Lactic Acid

Definition
Lactic acid is mainly produced in muscle cells and red blood cells. It forms when the body
breaks down carbohydrates to use for energy when oxygen levels are low. Times when your
body's oxygen level might drop include:
 During intense exercise
 When you have an infection or disease
A test can be done to measure the amount of lactic acid in the blood.

Alternative Names
Lactate test

How the Test is Performed

A blood sample is needed. Most of the time blood is drawn from a vein located on the inside of
the elbow or the back of the hand.

How to Prepare for the Test

DO NOT exercise for several hours before the test. Exercise can cause a temporary increase in
lactic acid levels.

How the Test will Feel

You may feel slight pain or a sting when the needle is inserted. You may also feel some
throbbing at the site after the blood is drawn.

Why the Test is Performed

This test is most often done to diagnose lactic acidosis.

Normal Results
4.5 to 19.8 mg/dL (0.5 to 2.2 mmol/L)
Note: mg/dL = milligrams per deciliter; mmol/L = millimoles per liter
Normal value ranges may vary slightly among different laboratories. Talk to your doctor about
the meaning of your specific test results.
The examples above show the common measurements for results for these tests. Some
laboratories use different measurements or may test different specimens.

What Abnormal Results Mean

Abnormal results mean that body tissues are not getting enough oxygen.
Conditions that can increase lactic acid levels include:
 Heart failure
 Liver disease
 Lung disease
 Not enough blood containing oxygen getting to a certain area of the body

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 Severe infection that affects the entire body (sepsis)
 Very low levels of oxygen in the blood (hypoxia)

Considerations
Clenching the fist or having the elastic band in place for a long time while having blood drawn
can result in a false increase in lactic acid level.
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Test Overview Lactic Acid

A lactic acid test is a blood test that measures the level of lactic acid made in the body. Most of it is
made by muscle tissue and red blood cells. When the oxygen level in the body is
normal, carbohydrate breaks down into water and carbon dioxide. When the oxygen level is low,
carbohydrate breaks down for energy and makes lactic acid.
Lactic acid levels get higher when strenuous exercise or other conditions—such asheart failure, a
severe infection (sepsis), or shock —lower the flow of blood and oxygen throughout the body. Lactic
acid levels can also get higher when the liver is severely damaged or diseased, because the liver
normally breaks down lactic acid.
Very high levels of lactic acid cause a serious, sometimes life-threatening condition called lactic
acidosis. Lactic acidosis can also occur in a person who takes metformin (Glucophage) to control
diabetes when heart or kidney failure or a severe infection is also present.
A lactic acid test is generally done on a blood sample taken from a vein in the arm but it may also be
done on a sample of blood taken from an artery (arterial blood gas).
At a Glance
Why Get Tested?

To detect high levels of lactate in the blood, which may be an indication of lack of oxygen
(hypoxia) or the presence of other conditions that cause excess production or insufficient
clearing of lactate from the blood; this test is not meant to be used for screening for health status.

When To Get Tested?

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When you have symptoms such as rapid breathing, nausea, and sweating that suggest a lack of
oxygen or an abnormal blood pH(acid/base imbalance); when a healthcare practitioner suspects
that you may be experiencing sepsis, shock, heart attack, severe congestive, kidney failure, or
inadequately treated (uncontrolled) diabetes; when a healthcare practitioner suspects that you
have inherited a rare metabolic or mitochondrial disorder; when you have symptoms of lactic
acidosis such as sweet-smelling breath, belly pain, confusion or cool and clammy skin

Sample Required?

A blood sample is obtained by inserting a needle into a vein in the arm. Sometimes, an arterial
sample is collected by inserting a needle into an artery. Occasionally, a sample of cerebrospinal
fluid is collected from the spinal column during a procedure called a spinal.

Blood lactate levels will usually be drawn either without the use of a tourniquet or with a
tourniquet that is not released during the blood draw. Tourniquet use and release and clenching
of the fist can increase lactate levels in the blood sample.

Test Preparation Needed?

In general, no test preparation is needed. In some cases, a healthcare practitioner may request
that you don't exercise for several hours before the test or refrain from eating or drinking
anything other than water for 8 to 10 hours prior to the test.

Looking for Test Results?

Looking for Reference Ranges?
What is being tested?

Lactate is one of the substances produced by cells as the body turns food into energy
(cell metabolism), with the highest level of production occurring in the muscles.
Depending on pH, it is sometimes present in the form of lactic acid. However, with the
neutral pH maintained by the body, most of it will be present in the blood in the form of
lactate. This test measures the amount of lactate in the blood or, less commonly, in
the ...

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Lactic Acid: Myth
However, research has revealed that lactate is formed and used continuously, even when
muscles are working with plenty of oxygen. In the human body most lactic acid is
present in the form of lactate. During vigorous exercise there is an increase in the acidity
in the blood and tissues. However, lactate makes a very small contribution to this. When
you're exercising hard, lots of ATP (the 'energy currency of life') is broken down to
release energy for muscle contraction. Each time an ATP molecule is broken down, one
hydrogen ion is released. It's actually the accumulation of hydrogen ions which reduce
pH (a measure of acidity/ alkalinity) and may be associated with 'the burn'.

When it comes to fatigue, neither lactate nor lactic acid are likely causes. The human
body is incredibly complex and it's more likely that the limiters to performance are a
result of many factors.

Lactate As An 'Ion Sponge'

So how and why is lactate produced? As exercise intensity increases, our body requires
more energy more quickly and energy metabolism shifts to use more carbohydrate and
less fat. Carbohydrate in the form of glucose is broken down in a chemical reaction
called 'glycolysis'. One of the end-products of this reaction is a molecule called
'pyruvate' which begins to accumulate along with the dreaded hydrogen ions. However,
pyruvate absorbs hydrogen ions in a 'reduction' reaction, which forms lactate. In stark
contrast to our commentator's contentions, lactate actually acts as a buffer – imagine
lactate as an 'sponge', mopping up ions to control pH in the muscle.

However, the speed of the 'mopping up' process has a limit. When this limit is reached,
hydrogen ions accumulate, pH begins to drop and we feel the burn, but if our muscles
did not produce lactate, fatigue would occur much more quickly.

How Does The Body Use Lactate?

The body uses lactate in a number of ways:

a) Lactate minimises acidity in the blood and tissues

As described above, lactate is the end result of pyruvate's reaction with hydrogen ions,
which reduces acidity and is associated with a delay in fatigue.

b) Lactate helps to preserve other fuel stores

When blood lactate concentrations are elevated, the body responds by down-regulating
the use of glucose and fat. In this way, lactate could be seen as preserving precious fuel
stores. Also, the body is able to generate glucose from non-carbohydrate sources
through a metabolic pathway called 'Gluconeogenesis'. Lactate is transported back to
the liver, enters a chemical process called the 'Cori cycle' and is converted into pyruvate
which is then used to generate glucose.

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c) Lactate is a direct source of energy for the muscles, heart and brain.
Muscles can extract lactate from the blood and oxidise it directly. This means that lactate can be used as a
source of energy for muscle contraction. In some cases, the body actually prefers to use lactate as a fuel.
Some research has illustrated that, during moderate intensity exercise, lactate from the working muscles
may be the primary fuel source for the heart.

d) Lactate acts as a 'shuttle' to transfer fuel between tissues.

Muscle glycogen stores are local, supplying the muscle they are stored within. This means that muscle
glycogen stored in your arms can't be directly transported to your legs. However, research suggests that
lactate can move both within and between cells. Consequently, during heavy exercise where high rates of
glucose and glycogen breakdown result in the accumulation of increasing amounts of lactate, lactate can be
'shuttled' from this site to other sites where is can be used as a fuel source or converted back into glucose.

e) Lactate is an important 'signalling molecule'.

Lactate may play the role of a signalling hormone, with a range of possible consequences. These include up
regulating the expression of genes associated with the use of lactate as a fuel, helping the body metabolise
lactate more effectively. Lactate may even stimulate an increase in formation of new mitochondria; an
important adaptation in endurance performance as mitochondrion represent the 'energy factories' of our
cells. It has also been suggested that lactate can influence lipolysis (the breakdown of fat for fuel).

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Lactate is GOOD for the patient and not BAD

It would appear that despite intense scientific inquiry most clinicians still believe
that the Earth is flat and that an increased serum lactate is the result of impaired tissue
oxygen delivery and anaerobic metabolism. This concept is perpetuated by The
Surviving Sepsis Campaign who state “we suggest targeting resuscitation to normalize
lactate in patients with elevated lactate levels AS A MARKER OF HYPOPERFUSION.”
These concepts are WRONG.

The understanding of Lactate is shrouded with misconceptions and myths. These are
briefly reviewed below.

1. Humans are not yeast and rarely produce lactate anaerobically. It is widely
regarded (and likely incorrect) that in the setting of sepsis, an increased lactate is
a marker of impaired microcirculatory flow and anaerobic metabolism. There is
however convincing clinical and experimental data that the increased lactate is as
a result of increased B2 adrenergic activation (as part of the stress response) with

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 greater production of pyruvate than can enter the Krebs cycle. Hence lactate
accumulates aerobically (analogous situation to increased lactate production
during exercise). B2 adrenergic stimulation increases glycogenolysis with
increased production of glucose, which is then metabolized to pyruvate at a rate
that exceeds its metabolic conversion in the Krebs cycle. This results in stress
hyperglycemia and stress hyperlactemia. Both are evolutionary preserved
responses which are designed to enhance survival during stress (and provide the
vital organs with a source of fuel). Blocking these survival responses increases the
risk of death during stress. It is likely that thiamine deficiency and decreased
activity of pyruvate dehydrogenase (due to cytokines) further increase the
likelihood of developing stress hyperlactemia. It has been demonstrated that the
GLOBAL anaerobic threshold of adults is about 4mls/kg/min (JAMA 1993;
270;1724) and this threshold does not change with sepsis. In adults this translates
into a hemoglobin of 4g/dl and a cardiac index of just over 1 L/minM2. This degree
of impaired oxygen delivery is quite uncommon in critical illness and usually a pre-
terminal event. From the above it is clear that the level of lactate is a measure of
the degree of activation of the stress response (and serum catecholamine levels)
and a prognostic marker. LACTATE IS GOOD FOR THE PATIENT AND NOT
BAD.
2. As a consequence of Myth No 1, it is widely believed that clinicians should
increase oxygen delivery (DO2) in response to a high lactate. WRONG. The
notion of increasing oxygen delivery to achieve some “magical target” DO2 or to
achieve a certain central venous/mixed venous oxygen saturation or lactate
concentration (or lactate clearance) has universally failed to improve patient
outcomes. Gattonni et al demonstrated this over 20 years ago (NEJM
1995;333:1025). It is striking that in the b-blocker in sepsis study, treatment with a
B1 antagonist (esmolol) decreased CI and DO2 was this associated with a more
rapid clearance of lactate (JAMA 2013;310:1683). The only intervention that I am
aware of that can actually decrease blood lactate level (and improve patient
outcome) is the administration of thiamine (Crit Care Med 2016;44;360).
Attempting to “titrate” therapy to a lactate level is as absurd as titrating treatment
to a White Blood Cell count (WBC). However, in patients with localized lactate

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 production (e.g ischemic bowel, ischemic limb etc) fixing the plumbing will reduce
lactate levels and improve patient outcome.
3. Probably one of the most remarkable of the Myths is the notion that the act of
measuring lactate in and of itself improves patient outcomes. This concept is
promoted by the Surviving Sepsis Campaign and is a core requirement of the
SEP-1 Federal mandate. This concept is as absurd as suggesting that measuring
a WBC improves the outcome of sepsis. While it is true that some studies have
shown a lower mortality in patients in whom the lactate is measured within 3 hours
(as opposed to later or never); this is not because measuring lactate improves
outcome. It is simply a marker of better care. Measuring a blood lactate within 3
hours is a marker of more timely recognition of sepsis, receipt of antibiotics and
earlier treatment.
4. Lactate causes an acidosis. The conversion of pyruvate to lactate consumes
rather than produces a hydrogen ion. Therefore lactate production retards, not
causing an acidosis (Am J Physiol 2004;287: R502). The presence of an acidosis
in many (not all) patients with an increased lactate is once again an association
and not causal. The cause of the acidosis in these patients is not exactly clear; the
hydrolysis of ATP has been one explanation that has been proposed.
5. “Medical Fables” suggest that Ringers Lactate is contraindicated in patients with
liver disease as this will cause a severe lactic acidosis. This is not correct; lactate
is given as the base and not the acid and cannot cause an acidosis, rather, the
opposite is true. The lactate is metabolized in the liver either by gluconeogenesis
or oxidation with both reactions consuming a hydrogen ion. This has been
demonstrated in both experimental models and clinical studies (even in presence
of severe liver disease). In a murine model of acetaminophen toxicity LR has been
demonstrated to improve liver recovery.(BMC Gasstroenerol 2011;11;125) In a
hemorrhagic shock model LR as compared to NS was associated with less
hepatic, renal and pulmonary injury (shock 2012;39268). Furthermore, LR has
been reported to be safe in patients undergoing hepatectomy. Most specifically
Goldstein evaluated the ability of dogs to handle a rapid infusion of Ringers lactate
solution in the presence of severe hepatic injury. (Can J Surg 1972; 15:318). In
this study they failed to demonstrate that exogenous lactate caused a prolonged

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 or progressive elevation of arterial lactate in animals with a severe disturbance of
hepatic function

References
 https://www.active com/cycling/articles/lactic acid math
 labtestonline.org/tests/lactate.

 Seifter JL. Acid-base disorders In: Goldman L, Schafer AI, eds. Goldman-Cecil
Medicine. 25th ed. Philadelphia, PA: Elsevier Saunders; 2016:chap 118.
Review Date: 5/3/2015