Lactic Acid

What Is It, What Increases It, and More

Author: Nikol Natalia Armata

Editors: Alyssa Haag, Ian Mannarino, MD, MBA, Kelsey LaFayette, DNP, RN

Illustrator: Jessica Reynolds, MS

Copyeditor: Sadia Zaman, MBBS, BSc

What is lactic acid?

Lactic acid, also known as lactate, is a substance the body produces mainly by the breakdown of glucose under anaerobic conditions (i.e., without oxygen), like anaerobic glycolysis. Anaerobic glycolysis refers to the main pathway responsible for supplying the cell with energy, both in the form of adenosine triphosphate (ATP) and nicotinamide adenine dinucleotide (NADH). The tissues that produce the most lactic acid include muscle cells and red blood cells, with lesser production from brain tissue, skin, and in the gastrointestinal (GI) tract. Lactic acid is subsequently released into the bloodstream to be metabolized by the liver and kidneys, where it can be used in gluconeogenesis. Gluconeogenesis refers to glucose and energy synthesis from noncarbohydrate substrates, such as lactate.

Typical lactate levels are usually low, less than 2 mmol/L, ranging between 0.5-1 mmol/L. Hyperlactatemia can occur when lactate levels rise to between 2-4 mmol/L. If the levels exceed 4 mmol/L, it is known as severe hyperlactatemia. Elevated serum lactate levels can be a risk factor indicating poor prognosis.

Illustrative outline of the last acid pathway with visual of blood vessels and liver.

What does lactic acid do?

Lactic acid is an important molecule in cellular respiration, glucose production, regulation of inflammation, and molecular signaling. Under anaerobic conditions, glucose (and more specifically, pyruvate) is converted into lactic acid in order to produce energy for the cells. Energy can also be produced in the kidneys, where lactate can be oxidized to produce energy with the generation of CO2, a process that consumes oxygen but generates ATP. Additionally, lactic acid can be used in gluconeogenesis, a process that takes place in both the liver and kidneys, that can convert lactic acid to glucose by consuming oxygen and ATP. Lactate also has anti-inflammatory effects and promotes immune tolerance and as a signaling molecule plays a major role in memory formation and neuro-protection, wound healing, ischemic tissue injury, cancer growth, and cancer metastasis. 

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What is lactic acidosis?

Lactic acidosis refers to the combination of elevated lactate levels and a decreased pH of the individual's blood serum equal to or less than 7.35. It is considered the most common cause of metabolic acidosis identified in hospitalized individuals.

There are two types of lactic acidosis; type-A and type-B. Type-A lactic acidosis is caused by hypoperfusion and long-term hypoxia of the tissues. It usually occurs when oxygen consumption is greater than oxygen delivery, resulting in cells undergoing anaerobic glycolysis for energy. Type-A lactic acidosis can be caused by all subtypes of shock (e.g., septic, cardiogenic, hypovolemic, obstructive), regional ischemia (e.g., limb, mesenteric), and anaerobic muscle activity (e.g., high intensity interval training, weight lifting). 

On the other hand, type-B lactic acidosis results from sources other than hypoperfusion and tissue hypoxia that result in impaired tissue function and an inability to process available pyruvate. Consequently, alternative metabolic pathways to generate pyruvate occur, activating the lactic acid cycle, thereby resulting in high levels of lactate. Causes of type-B lactic acidosis include liver disease, malignancies, medications (e.g., metformin, epinephrine), thiamine deficiency, excessive exercise, diabetic ketoacidosis, and alcohol intoxication.

Lactic acidosis contributes to a worsening of underlying comorbidities and therefore impacts an individual’s mortality. For example, individuals with even mildly elevated levels of lactic acid along with sepsis have a greater risk of in-hospital mortality within 30 days. Similarly, severely elevated lactic acid levels can have profound hemodynamic consequences, as it has been shown to reduce the heart’s and blood vessels’ contractility. The higher the lactate levels and the longer their value remains elevated, the greater the risk of death. 

What causes lactic acid build-up in the body?

Elevated lactate can be the result of increased lactic acid production, decreased lactic acid clearance, or a combination of both. There are multiple causes for lactic acid build-up in the body, of which include septic shock, tissue hypoperfusion (e.g., due to carbon monoxide exposure), post-cardiac arrest, regional tissue ischemia, anaerobic muscle activity, diabetic ketoacidosis, toxins and pharmacological agents, thiamine deficiency, malignancies, and liver failure. 

Septic shock is often associated with cardiovascular dysfunction causing arterial hypotension, as well as decreased perfusion in the peripheral tissues for oxygen and nutrient exchange. As a result, lactic acid that has subsequently accumulated in the blood can be a useful monitoring marker for individuals in shock. Similarly, any form of ischemia (i.e., restricted or inadequate oxygen delivery) as seen in the other types of shock (e.g., cardiogenic, obstructive, hemorrhagic shock), cardiac arrest due to lack of flow during the arrest, carbon monoxide poisoning, or local tissue ischemia can cause lactic acid build-up. A very common and benign cause of lactic acid increase is anaerobic muscle activity, which results in muscle soreness after intense exercise. During exercise, the skeletal muscles produce more lactate than the liver can metabolize. In addition, diabetic ketoacidosis can affect lactate levels as a result of hypoperfusion and metabolic stress. Several medications and toxins, like alcohol, biguanides (e.g., metformin), nucleoside reverse transcriptase inhibitors, salicylates, and isoniazid, can also increase lactic acid levels. Thiamine deficiency shifts metabolism to increased anaerobic carbohydrate metabolism, as thiamine is a crucial co-factor for multiple cellular enzymes including pyruvate dehydrogenase, an essential component of aerobic carbohydrate metabolism. Lastly, malignancies and liver failure mainly increase lactate due to the inability of the liver to remove excessive lactic acid. 

How do you get rid of lactic acid?

Under most circumstances, lactate is rapidly cleared by the liver, where it is reconverted into glucose by the processes of gluconeogenesis. A smaller amount of additional lactate is cleared by the kidneys. Notably, lactate is oxidized with NAD+ within the mitochondria by the enzyme lactate dehydrogenase to produce pyruvate and NADH.

Treatment options for excessive lactic acid levels depend on how elevated the lactate levels are and what caused the increase. If a medical history reveals strenuous exercise, health care professionals must ensure that the individual is adequately hydrated, is breathing sufficiently, is warm, and is resting. Lactic acidosis secondary to septic shock generally requires administering broad-spectrum antibiotics in order to manage the underlying infection. Equally important is administering crystalloid fluids, typically 30 mL/kg within three hours of the initial assessment. The use of vasopressors becomes necessary depending on the severity of the shock. Hemodialysis can sometimes be used to manage severe lactic acidosis, especially in patients who have renal failure. In the vast majority of cases, lactic acidosis is caused by inadequate blood flow, therefore tissue perfusion must be improved first. Initiation of inotropic medications (e.g., dobutamine, dopamine) and vasoconstrictors (e.g., epinephrine, vasopressin analogs) may be helpful, providing better circulation of the intravascular volume. Further supportive care must then be individualized.

What are the most important facts to know about lactic acid?

Lactic acid, also called lactate, is a product of pyruvate metabolism under anaerobic conditions. The tissues that produce most lactic acid are the muscle cells and red blood cells. An elevated lactate level and a pH equal to or less than 7.35 cause lactic acidosis. There are two types of lactic acidosis; type-A and type-B. Type-A lactic acidosis is typically caused by hypoperfusion and long term hypoxia of the tissues whereas type-B lactic acidosis is related to the inability to process the available amount of pyruvate due to impaired tissue function, unrelated to hypoxia. Elevated lactate can be the result of increased lactic acid production, decreased lactic acid clearance, or a combination of both. Treatment options for excessive lactic acid levels depend on the underlying cause and extent of lactate level elevation.

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Related links

Physiological changes during exercise
Metabolic and respiratory acidosis: Clinical practice

Resources for research and reference

Andersen, L. W., Mackenhauer, J., Roberts, J. C., Berg, K. M., Cocchi, M. N., & Donnino, M. W. (2013). Etiology and therapeutic approach to elevated lactate levels. Mayo Clinic proceedings, 88(10), 1127–1140. DOI: 10.1016/j.mayocp.2013.06.012 

Foucher, C. D., & Tubben, R. E. (2021, July 19). Lactic Acidosis. In: StatPearls [Internet]. Retrieved Aprill 22, 2022, from 

Plowman, S., & Smith, D. (2003). Anaerobic metabolism during exercise. In Donatelli, R. (Ed.), Sports-Specific Rehabilitation (pp. 39–63.)  St. Louis: Churchill Livingstone. 

Sun, S., Li, H., Chen, J., & Qian, Q. (2017). Lactic acid: No longer an inert and end-product of glycolysis. Physiology, 32(6), 453–463. DOI: 10.1152/physiol.00016.2017