasing exercise intensity. This connection resulted in lactate being associated with numerous other events associated with high-intensity exercise including muscle cramps, fatigue, acidosis and post-exercise muscle soreness. Nobel prize-winning research by AV Hill and Otto Meyerhof provided a rational explanation linking lactate to anaerobiosis and acidosis, which resulted in this relationship being widely accepted as fact. It was only following isotopic tracer studies of George Brooks and others that the true role of lactate during rest and exercise was revealed. Conclusions. Lactate is now acknowledged as an important intermediate of carbohydrate metabolism, taken up from the blood by tissues such as skeletal and cardiac muscle as a substrate for oxidation. Furthermore, lactate formation consumes a proton, thereby buffering against muscle acidosis. For this reason, lactate production forms an essential aid to endurance performance rather than a hindrance.”

Key points from Mann, 2007:

Prior to the discovery of the lactate shuttling systems, “scientists had determined that blood and muscle lactate concentrations return to resting levels within an hour of the exercise session.”  Unlikely that lactate causes the pain and stiffness that occurs 12 – 24 hours after exercise. Evidence indicates that lactate might be beneficial for muscle recovery by serving as a substrate for glycogen re-synthesis.

“Post-exercise muscle soreness is now largely accepted to be as a result of mechanical damage to the muscle and the associated inflammation” Inflammation leads to changes in chemical, temperature and pressure fluctuations, which often contribute to pain (pain is a concept-complex, physiological, social and psychological factors involved).

The link between increased lactate and decreased blood and muscle pH – has  long been believed to result from the dissociation of protons from lactate. Recent research indicates the association is a correlation and not a cause and effect relationship.

It is proposed that rapid turnover of ATP, and not increased lactate production, is ultimately responsible for the accumulation of protons at high exercise intensity. Lactate resists rather than contributes to a fall in pH “as formation of lactate from muscle glycogen actually consumes two protons.”

Lactate production is not inherently bad, but rather it may be an advantage

Abstract- Brooks, 2009:

“Once thought to be the consequence of oxygen lack in contracting skeletal muscle, the glycolytic product lactate is formed and utilized continuously in diverse cells under fully aerobic conditions. ‘Cell–cell’ and ‘intracellular lactate shuttle’ concepts describe the roles of lactate in delivery of oxidative and gluconeogenic substrates as well as in cell signalling. Examples of the cell–cell shuttles include lactate exchanges between between white‐glycolytic and red‐oxidative fibres within a working muscle bed, and between working skeletal muscle and heart, brain, liver and kidneys. Examples of intracellular lactate shuttles include lactate uptake by mitochondria and pyruvate for lactate exchange in peroxisomes. Lactate for pyruvate exchanges affect cell redox state, and by itself lactate is a ROS generator. In vivo, lactate is a preferred substrate and high blood lactate levels down‐regulate the use of glucose and free fatty acids (FFA). As well, lactate binding may affect metabolic regulation, for instance binding to G‐protein receptors in adipocytes inhibiting lipolysis, and thus decreasing plasma FFA availability. In vitro lactate accumulation upregulates expression of MCT1 and genes coding for other components of the mitochondrial reticulum in skeletal muscle. The mitochondrial reticulum in muscle and mitochondrial networks in other aerobic tissues function to establish concentration and proton gradients necessary for cells with high mitochondrial densities to oxidize lactate. The presence of lactate shuttles gives rise to the realization that glycolytic and oxidative pathways should be viewed as linked, as opposed to alternative, processes, because lactate, the product of one pathway, is the substrate for the other.”

Key points from Brooks, 2009:

“Once thought to be the consequence of oxygen lack in contracting skeletal muscle, we know now that lactate is formed and utilized continuously under fully aerobic conditions. Lactate is actively oxidized at all times, especially during exercise when oxidation accounts for 70–75% of removal and gluconeogenesis for most of the remainder.”

Lactate is used by glygolytic and oxidative fibers. Lactate has an influence on metabolic regulation in multiple cells at diverse levels.”The presence of cell–cell and intracellular lactate shuttles gives rise to the notion that glycolytic and oxidative pathways be viewed as linked, as opposed to alternative, processes, because lactate, the product of one pathway, is the substrate for the other.”

References are available upon request

Jamie Hale