Muscle soreness from ‘lactic acid buildup’? Lactic acid has been a black pot for a hundred years

Climbing several floors in a row, there is a burning pain in the thigh. Is this the accumulation of lactic acid? The day after exercising, the muscles hurt to the point of exertion. Why hasn’t the lactic acid gone?
 “Accumulation of lactic acid causes muscle soreness” is common knowledge among many people. Fitness coaches say this, and similar explanations can be seen everywhere on the Internet and in books. But in fact, lactic acid is a sore pot for other accomplices. 

Too long to read the version

  • Sugar breaks down to produce “lactate”, not “lactic acid”

  • Lactate buildup accompanies muscle soreness during exercise, but not alone

  • Post-exercise, lactate concentrations recovered within 1 hour, independent of second day soreness

  • Lactate can provide energy, transmit signals

z-ILW-V-NrWeAYzrYZdDlKTnBp9fU4BXYEIfDkvO 1~2 days after training hips and legs or climbing | giphy

Lactic acid was once thought to be the main cause of soreness

 
When lactic acid was first discovered, it was not associated with muscles. In 1780, a Swedish medicinal chemist discovered it in yogurt, so it was named lactic acid [1]. Over the next 100 years, scientists have gradually linked lactic acid to muscle soreness and acidification through a study: 

After multiple contractions of a single muscle, lactate levels increase, pH decreases (acidification), and muscle strength decreases, and these changes are more pronounced when oxygen is deficient;

After the whole person is tired from exercising, there are similar changes, and they feel muscle soreness;

The higher the lactate level, the more severe the muscle soreness and weakness;

Lactate levels are also elevated in some people who are sick;

Lactic acid is very acidic (pH 3.86), which can cause soreness.

 
Piecing these findings together, researchers in the 1920s hypothesized that when muscles contract in an oxygen-deficient environment, sugar is forced to break down to produce lactic acid, a metabolic waste that causes acidification; lactic acid only makes muscles sore and tired . and other harm, no benefit. This speculation thus put the pot on the lactic acid head and made it notorious for the next century [2]. 

Related non-causal, “lactate” not “lactic acid”

 However, careful scrutiny shows that the hypothesis that “lactic acid causes muscle soreness” is not perfect. Although it is true that muscle soreness and weakness are co-occurring with elevated lactate levels during exercise and are correlated in magnitude, causality cannot be established. In fact, in addition to lactate, muscle fatigue is accompanied by many physiological changes, such as acidification, decreased ATP levels, etc. [2]. In addition, the traditional concept is that lactic acid is produced when sugar is broken down, and it is immediately broken down into lactate and hydrogen ions, which leads to acidification of the environment, resulting in muscle soreness and weakness. But in 1983, scientists put forward another point of view, which was affirmed by more researchers after 2004: the word lactic acid” itself is not accurate, because there is no research to prove that muscle contraction produces lactic acid, which is produced when sugar is broken down. Lactate”, a process of decomposition that, instead of directly producing acid, may consume a hydrogen ion, alkalizing the cell [3]. Muscles are indeed acidified during exercise, but the source of hydrogen ions is still under debate. At present, most people believe that lactic acid is not the direct source, and the hydrogen ions may mainly come from the process of ATP hydrolysis [1, 4]. 178 The decomposition of pyruvate to lactate does not produce hydrogen ions | Reference [5]

Lactate does not directly cause soreness during exercise

 In addition to theoretical analysis, actual test results do not support lactate directly causing muscle soreness during exercise. A 2014 study injected lactate directly into the muscles of the palms of people and found that the solution did not cause significant pain, even at concentrations significantly higher than what can be achieved with exercise (50 mmol/L). Two other metabolites commonly found in muscle contraction, ATP and hydrogen ions, also caused little pain when injected alone. However, simultaneous injection of these three substances can cause significant muscle pain [6]. The trial cleared the culprit of muscle soreness for lactate. On its own, no amount of concentration is enough to ignite your muscles. 214 Elevated lactate concentrations alone are not sufficient to cause soreness | Ref [6]
The reason why muscles are sore during exercise is that repeated forced contractions produce many metabolites, some of which can bind to receptors to activate pain afferent neurons in the muscle, which then transmit pain signals to the brain. A hundred years ago, scientists speculated that the most important of these metabolites was lactic acid. In the past two decades, under conditions closer to the actual situation of the human body, many studies have gradually denied the decisive role of lactate, and found that pain is a variety of the result of the interaction of substances. Among all metabolites, the three most influential on pain are lactate, ATP and hydrogen ions. When the three exist alone or when only the two are added together, the effect is relatively weak, but when the three appear at the same time, there will be a synergistic effect of mutual enhancement, and the pain signal will be significantly enhanced. Low concentrations of these three induce a feeling of warmth, while elevated concentrations produce pain and burning sensations [6-8]. In addition, there are a number of substances that increase in concentrations during muscle contraction and may enhance pain perception, including bradykinin, potassium, and various cytokines [2, 6, 7]. Therefore, the muscle soreness at the time of exercise is the result of the combined force of many substances. Although the status of lactate is important, it should not be responsible for this pot alone. 

Lactate not linked to soreness on day two of exercise

 As for muscle soreness on the second or third day after exercise, it has less to do with lactate, because lactate has been metabolized as early as the end of exercise. At rest, people’s blood lactate concentrations range from 0.5 to 2.2 mmol/L. Once you start exercising, lactate levels typically rise gradually, and the higher the intensity of the exercise, the faster it rises. After cessation of exercise, blood lactate concentrations generally continue to rise, reaching a peak (10–30 mmol/L) 5 minutes after exercise , and then gradually decline, usually falling back to resting levels within 1 hour [5] ]. Now that the concentration has recovered, muscle soreness the day after exercise has nothing to do with lactate buildup. For this kind of soreness that begins 6-12 hours after exercise and peaks at 48-72 hours, the mechanism has not yet been identified, and it is currently believed to be mainly related to skeletal muscle mechanical damage and inflammatory response, rather than lactate.
424 Changes in blood lactate levels after exercise cessation | Reference [9]

Lactate is actually very useful

 Lactate bears the notoriety of muscle soreness for many other substances, but its important role in the human body is rarely mentioned. In recent years, studies have gradually found that lactate is not a metabolic waste, but an important fuel, and has the function of transmitting signals [1, 4]. When a person needs to obtain a lot of energy in a short time, sugar is broken down in the cytoplasm to form lactate. These lactates can enter the mitochondria for oxidation and provide energy, and can also be transported to the outside of the cell to be taken up by adjacent skeletal muscle, heart, brain, liver, kidney and other cells for oxidative energy supply or resynthesis of sugars [5, 10] ]. In some cases, lactate is even an energy source superior to glucose [4]. There is also an extreme case where the role of lactate can be tested, and that is to observe how the movement status of patients who cannot produce lactate changes. They are unable to break down sugar into lactate due to a lack of muscle phosphorylase, however, avoiding lactate accumulation did not enhance their exercise performance, but instead made fatigue earlier [11]. In short, lactate is not a metabolic waste that harms muscles. Next time you feel sore, don’t blame “lactic acid accumulation” again. 9PjDm1mxUEeUiFc0NJdkl6QfDEwZRoSo1I_vF-RO Really not my lactate dry | giphy 

references

[1] Ferguson BS, Rogatzki MJ, Goodwin ML, Kane DA, Rightmire Z, Gladden LB. Lactate metabolism: historical context, prior misinterpretations, and current understanding. Eur J Appl Physiol. 2018;118(4):691-728.

[2] Cairns SP. Lactic acid and exercise performance: culprit or friend? Sports Med. 2006;36(4):279-91.

[3] Hochachka PW, Mommsen TP. Protons and anaerobiosis. Science. 1983;219(4591):1391-1397.

[4] Hall MM, Rajasekaran S, Thomsen TW, Peterson AR. Lactate: Friend or Foe. PM R. 2016;8(3 Suppl):S8-S15.

[5] National Strength and Conditioning Association; G. Gregory Haff, N. Travis Triplett, editors. Essentials of Strength Training and Conditioning, 4th ed. 2016.

[6] Pollak KA, Swenson JD, Vanhaitsma TA, Hughen RW, Jo D, White AT, Light KC, Schweinhardt P, Amann M, Light AR. Exogenously applied muscle metabolites synergistically evoke sensations of muscle fatigue and pain in human subjects. Exp Physiol. 2014;99(2):368-380.

[7] Gregory NS, Whitley PE, Sluka KA. Effect of Intramuscular Protons, Lactate, and ATP on Muscle Hyperalgesia in Rats. PLoS One. 2015;10(9):e0138576.

[8] Light AR, Hughen RW, Zhang J, Rainier J, Liu Z, Lee J. Dorsal root ganglion neurons innervating skeletal muscle respond to physiological combinations of protons, ATP, and lactate mediated by ASIC, P2X, and TRPV1. J Neurophysiol . 2008;100(3):1184-1201.

[9] Fukuba Y, Walsh ML, Morton RH, Cameron BJ, Kenny CT, Banister EW. Effect of endurance training on blood lactate clearance after maximal exercise. J Sports Sci. 1999;17(3):239-248.

[10] Brooks GA. Cell-cell and intracellular lactate shuttles. J Physiol. 2009;587(Pt 23):5591-5600.

[11] Lewis SF, Haller RG. The pathophysiology of McArdle’s disease: clues to regulation in exercise and fatigue. J Appl Physiol (1985). 1986;61(2):391-401.

Author: Dai Tianyi Editor: odette

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