The Truth About Lactic Acid

I. Introduction
II. Delayed onset muscle soreness
III. Cramping
IV. Muscular acidosis
V. Fatigue
VI. As fuel and in exercise
VII. Conclusion

Lactic acid has been unfairly demonized for everything from delayed onset muscle soreness to cramping to robbing banks. Well, maybe not robbing banks, but you get the point.

In this article we will dispel all myths about lactic acid, and cover physiologic explanations for the phenomena supposedly associated with lactic acid. If you have one that I have not covered please comment at the bottom of the article, and I will integrate it in later.

This is the first post in a series on the metabolic pathways.

Lactic acid is not responsible for delayed onset muscle soreness.

Delayed onset muscle soreness (DOMS) is caused by a couple factors. Exercise, especially eccentric exercise, creates microtrauma within the muscles. The body initiates an inflammatory response to repair the damaged area. There are a couple theories on how this produces DOMS, but none involve lactic acid.

• The inflammatory response itself may be responsible for aggravating afferent sensory neurons which would “cause” the pain associated with soreness.
• Microtrauma in the muscles allows ions to leak out into the surrounding musculature. This may also aggravate afferent neurons as many of these are ion sensitive. For example, neurons activate by firing action potentials which may be more easily set off by accumulated ion concentrations from the tears in the muscles.
• Enlarging of the area due to swelling and/or muscle growth may cause fascia stretching which may aggravate afferent neurons causing pain.

Lactic acid is a metabolite not involved with any of the factors in delayed onset muscle soreness.

In fact, lactic acid is removed almost totally from the muscles within 30 minutes of cessation of exercise. How it could even begin to explain delayed onset muscle soreness which comes 24-72 hours later is beyond me.

Lactic acid is not responsible for muscle cramping.

Cramping occurs due to a few reasons.

• Impact/injury may cause cramping. What this means is if there is trauma to an area of the body, the body will generally tighten up to protect the area which thusly may cause cramping.
• Low blood flow. This may be due to already cramping muscles, too much scar tissue, or poor circulation. If there is very little blood flow to an area there is less oxygen. Less oxygen means poor metabolic functioning. If there is not enough oxygen to facilitate production of ATP, pumping of Ca2+ back into the sarcoplasmic reticulum cannot occur. This leads to sustained contraction of the muscle.
• Improper or overactive motor neuron function. Some diseases such as muscular (myoclonic) dystonia are caused by this. Similarly, twitching of random muscles may lead to cramping.
• Alternatively, cramps can also be due to overuse. Similarly to the low blood flow, we have a case where the muscle cannot keep up metabolically supplying the sarcoplasmic reticulum transporters with ATP to pump Ca2+. Thus, Ca2+ runs loose and initiates sustained contractions
• vElectrolytic imbalances from intake of too many nutients or lack of nutrients also may contribute to cramping.

Apparently, loss of electrolytes does not cause cramps, especially from sweating during physical exertion.

Secondary cause:

• Poor range of motion. When muscles are moved into a short range of motion and contracted, they are likely to cramp. For example, the quads are likely to cramp if you try to do an L-sit or V-sit the first time you try. This goes back the poor blood flow scenario where a sustained contraction cuts off oxygen availability and the muscles cramp due to lack of ATP. People that are inflexible usually have tight musculature and lots of scar tissue already and are thus “predisposed” to poorer blood flow and easier cramping. Foam rolling, massage, and static stretching are musts.

As you can see, lactic acid is not involved with cramping. High quantities of it may be detected in severely oxygen limited muscle cells with diminished amounts of ATP. However, this is only a correlation and not the actual causation of cramping.

Note: the basis of massage and techniques such as ART/trigger points aim at releasing contracted muscles. This frees up blood flow for healing and ATP production as well as breaks up scar tissue and reintroduces inflammation to heal the prolonged damaged and contracted areas of muscle.

Lactic acid is not responsible for muscular acidosis.

Muscular and systemic acidosis is caused by three factors.

1. ATP depletion: ATP + H2O -> ADP + P + H+

2. Oxidation of glucose (C6H12O6) releases the hydrogen atoms as it is metabolized. Before the H+ ions get converted into H2O with oxygen at the end of the electron transport, they are released as H+ ions mostly in the krebs/citric acid cycle. All of the NADH generating reactions release H+.

2 NADH from Glycolysis + 1 (*2) NADH from Acetyl-CoA generation + 3 (*2) NADH from citric acid cycle generate 10 H+ per glucose molecule. The other two H+ are “absorbed” by FADH2 (QH2).

Hydrogen ions are buffered by microchondria through H+ ion gradients which drive the ATP synthase enzyme (this has very important implications which will be discussed later). ATP synthase is responsible for production of all ATP in the body by combining ADP + P and literally “smashing” them together to form ATP.

3. CO2 in the blood combines with water.

CO2 + H2O -> HCO3- + H+

This drops pH. The body has monitors up near the heart to detect blood pH levels. If the pH of the blood drops, this tells the body that there is too much CO2 in the blood making it too acidic. Thus, we increase our inhalation and exhalation rate. Thus, we breath not because we need oxygen but because we need to exhale CO2.

4. Incorrect: pyruvic acid + NADH -> NAD+ + lactic acid

Do NOT be confused here. Pyruvic acid –> lactic acid conversion does not release H+. Hence lactic acidosis is a misnomer and untrue because the pyruvate’s carboxylic acid group already has the hydrogen ion dissociated from it.

Lactic acid is not responsible for fatigue, especially muscular fatigue.

There are a large number of reasons for decline and failure of contraction and peak tension in muscles. None are due to fatigue.

Muscular acidosis is indeed one cause of fatigue; however, as we already examined lactic acid is not involved in “creating” muscular acidosis.

Similarly, other causes of fatigue may include (going down the chain): CNS, motor nerves not being activated, nerve impulses not being transmitted correctly through lack of ion gradient, depletion of neurotransmitters at the neuromuscular junction, actin/myosin or muscle damage especially in eccentric contractions, calcium dysregulation, lack of metabolic substrates, blood flow or oxygen leading to ATP depletion, etc.

Metabolically, the accumulation of lactic acid does usually signal that the body is fatiguing; however, it is not directly involved and may only be used as a measuring stick especially in anaerobic exhaustion.

Some “recent” articles in the media here and here have given the public an image that lactic acid is a fuel.

This is false.

This is the Cori Cycle discovered in 1929 by the biochemists Carl and Gerty Cori.

There are two lactate transporters, MCT1 and MCT4, involved with symporting lactate/H+ out of the muscle cells into the blood stream. These are transported as you can see in the image to the liver which metabolizes the lactate to glucose. Glucose is then shipped back to the muscle cells. The liver also releases glycogen stores as well.

The alternative reaction that lactate can undergo within the muscle if exercise intensity decreases is that it can be reformed to pyruvate with NAD+ and then remetabolized into the citric acid cycle normally.

Thus, lactate is indeed a substrate used to resynthesize glucose. But saying it is a “fuel” itself is an stretch at best, and calling it new is certainly absurd.

For more on the discovery of the Cori Cycle, see this article.

But wait…

The Cori Cycle is only one of the important “alternate” metabolic pathways in the body for resynthesis of glucose in the liver.

The other is the Glucose-Alanine Cycle.

If oxidative metabolism is limited by the number of mitochondria, then excess pyruvate is converted into alanine from pyruvate and another amino acid.

This leads to a dual interplay between the Cori Cycle (CC) and Glucose-Alanine cycle (GAC) which shifts the metabolic “debt” over to the liver. Since the GAC conserves NADH as opposed to the CC due to the pyruvate-lactate reaction (pyruvic acid + NADH -> NAD+ + lactic acid), the GAC allows more energy to be produced within the muscle because the NADH can be used to create 3 ATP in electron transport. This assumes, of course, that the intensity is not high enough that the extra NAD+ is needed for glycolysis.

So basically we have both pathways playing off each other to send off substrates to the liver to help resupply glycogen to the muscles. If the intensity is higher, the Cori Cycle tends to be used a bit more. If the intensity is lower but above lactate threshold, the Glucose-Alanine Cycle is more prevalent. There is a mix of moderately-high intensity where both are used simultaneously.

For more information see Exercise Biochemistry Page 220.

Let me clarify a little bit here. The during exercise, excess lactate within the blood stream can be uptaken by the brain, heart, and slow twitch muscles as a source of energy besides being used by existing muscles.

I argue that this is NOT to be considered a “fuel” rather as an intermediary metabolite during a vast set of biochemical reactions. It’s not a “fuel” just because everyone thought it was a “dead end” reaction and found it that it does get reprocessed by other tissues or used by the tissues its in.

Lactic acid must still be reconverted into pyruvate before it’s oxidation in the CAC and electron transport which is typical of the primary carbohydrate energy pathway. Shunting lactic acid from one place to another (as in the Cori cycle or to the brain, heart or slow twitch muscles) does not make it a fuel — rather a way for the body to transfer some of its metabolic load to other tissues.

Basically, I see it as dispersing the energy load from the hard working muscles to other tissues through intermediary metabolites. If this constitutes fuel to you, then by all means call lactic acid a fuel.

In conclusion, we know that lactic acid does not cause DOMS, cramping, muscular acidosis, fatigue, and it is certainly not a fuel source although it may be used to resynthesize metabolites used for further production of energy.

Lactic acid is a metabolic byproduct of high intensity exercise. The fact that it correlates fairly well with the above symptoms and ailments does not mean it is a causative factor.

Most laypeople and even medical and exercise physiology texts still follow “conventional wisdom” without fact checking their sources. The only way to combat the ignorance is with correct information.

Next time someone blames lactic acid for anything please set them straight.

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