Lactic acid, often referred to as lactate, is an organic acid naturally generated as a byproduct of cellular metabolism. When it enters the bloodstream, it quickly dissociates into its conjugate base, lactate, and a hydrogen ion. This substance is constantly produced and consumed within the body, maintaining a stable concentration in the blood even at rest. Although most commonly associated with intense exercise, lactate is a circulating molecule that serves continuous functions in multiple organ systems.
Lactate is an alpha-hydroxy acid. The body primarily produces the L-isomer of lactate, which is involved in various biochemical processes. Its continuous presence in the bloodstream highlights its status not merely as a waste product, but as an active intermediate in energy production.
How the Body Produces and Uses Lactic Acid
Lactate production occurs primarily through anaerobic glycolysis, the breakdown of glucose without requiring oxygen. This process is active in cells lacking mitochondria, such as red blood cells, or in muscle fibers when energy demand exceeds oxygen supply. During this high-demand state, the enzyme lactate dehydrogenase converts pyruvate, a product of glycolysis, into lactate.
The majority of lactate is generated in skeletal muscles, especially during high-intensity exercise, but it is also produced consistently by the gut, brain, and red blood cells. This mechanism allows for the regeneration of NAD+, which is necessary to keep glycolysis running, ensuring a rapid source of cellular energy. Lactate plays a significant role in energy substrate shuttling between different tissues.
The body efficiently clears lactate from the bloodstream, maintaining concentration balance through the Cori cycle. In this cycle, lactate produced by muscles or red blood cells is transported to the liver. The liver utilizes energy to convert the lactate back into glucose through gluconeogenesis.
This newly formed glucose is released back into the circulation, where it can be used for energy by muscles or other tissues. Beyond this recycling mechanism, approximately 70–80% of lactate is oxidized directly by tissues like the heart and brain, which efficiently use it as a fuel source. The kidneys also contribute to lactate clearance, metabolizing about 30% of the circulating amount.
Understanding Normal Resting Blood Lactate Levels
The concentration of lactate in the blood reflects the balance between its continuous production and its clearance by the liver, heart, and kidneys. For a healthy, resting adult, the typical reference range for lactate levels is between 0.5 and 2.2 millimoles per liter (mmol/L). This is equivalent to approximately 4.5 to 19.8 milligrams per deciliter (mg/dL).
This measurement must be taken while the individual is at rest, as exercise can temporarily elevate the concentration significantly. Blood collection protocols often specify avoiding strenuous activity for several hours before the test to ensure an accurate baseline reading. Clinically, any value consistently above 2.2 mmol/L is considered elevated, a condition known as hyperlactatemia.
Testing methodology affects the reported normal range, specifically whether the sample is drawn from an artery or a vein. Arterial blood is the standard for assessing true systemic lactate levels and acid-base status. Venous lactate levels tend to be slightly higher than arterial levels because venous blood carries lactate from the tissues back toward the liver for processing.
Venous measurements are simpler to obtain and correlate well with arterial levels when concentrations are normal. However, the absolute values can differ when levels become highly elevated. Consistency in the sampling site is important when monitoring trends in a patient’s lactate concentration over time.
Primary Reasons for Elevated Lactic Acid
Elevated lactate levels occur when the rate of production surpasses the body’s ability to clear it, signaling a disruption in cellular oxygen delivery or metabolism. Clinicians categorize sustained elevation into two primary types: Type A, related to a lack of oxygen, and Type B, not primarily caused by tissue hypoxia. Type A hyperlactatemia is the most common and concerning, resulting from inadequate tissue perfusion or oxygenation.
Causes of Type A elevation include shock states, such as septic, cardiogenic, or hypovolemic shock. Poor blood flow in these states leads to insufficient oxygen delivery to the tissues. When cells are deprived of oxygen, they rely heavily on anaerobic glycolysis, which rapidly increases lactate production. Regional ischemia, such as a blocked blood vessel, also forces local cells into this anaerobic pathway.
Type B hyperlactatemia arises when oxygen delivery is adequate, but there is either an overproduction of lactate due to cellular dysfunction or a failure in clearance mechanisms. Strenuous, short-duration exercise is a physiological example of Type B, where the surge in muscle activity temporarily overwhelms clearance capacity. This exercise-induced increase is transient and resolves quickly with rest.
Pathological Type B causes include conditions that impair the liver’s ability to convert lactate back to glucose, such as liver failure. Certain medications, notably the diabetes drug metformin, can interfere with the metabolic pathways that clear lactate, leading to accumulation. Other causes include malignancies, severe thiamine deficiency, and toxins like methanol and ethylene glycol.
Recognizing and Treating Lactic Acidosis
Lactic acidosis is a severe condition defined by blood lactate elevation, typically above 4 mmol/L, accompanied by a drop in the blood’s pH level below 7.35. This acidic state profoundly disrupts normal physiological functions and is a sign of a medical emergency. Symptoms can include shallow, rapid breathing, often called Kussmaul breathing, as the body attempts to expel excess carbon dioxide to compensate for the acid buildup.
Patients may also experience serious symptoms like nausea, vomiting, profound fatigue, confusion, and a rapid heart rate. If the underlying cause involves liver impairment, jaundice (yellowing of the skin and eyes) may be present. Because the symptoms are similar to those of the underlying disease, the lactate measurement is an indispensable diagnostic tool in the hospital setting.
The primary goal of treatment is to identify and reverse the underlying cause of lactate accumulation, not to directly neutralize the lactate itself. For Type A acidosis, the immediate focus is on restoring tissue oxygenation and perfusion. This involves administering intravenous fluids to improve blood volume, providing supplemental oxygen, and treating severe infections like sepsis with antibiotics.
In cases of Type B acidosis, treatment involves addressing the specific metabolic disruption, such as discontinuing an offending medication or managing liver disease. While bicarbonate therapy to raise the blood pH is sometimes considered in extremely severe cases (pH below 7.0), the most effective approach remains resolving the root cause. Serial lactate measurements are routinely used to monitor treatment effectiveness, with decreasing levels indicating clinical improvement.