Nearly 100 years ago, researchers of exercise physiology found that as the harder the muscles worked, the more fatigued the muscle became, and the more lactic acid accumulated within the muscles. In other words, as the concentration of lactic acid increases in the muscles, the more fatigued the muscles become. This association between lactic acid and muscle fatigue has guided how we perceive exercise fatigue and muscle soreness. However, as any good critical thinker knows, association is not causation. This cause-effect relationship between lactic acid and muscle fatigue has been disproven repeatedly in published research over the last 25 years. Yet, there are still many horse owners, trainers, and even equine veterinarians that believe when a horse experiences exercise-induced fatigue, muscle soreness, or severe muscle cramping (otherwise known as tying-up), this is caused by lactic acid. Once again, these notions are false. This article aims to explain why lactic acid is no longer thought to cause exercise fatigue or muscle soreness, and that lactic acid is actually a beneficial bi-product of exercise metabolism rather than a ‘waste product.’
To clear things up, lactic acid actually isn’t the molecule that accumulates in the muscle cell during hard exercise, lactate is. Lactate is the conjugate base of lactic acid. I will cover more on that later, but for now just associate lactic acid with lactate. How much lactate the body is producing can be measured by the concentration of lactate in the blood, otherwise known as "blood-lactate concentration".
So what is lactate exactly? Lactate is the product of anaerobic glycolysis (one of three pathways that makes energy for the muscle cell). When the muscle cell is in demand for energy, the cell may take carbohydrates stored within the cell or blood and break it down into glucose (a sugar molecule). This sugar molecule then goes through a series of chemical reactions that results in 2 molecules called pyruvate. During the process of forming pyruvate, energy (in the form of ATP) is formed for the muscle cell. This process is called glycolysis.
Image of aerobic and anaerobic pathways of glycolysis.
Pyruvate can then go through one of 2 pathways:
1) Convert into Acetyl-CoA and go into the mitochondria (the ‘powerhouse’ of the cell) to be further broken down into energy with the assistance of oxygen, Aerobic Glycolysis.
Or 2) Pyruvate is converted to lactate, Anaerobic Glycolysis.
These processes are shown in the previous image.
What dictates whether pyruvate goes to the mitochondria to form more energy or converts into lactate? The muscle cell’s demand for energy. If the muscles need a high amount of energy very quickly, such as during an extended fast gallop, then glycolysis will be repeated rapidly, producing a lot of energy over a short period of time, with lactate being the end product. Thus, lactate accumulates quickly in the cell, regardless of how abundant oxygen is within the muscle cell. If the demand of energy is low, such as a trot, canter, or even a light gallop for fitter horses, then glycolysis will occur at a lower rate and the pyruvate that are formed will be sent to the mitochondria to form more energy rather than converting into lactate.
What is the purpose of pyruvate turning into lactate? Wouldn’t it be more efficient for the pyruvate to go to the mitochondria to form more energy for the cell?
Not exactly. You see, glycolysis is one of the fastest pathways of creating energy for the muscle cell. But glycolysis has a downside, the process produces hydrogen ions (H+). The concentration of hydrogen ions can determine the pH (acidity or alkalinity) of the muscle cell. As the number of hydrogen ions increases in the cell, the lower the pH and the more acidic the cell becomes. If the cell becomes too acidic, metabolic processes, such as forming energy, become impaired and slow down. Some molecules can even become damaged within the cell if the pH gets too low. During low energy demand, glycolysis produces hydrogen ions at a very low rate. The cell can tolerate this low accumulation of hydrogen ions by removing them out of the cell or taking them up by other molecules. Thus, not significantly changing the pH of the cell. But as mentioned before, in times of high energy demand, glycolysis will repeat rapidly. This will cause a rapid accumulation of acidic hydrogen ions within the cell. This influx of hydrogen ions occurs too rapidly than the cell can handle and pH begins to drop. However, there is a molecule that can help buffer this rapid increase in acidity: lactate!
When pyruvate is converted into lactate, it takes up 2 hydrogen ions. By absorbing hydrogen ions formed inevitably by glycolysis, the acidity of the cell can be reduced. Essentially, the conversion of pyruvate to lactate helps reduce the accumulation of acid within the cell, thus improving the capacity of the muscle cell to perform more glycolysis to meet the high demand of energy. This is why it is more energy efficient to produce lactate following glycolysis than have pyruvate enter the mitochondria to form more energy (which is a time consuming process and is not as efficient in times of high energy demand). Glycolysis is an imperative energy pathway to form energy very quickly during high intensity exercise, but if hydrogen ions are not taken up by lactate, acidity accumulates in the muscle cell quickly and glycolysis is slowed down- overall, slowing down energy production and causing muscle acidosis and fatigue. But when pyruvate is converted to lactate, hydrogen ions are able to be taken up and the acidity of the cell is reduced.
Image of pyruvate converting to into lactate by taking up two acidic hydrogen ions.
Let’s look at more of the science showing why lactate does not cause fatigue but actually aids in preventing fatigue:
If you actually look at the acidity of pyruvate vs lactate, pyruvate is actually a more acidic molecule than lactate. In chemistry, a molecule’s acidity can be measured by using pKa. The smaller the pKa, the more acidic the molecule is.
Pyruvate has a pKa of 2.50.
Lactate has a pKa of 3.87.
Thus, making pyruvate much more acidic than lactate for the cell. If you have a chemistry background and want to learn more about the biochemistry of muscle fatigue, you may be interested in this article: “Biochemistry of exercise induced metabolic acidosis” R Robert’s et al. (2004)
This article goes on to state that lactate inhibits, not causes, muscle acidosis.
To further prove this point, another very fascinating study performed in 2001 looked at the effects of injecting lactic acid into the muscles of rats during fatiguing muscle contractions. Researchers isolated the muscles of rats and forced it to contract using an electric shock. They repeated these shocks while recording the force production of the muscle over time. As expected, the more the muscle was shocked, the weaker the force the muscles were able to produce over time due to muscle fatigue. The pH of the muscles were also measured over time. As the muscles fatigued, the lower the pH (more acidic) the muscles had. However, once they injected a solution of lactic acid into the fatigued muscles, when they went to shock the muscles again, the force production was able to recover almost as high as the initial force produced at the start of the exercise. The conclusion of this study was that lactate actually has a protective effect against exercise-induced muscle fatigue.
So what happens to lactate after it takes up hydrogen ions to help buffer cell acidity? Well it can do one of two things:
1) Be transported out of the cell and into the blood, where it can be transported to the liver and converted back into glucose/sugar for energy.
Or 2) The lactate is taken into the mitochondria of the muscle cell and is further broken down into energy.
I will explain these mechanisms and what it means for a horse’s performance in future articles. But for now, understand that lactate is not only a buffer, but a source of energy for the cell. Not an acid. Not a waste product.
Image of lactate pathways.
The “burn” and fatigue your horse’s muscles feel during high intensity exercise is a combination of muscle acidosis caused by the influx of hydrogen ions (formed by glycolysis) and also possibly micro-damage of muscle fibers during high-force muscle contractions depending on the fitness of the horse. Not lactic acid/lactate.
So what about muscle soreness following vigorous exercise? This can’t be caused by lactate because lactate concentration in the muscle and blood actually return to normal resting levels within 1 hour of exercise, regardless of how hard the exercise was. This is because lactate is immediately recycled back into glucose or energy as previously mentioned. Research has shown that muscle soreness is caused by micro-tears within the muscle fibers. When these micro-tears occur, a molecule called Creatine kinase (CK), as well as other protein molecules that make up the muscle cell, leaks out into the extracellular space and blood. This is why CK is elevated in the blood days following exercise. Exercise physiologists and vets use blood CK as a measure of muscle damage following exercise.
Micro-tears in the muscle following rigorous exercise can also result in a horse tying-up (muscle cramping or rhabdomyolysis) if the damage is severe enough. As mentioned before, this causes CK and damaged muscle proteins to be elevated in the blood. Eventually, the horse’s kidneys filter these proteins out of the blood and into the urine, causing a very dark-smelly urine color. The dark color in the urine are the damaged muscle proteins and CK. This is why it is common to see horses urinate this dark-smelly urine after a rhabdomyolysis episode or severe exercise.
Image of muscle micro-tears under microscope.
Micro-tears in the muscle can take several days to repair depending on the severity of damage to the muscle, the horse’s diet, and the exercise regimen following the initial exercise. The horse may not actually feel muscle sore until 1-2 days following the initial exercise. This is called "delayed onset muscle soreness" (DOMS). The exact reasoning for why DOMS occurs is not yet well understood.
Often horse owners, riders, or trainers will exercise their horse the days following a hard workout with the hopes of “flushing out” the lactic acid from the muscle. But as mentioned before, this concept does not make any physiological sense considering lactic acid/lactate is already “flushed” out of the muscle within an hour following a hard workout. And the acidity level of the muscle caused by hydrogen ions is also recovered within a few hours following a hard workout as well. So the idea that you are helping “flush out” lactic acid out of the horse’s muscles by exercising them in the days following a hard workout is false. However, this does not mean that light exercise the days following a hard workout is not beneficial to overall muscle recovery. Also, lactate can be "flushed out" of the muscles faster with light exercise such as a light canter, trot, or walk- but only within the minutes (not hours or days) following a hard bout of exercise. Additionally, I’m sure many horsemen have heard “horse physical therapists” saying their massaging, PEMF, laser light, cryotherapy, etc. “helps reduce lactic acid from the muscles” several hours or days after exercise. But once again, these claims are not congruent with the physiology.
Graph of blood lactate over time before, during, and after exercise.
To conclude:
Lactic acid does not cause muscle acidosis, hydrogen ions do.
Lactic acid, or more correctly termed lactate, is actually a buffer and helps to prevent muscle acidosis. Therefore, lactate is actually protective against muscle fatigue.
Lactate does not cause muscle soreness following exercise, muscle damage does.
Lactate is brought back to normal levels in the body within 60 minutes following hard exercise. Furthering the point that lactate cannot and does not cause muscle soreness the days following exercise.
Muscle cramping is not caused by lactate, but most likely by the acidosis of hydrogen ions and muscle damage.
Hopefully you are now better equipped with the knowledge of what actually causes muscle acidosis and have an improved understanding of the protective mechanisms lactate has against muscle fatigue. In future articles, I plan to cover more about how lactate can be used to measure a horse’s fitness as well as the molecule’s important mechanisms during exercise that can dictate exercise performance.
If you want more resources on this topic, I have a list of links to peer-reviewed research papers, articles, and videos explaining some of the concepts I mentioned in this article down below. If you have any questions, please feel free to email me at gallopscience@gmail.com.
Published Journal Articles:
“Biochemistry of exercise induced metabolic acidosis” (R Robert’s et al. 2004) https://pubmed.ncbi.nlm.nih.gov/15308499/
“Protective effects of lactic acid on force production in rat skeletal muscle” (Nielson et al. 2001)
“Lactate: metabolic fuel or poison for racehorses?” (Lindinger 2011)
“Lactate Doesn't necessarily cause fatigue: why are we surprised?” (Brooks 2001)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2278833/#:~:text=Since%20the%20work%20of%20Fletcher,until%20fatigue%20accumulate%20lactic%20acid.
Other Newsletter Articles:
“Myths about lactic acid debunked”
“The Lactic Acid Myth”
Videos:
“Glycolysis Explained (Aerobic vs Anaerobic, Pyruvate, Glyconeogenesis)”
“What Lactate is & What it ACTUALLY does: 5 Min Phys”