For years, it was considered garbage in our cells, a waste product of our metabolism. It was considered to be the cause of muscle soreness. We are talking about lactate. It should be noted at this point that its role in the body is by no means fully understood at this point. However, some “truths” related to lactate have proven to be definitely false. Misinformation still circulates and even experts are on a wrong and outdated steamer when interpreting its occurrence, as in performance diagnostics. Modern testing methods help clear the fog around lactate. The new lactate theories suggest that lactate can and is much more than previously believed.
In a three-part series, I would like to present older and current scientific findings here. If you have any questions or comments on the topic, please do not hesitate to contact me. Have fun reading.
What is lactate?
Fat is our body’s main source of energy. At rest, our body gets three-quarters of its energy from fat. The remaining energy comes mainly from carbohydrates. These are broken down into simple sugars for energy production. 75 percent of these are used by our nervous system and especially the brain, since the brain can only utilize a few types of fatty acids. The remaining sugar is mainly used by the red blood cells, as they do not have mitochondria to process fat for energy. The mitochondria, provide energy using oxygen. Since oxygen is necessary, this is referred to as aerobic energy supply. Not only fat can serve as a starting material for aerobic energy supply via the mitochondria. Carbohydrates are also used for aerobic energy production. In contrast to fat, however, carbohydrates are also suitable for energy production without the aid of oxygen. This is known as anaerobic energy production. This is where the so-called lactic acid fermentation comes into play, during which lactate is produced.
Lactate is often referred to as lactic acid and is held responsible for over-acidification of the muscle and its fatigue. In English, the terms “lactic acid” and “lactate” exist. Here, a differentiation is made between lactate and lactic acid. Chemically, lactate is the salt of lactic acid. In German, no distinction is made between lactic acid and lactate. In the body, the resulting lactic acid decomposes almost completely into lactate and a positively charged hydrogen particle H+. Whether a fluid or a muscle is acidic or hyperacidic depends on the pH value, which is defined as the potential of hydrogen (lat. pondus hydrogenii ). The more hydrogen ions (H+) present, the more acidic the fluid and tissue are classified. These H+ ions have long been seen as the cause of muscular fatigue, as the muscle becomes increasingly acidic. Thus, it is not the lactate that makes acidic, but the hydrogen ions that are formed simultaneously. On the contrary, lactate even has a weakly alkaline effect. Recent scientific studies no longer consider lactate to be the cause of muscular fatigue, but blame changes in metabolism. These metabolic changes have a negative effect on the muscle contraction and/or activation process of the muscles. According to recent studies, intracellular acidosis shows little direct effect on muscle function and does not appear to affect energy production from carbohydrates (glycolysis) even at high intensities. Instead, another major cause of muscle fatigue is seen in phosphate, which increases during fatigue due to the breakdown of creatine phosphate. In addition to the fact that various other factors are seen as the cause of muscular fatigue, acidosis tends to no longer be considered as a trigger of fatigue.
Lactate and its role in energy production
We supply potential energy with food. In the digestive process, all long-chain carbohydrates are broken down into simple sugars as far as possible. Dietary fibers are also carbohydrates in part, but cannot be broken down by our body’s enzymes to produce energy. Some dietary fiber can be indirectly converted into energy by bacteria in the intestinal flora or is excreted undigested. The following applies to the majority of carbohydrates eaten and drunk: If carbohydrates or simple sugars are used for energy production, this is initially done via so-called glycolysis, the breakdown of simple sugars. Glucose (also known as dextrose) is the main sugar converted. During glycolysis, glucose is converted into pyruvate. Pyruvate is an energy carrier, which is sometimes also supplied as a supplement. This conversion of glucose to pyruvate happens with the release of energy in the form of ATP (adenosine triphosphate). ATP is the main energyiferant of our body. ATP production by glycolysis can be adjusted to the current energy demand within a few seconds. Even though aerobic energy provision with oxygen (e.g. through fat) provides significantly more energy overall, glycolysis can provide an amount of energy twice as fast, which is important in sports during intense exercise. However, energy production via glycolysis is limited. The process requires a specific coenzyme, NAD (nicotinamide adenine dinucleotide). However, the coenzyme NAD is “consumed” during glycolysis. Therefore, even with an infinite amount of available glucose, only a certain amount can serve for anaerobic energy production. In order to quickly generate new NAD, the body converts the resulting pyruvate into lactate, creating new NAD, which is again available for anaerobic energy production through glycolysis. In the process, lactate increasingly accumulates. The formation of lactate thus supports anaerobic energy production from carbohydrates. This anaerobic energy production of ATP from glucose is four times higher in the same time compared to energy production from fatty acids. An increase in lactate is observed with increasing physical exertion and thus increasing energy demand. Lactate is formed when pyruvate production exceeds demand and is not necessarily the result of anaerobic conditions with oxygen deficiency. Pyruvate is a key intermediate for a wide variety of metabolic pathways and can serve both aerobic and anaerobic energy production in addition to new glucose production (gluconeogenesis). Pyruvate can also be derived from lactate if required. This process is called lactate oxidation. So lactate is also an important and potent energy source for the body! The conversion of pyruvate to lactate, after glycolysis has taken place, occurs with the help of the enzyme LDH (lactate dehydrogenase). Pyruvate is reduced to lactate anaerobically, i.e. without the participation of oxygen. This process is reversible and also takes place via the enzyme LDH. During intense athletic exertion, our body makes greater use of lactic acid fermentation, and LDH levels increase. LDH is used as a diagnostic parameter in medicine. LDH can be used, for example, as an indicator of damage to muscle cells after heavy exercise. LDH can also be used for diagnosis in diseases. For example, malignant cancer cells often show an increased glucose turnover, especially since mitochondrial function and the associated fat utilization are disturbed (Warburg effect). Five different (iso)forms of the enzyme LDH are known to date, which, depending on their expression, tend either to generate lactate or to break down the lactate. In muscle, the type of LDH depends strongly on the type of muscle fiber. Especially in the fast-twitch glycolytic muscle fibers (type 2x fibers), the M isoform (muscle isoform) dominates, catalyzing the conversion of pyruvate to lactate (lactate production). LDH activity is lower in the slow-twitch red type-1 fibers (oxidative fibers), which dominate in endurance specialists. Here, mainly the H isoform is found, which favors the conversion of lactate to pyruvate (lactate elimination). Due to the isoenzyme distribution within the muscle, there is a preferential flow of lactate from the fast-twitch, glycolytic fibers to the slow-twitch, oxidative fibers. Lactate is not only generated or converted to pyruvate by LDH in the muscles, LDH is also present in organs and tissues. In the heart, the H isoform (cardiac isoform) dominates, which oxidizes the lactate. Especially under high athletic stress, the heart gains well over 50 percent of its energy from lactate.
The brain also absorbs lactate, the higher the lactate concentration, the more, replacing some of the glucose otherwise needed to supply energy. The rate of lactate production differs between muscle fiber types. It is significantly higher in fast-twitch muscle fibers than in slow-twitch muscle fibers. The metabolic capacity, which provides information about lactate elimination, also differs. In the oxidative fibers, the change from a net release to a net uptake of lactate already occurs at low concentrations (1-2 mmol/l). Only at higher concentrations (3-4 mmol/l) does this happen in the glycolytic fibers. Lactate exchange and thus lactate elimination also depend on the blood flow velocity between different tissues, which influences the concentration gradient of lactate. Trained athletes exhibit better fat burning and altered lactate utilization compared to the untrained. During casual training in the fasting state, this contributes to a decrease in gluconeogenesis relative to glycolysis. Not only are decreased lactate levels seen in exercisers under low intensity training in the recovery zone, but also lower glucose concentrations. The lactate produced at rest may be transported predominantly via the bloodstream from muscle cells to the liver and kidney for gluconeogenesis. The exact cause of the lower glucose levels is not clear. Key enzymes activated by fatty acid oxidation and hormonal responses of gluconeogenesis may inhibit enzymes associated with glycolysis. Decreased blood lactate and glucose levels at low exercise levels may be an indicator of the recovery ability of well-trained athletes. In contrast, people with certain (metabolic) diseases exhibit elevated blood lactate concentrations even at low levels of exercise.
Lactate is the salt of lactic acid. When lactate is formed, a hydrogen ion H+ is also always generated, which causes the pH value in the surrounding tissue to drop and it becomes increasingly acidic. According to current knowledge, increasing acidity in the muscle with constant lactate formation is not the cause of muscle fatigue. Anaerobic energy supply – i.e. without oxygen – is supported by lactate formation and lactate utilization (via lactate oxidation). Lactate is also a potential energy carrier. Especially under high athletic stress, the heart gains well over 50 percent of its energy via lactate. The brain also absorbs lactate, the higher the lactate concentration, the more, replacing some of the sugar (glucose) otherwise needed for energy. The enzyme LDH (lactate dehydrogenase) is used in various forms to convert lactate and is an important medical diagnostic parameter. Elevated LDH levels are not only caused by physical activity, but also by metabolic diseases such as diabetes or cancer. During exercise, lactate is produced primarily in fast-twitch, glycolytic muscle fibers. In the slow-twitch, oxidative, red type 1 muscle fibers, lactate is sometimes eliminated at lower intensities. Trained athletes exhibit better fat burning and altered lactate utilization compared to the untrained.
Check out: Newsletter
Literature on the topic:
Hall MM, Rajasekaran S, Thomsen TW, Peterson AR. Lactate: Friend or Foe. PM R. 2016 Mar;8(3 Suppl):S8-S15. doi: 10.1016/j.pmrj.2015.10.018. PMID: 26972271.
Rasmussen, P., Wyss, M. T., Lundby, C. Cerebral glucose and lactate consumption during cerebral activation by physical activity in humans. FASEB J. 25, 2865– 2873 (2011). www.fasebj.org
Quistorff, B., Secher, N.H. and Van Lieshout, J.J. (2008), Lactate fuels the human brain during exercise. The FASEB Journal, 22: 3443-3449. https://doi.org/10.1096/fj.08-106104
Wahl P. et al.. Moderne Betrachtungsweisen des Laktats: Laktat ein überschätztes und zugleich unterschätztes Molekül. Schweizerische Zeitschrift für «Sportmedizin und Sporttraumatologie» 57 (3), 100–107, 2009
Yang WH, Park H, Grau M, Heine O. Decreased Blood Glucose and Lactate: Is a Useful Indicator of Recovery Ability in Athletes? Int J Environ Res Public Health. 2020 Jul 29;17(15):5470. doi: 10.3390/ijerph17155470. PMID: 32751226; PMCID: PMC7432299.
Westerblad H, Allen DG, Lännergren J. Muscle fatigue: lactic acid or inorganic phosphate the major cause? News Physiol Sci. 2002 Feb;17:17-21. doi: 10.1152/physiologyonline.2002.17.1.17. PMID: 11821531.
Allen DG, Westerblad H. Role of phosphate and calcium stores in muscle fatigue. J Physiol. 2001 Nov 1;536(Pt 3):657-65. doi: 10.1111/j.1469-7793.2001.t01-1-00657.x. PMID: 11691862; PMCID: PMC2278904.
Goodwin ML, Gladden LB, Nijsten MW, Jones KB. Lactate and cancer: revisiting the warburg effect in an era of lactate shuttling. Front Nutr. 2015 Jan 5;1:27. doi: 10.3389/fnut.2014.00027. PMID: 25988127; PMCID: PMC4428352.
Kaijser L, Berglund B. Myocardial lactate extraction and release at rest and during heavy exercise in healthy men. Acta Physiol Scand. 1992 Jan;144(1):39-45. doi: 10.1111/j.1748-1716.1992.tb09265.x. PMID: 1595352.
Emhoff, C.-A.W., Messonnier, L.A., Horning, M.A., Fattor, J.A., Carlson, T.J. and Brooks, G.A. (2013), Gluconeogenesis and hepatic glycogenolysis during exercise at the lactate threshold. The FASEB Journal, 27: 1132.2-1132.2. https://doi.org/10.1096/fasebj.27.1_supplement.1132.2
Nitzsche N, Baumgärtel L, Schulz H. Comparison of maximum lactate formation rates in ergometer sprint and maximum strength loads. Dtsch Z Sportmed. 2018; 69: 13-18. doi:10.5960/dzsm.2017.312
König D, Braun H, Carlsohn A, Großhauser M, Lampen A, Mosler S, Nieß A, Oberritter H, Schäbethal K, Schek A, Stehle P, Virmani K, Ziegenhagen R, Heseker H (2019) Carbohydrates in sports nutrition. Position of the working group sports nutrition of the German Nutrition Society (DGE). Ernahrungs Umschau 66(11): 228–235
Onakpoya I, Hunt K, Wider B, Ernst E. Pyruvate supplementation for weight loss: a systematic review and meta-analysis of randomized clinical trials. Crit Rev Food Sci Nutr. 2014;54(1):17-23. doi: 10.1080/10408398.2011.565890. PMID: 24188231.