Let’s set the story straight up front, there is virtually no lactic acid in the human body. Yes, that includes muscles. Based on the laws of physics, and the fundamentals of metabolic biochemistry, physiology, and acid-base chemistry, lactic acid cannot be produced in living systems where the pH is regulated between 6.0 and 7.5. That one silly little proton (positively charged hydrogen molecule) will not stick to the lactate molecule to make it lactic acid. So why does everyone say that lactic acid causes muscle fatigue?
To understand why we think that we must flush the lactic acid from our legs after some intense assault bike sprints, we need to look back at the history of lactate and lactic acid. In 1789 Carl Sheele, a Swedish chemist, isolated lactic acid from samples of sour milk (1). By 1869, scientists had discovered the formation of lactic acid in fermentation reactions, you know that process to make beer and kombucha (2). Since then it has been widely used in the food industry as a flavoring additive and preservative.
In 1907 Fletcher and Hopkins were some of the first individuals to demonstrate that there are low levels of “lactic acid” in muscle at rest and after muscle contractions the amount of “lactic acid” increased. This increase reduced quickly when the muscles were exposed to oxygen. While they discuss these changes as alterations in “lactic acid”, they were actually measuring lactate, which they indicate in the paper’s methodology (3). This initial study laid the groundwork for the next few decades of research. A common misconception of this original research is that “lactic acid” causes fatigue. Fletcher and Hopkins do not make this claim they simple suggest that the increase in lactate occurs at a similar time as fatigue.
When 1922 rolled around two Nobel Prize winning scientists, Otto Meyerhoff and Archibald Hill, who trained under Hopkins and Fletcher, suggested that lactic acid was a side reaction to anaerobic glycolysis (breaking down sugar when oxygen is not present); although, there were never any experiments run to prove that that lactate production caused acidosis (4). Additionally, they demonstrated that lactate can be converted back into glycogen. Unfortunately, at that time they still had an incomplete understanding of cellular metabolism (how our cells make energy).
Hill continued to research the association of lactate and fatigue using humans. From his 1924 experiments he concluded that the rise in lactate that occurs at the start of exercise is due to a deficit in oxygen in the working skeletal muscle (5-6). This work became the basis for the idea that lactate produced by the muscle during exercise causes fatigue, but still no one had proven cause-and-effect of lactate production and acidosis. The unquestioned acceptance of lactic acidosis is a hallmark and basis for much of the research in the field of muscle metabolism since the 1920’s.
Several studies have been conducted since the 1920’s that shed more light on the idea of lactic acidosis (accumulation of lactate and accompanying accumulation of hydrogen ions) causing fatigue. Studies utilizing isolated muscle demonstrate that when placed in an acidic environment the muscle cannot produce the same amount of force when stimulated to contract. Acidosis is thought to inhibit muscle function through a variety of methods including, inhibition of calcium release and uptake by the sarcoplasmic reticulum (this calcium is required for muscle contraction), inhibition of myosin ATPase activity (required for actin-myosin binding and muscle contraction), inhibition of glycolysis (breaking down of sugar to make energy), and decreases in the amount of free energy (ATP) (7-8). By the 1980s it was widely accepted that acidosis was a likely cause of fatigue in the muscle. In the 1990s this was challenged by experiments that were performed in more physiological conditions. Although many of the earlier results were proven to be less substantial, it is likely that acidosis is a contributor to muscle fatigue independent of lactate.
Since the early 1920’s we have come a long way in our understanding of metabolism, fatigue, lactate, and metabolic acidosis. While early studies thought that lactate was a waste product from the breakdown of sugars, we now know that lactate is actually a very useful fuel source for the muscle, heart, liver and brain. Studies by George Brooks demonstrated that lactate is a very mobile compound that can leave the muscle to enter the bloodstream and travel to other tissues to be used as fuel. Brooks also showed that in addition to being used as fuel, the production of lactate in muscle during exercise is very beneficial and actually helps prevent fatigue (9).
In summary, lactate, formerly known to us as “lactic acid”, is not bad. We do not need to “flush” the lactic acid from our muscles after intense exercise. In fact, lactate is a misunderstood byproduct of anaerobic glycolysis that actually plays a pivotal role in helping our muscles and bodies continue to function during high-intensity exercise.
Written by:
Mel Puppa-Lasher, PhD
References
1) Scheele KW (1788–1789) Opuscula chemica et physica. Leipzig
2) Holten CH, Muller A, and Rehbinder D. Lactic Acid: Property and Chemistry of Lactic Acid and Derivatives. Germany: Verlag Chemie, 1971.
3) Fletcher WM. and Hopkins G. Lactic acid in amphibian muscle. The Journal of physiology. 1907;35(4):247-309.
4) Hill, A. V. and Meyerhof, O. (1923). Ueber die vorgange bei der muskelkontraktion. Ergeb. Physiol. Biol. Chem. Exp. Pharmakol. 22, 299-344
5) Hill, A. V., Long, C. N. H. and Lupton, H. (1924a). Muscular exercise, lactic acid, and the supply and utilisation of oxygen. Parts I-III. Proc. R. Soc. Lond. B 96, 438-475.
6) Hill, A. V., Long, C. N. H. and Lupton, H. (1924b). Muscular exercise, lactic acid, and the suppply and utilisation of oxygen. Parts IV-VI. Proc. R. Soc. Lond. B 97, 84-138.
7) Cairns, S. P. (2006). Lactic acid and exercise performance. Sports Medicine, 36(4), 279-291.
8) Robergs, R. A., Ghiasvand, F., & Parker, D. (2004). Biochemistry of exercise-induced metabolic acidosis. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 287(3), R502-R516.
9) Brooks, G. A. (2007). Lactate. Sports medicine, 37(4-5), 341-343.
