Ah, yes. Lactic acid, the ultimate exercise enemy. Lactic acid has been blamed for causing issues all the way from muscle soreness to exercise fatigue and probably even global warming. Interestingly enough, almost every single thing we blame on lactic acid is erroneous, misguided, or just plain outdated. We’re going to dispel a lot of myths over the next few minutes so leave the pitchforks and torches at home and try to keep an open mind.
Let’s first cover what exactly lactic acid is. It gets blamed for almost every negative outcome during exercise, but when pressed, most people probably couldn’t give you a solid description of this evil culprit. Here’s where our first myth lies – lactic acid actually does not exist as such in our bodies, it’s more so just a general expression since we’re too lazy to differentiate between terms. “Lactic acid” is actually presented as two separate species in our bodies – lactate and hydrogen ions (8). Both have unique actions on metabolism and fatigue so we’ll cover them separately as we go along. Lactate is produced during glycolysis, which is the main metabolic pathway we use during intense exercise bouts that last anywhere from 15-seconds to 2-minutes (2,25). Hydrogen ions are produced by other metabolic processes that coincide with glycolysis which is why we see lactate and hydrogen ion accumulation occur simultaneously (8). This 15-second to 2-minute range covers most resistance training exercises and is the exact reason why high rep sets give such a “burn.” This burn is caused by the presence of hydrogen ions which reduce the pH within the muscle (2,8,12).
Glycolysis is the metabolic process of turning stored sugars or ingested carbohydrates into energy. Lactate is produced when exercise intensity increases (15) and not all of the byproducts of glycolysis can make it to the cell mitochondria to be converted into even more energy (8,13). The best part about lactate is that it doesn’t have to travel to the cell mitochondria to be converted to energy – it can undergo a similar process to glycolysis and can be turned into energy instantly or can be shuttled to nearby cells for the same process. In fact, during intense isometric muscle actions, lactate is responsible for 60% of energy production (15). It seems, then, that lactate isn’t much of an enemy since we can readily use it for energy to maintain performance. The only time that lactate could potentially expedite the fatigue process is during a dehydrated state as lactate accumulation may force water out of the muscle cell (2,16). An extensive review on muscle fatigue states, however, that under normal conditions, lactate is not a major determinant of fatigue (2).
Now, on to hydrogen ions. We already know that hydrogen ions are responsible for the “burn” we feel during workouts which we typically associate with lactic acid in general. The accumulation of hydrogen ions will lower cellular pH during maximum exercise – at rest, our muscles are usually somewhere around 7.05 but researchers have seen muscles maintain activity with a pH as low as 6.2; the lowest that we usually see is around 6.5 (2,8,29,30). Many studies have found that muscle force production decreases with a drop in pH but what we don’t often hear is that following fatiguing stimulations, muscle force production recovers to baseline more quickly than pH does (2,8). So it seems that pH and fatigue may not be directly related in this instance. In fact, the majority of studies that found acidosis to be a determinant of fatigue were performed on isolated muscle fibers in controlled environments between 10-20 degrees Celsius. When intact muscle is studied at normal tissue temperatures, acidosis has little effect on fatigue (8,21,33). So hydrogen doesn’t seem to be much of an enemy, either.
It’s starting to get a little controversial so we’re just going to come out and say it: lactic acid is good for you. Oh yeah, we went there. We already somewhat covered the positive aspects of lactate production, but let’s delve into the positive aspects of hydrogen ion accumulation.
By now we know that hydrogen ions are responsible for lowering the pH of a muscle cell. We’ve reverberated that point several times now but it’s important because it appears that lowering the pH of a muscle cell may have an ergogenic (performance-enhancing) effect. One of the main positive effects of lowering cellular pH is that the calcium binding affinity at several sites within the cell is lowered (2,3,10). This is huge because we need calcium to bind to proteins within the cell to cause muscle contraction. If other parts of the cell are also signaling for calcium, then calcium might not bind to these contractile proteins as well (4,18,24). Lower cellular pH may also enhance the ability of electrolytes to move through the cell membrane (14,20) – we can’t achieve muscle activation without this movement of electrolytes, so improving that ability is paramount to maintaining force production and warding off fatigue (2). This effect lowers the amount of brain signal needed to activate a muscle and may be one of the reasons why BFR training increases muscle activation. Ultimately it seems like both lactate and hydrogen ions are actually beneficial for performance. So what causes fatigue, then?
Lactate and hydrogen ions are not the only byproducts of cell metabolism during intense exercise. Our main energy source in a cell is known as adenosine triphosphate, or ATP. We break down food to produce ATP and then we break down ATP to create energy. When ATP breaks down it loses a phosphate group and becomes ADP. Stored creatine phosphate within the cell donates its phosphate group to ADP to reproduce ATP and start the cycle all over again. Under normal conditions, this process happens without a hiccup. But as exercise intensity increases our cells work hard to maintain ATP concentrations but start to accumulate unbound creatine and phosphate ions (2). This accumulation of phosphate ions seems to be one of the masterminds working in the background while lactic acid takes all of the blame.
Studies performed on inorganic phosphate accumulation and fatigue have shown a strong correlation between high phosphate levels and decreasing levels of muscle force production (2,22). The presence of inorganic phosphate may also lower the calcium sensitivity of the contractile proteins within the cell (2,17,19) – so while lowering cellular pH may improve calcium sensitivity, phosphate accumulation does the exact opposite (2). In fact, research has been performed on genetically altered muscle fibers that lack the necessary enzymes to accumulate phosphate during exercise. The fibers that lacked phosphate accumulation were compared to normal fibers in a condition where both underwent 100 fatiguing stimulations. The normal fibers experienced a 30% decrease in force production throughout the trial while the altered fibers exhibited no significant signs of fatigue (2,31). Other studies have also found decreased force production to be associated with higher levels of phosphate accumulation (2,6,7,23). This leads many to believe that phosphate accumulation is a major determinant of fatigue (2,32). But wait, there’s more!
The majority of fatigue is derived from electrolytes and muscle cell excitability. When our brain sends signals to our muscles to contract, electrolytes move around our cell membrane to “depolarize” the muscle cell which ultimately causes it to activate and contract (5). As we send more and more signals with increasing frequency, like we would with exercise, these electrolytes can easily become imbalanced around the cell membrane (11,26,27). Having the correct balance of these electrolytes around the cell is crucial to maintaining the cell’s conductivity to the signals from our brain. As this issue increases in magnitude many of the channels that shuttle electrolytes around the cell membrane start to shut down (1,28). This greatly increases the brain signal required for the muscle to activate (11) and ultimately lowers muscle force production by close to 25% alone (9). This is why it’s so important to properly hydrate and ensure appropriate electrolyte consumption as they are directly related to exercise performance.
So, after lots of huge words and complicated science, I think we can conclude that “lactic acid” isn’t the villain we thought it was. I know a lot of this was probably hard to digest but cellular physiology and biochemistry can be incredibly perplex. If you are interested in learning more I highly suggest the comprehensive reviews by both Cairns (2006) and Allen, Lamb & Westerblad (2008) that are referenced often in this article. There’s a ton of really good information in both that we just don’t have the time to mention in a single article here.
In review, “lactic acid” may help boost performance by providing extra energy through lactate and improving cell processes by way of hydrogen ions and the resulting drop in cellular pH. Fatigue seems to mostly stem from phosphate accumulation and electrolyte imbalances caused by intense exercise and repeated muscle stimulation. Proper hydration, electrolyte intake, and even creatine supplementation may help reduce the fatigue produced by these pathways.
- Adrian, R. H., Chandler, W. K., & Rakowski, R. F. (1976). Charge movement and mechanical repriming in skeletal muscle. The Journal of Physiology, 254(2), 361-388.
- Allen, D.G., Lamb, G.D., Westerblad, H. (2008). Skeletal Muscle Fatigue: Cellular Mechanisms. Physiology Review. 88: 287-332.
- Baker, A. J., Brandes, R., & Weiner, M. W. (1995). Effects of intracellular acidosis on Ca2+ activation, contraction, and relaxation of frog skeletal muscle. American Journal of Physiology-Cell Physiology, 268(1), C55-C63.
- Baylor, S. M., & Hollingworth, S. (2003). Sarcoplasmic reticulum calcium release compared in slow‐twitch and fast‐twitch fibres of mouse muscle. The Journal of Physiology, 551(1), 125-138.
- Blijham, P. J., Hengstman, G. J., Ter Laak, H. J., Van Engelen, B. G., & Zwarts, M. J. (2004). Muscle‐fiber conduction velocity and electromyography as diagnostic tools in patients with suspected inflammatory myopathy: A prospective study. Muscle & Nerve: Official Journal of the American Association of Electrodiagnostic Medicine, 29(1), 46-50.
- Bruton, J. D., Westerblad, H., Katz, A., & Lännergren, J. (1996). Augmented force output in skeletal muscle fibres of Xenopus following a preceding bout of activity. The Journal of Physiology, 493(1), 211-217.
- Bruton, J. D., Wretman, C., Katz, A., & Westerblad, H. (1997). Increased tetanic force and reduced myoplasmic [P (i)] following a brief series of tetani in mouse soleus muscle. American Journal of Physiology-Cell Physiology, 272(3), C870-C874.
- Cairns, S.P. (2006). Lactic Acid and Exercise Performance, Culprit or Friend? Sports Medicine 36(4), 279-291.
- Cairns, S. P., Hing, W. A., Slack, J. R., Mills, R. G., & Loiselle, D. S. (1997). Different effects of raised [K+] o on membrane potential and contraction in mouse fast-and slow-twitch muscle. American Journal of Physiology-Cell Physiology, 273(2), C598-C611.
- Fabiato, A., & Fabiato, F. (1978). Effects of pH on the myofilaments and the sarcoplasmic reticulum of skinned cells from cardiace and skeletal muscles. The Journal of Physiology, 276(1), 233-255.
- Filatov, G. N., Pinter, M. J., & Rich, M. M. (2005). Resting Potential–dependent Regulation of the Voltage Sensitivity of Sodium Channel Gating in Rat Skeletal Muscle In Vivo. The Journal of General Physiology, 126(2), 161-172.
- Fitts, R. H. (1994). Cellular mechanisms of muscle fatigue. Physiological reviews, 74(1), 49-94.
- Gladden, L. B. (2004). Lactate metabolism: a new paradigm for the third millennium. The Journal of Physiology, 558(1), 5-30.
- Hansen, A. K., Clausen, T., & Nielsen, O. B. (2005). Effects of lactic acid and catecholamines on contractility in fast-twitch muscles exposed to hyperkalemia. American Journal of Physiology-Cell Physiology, 289(1), C104-C112.
- Katz, A., Sahlin, K. (1988). Regulation of lactic acid production during exercise. Journal of Applied Physiology. 65(2): 509-518.
- Lamb, G. D., Stephenson, D. G., & Stienen, G. J. (1993). Effects of osmolality and ionic strength on the mechanism of Ca2+ release in skinned skeletal muscle fibres of the toad. The Journal of Physiology, 464(1), 629-648.
- Martyn, D. A., & Gordon, A. M. (1992). Force and stiffness in glycerinated rabbit psoas fibers. Effects of calcium and elevated phosphate. The Journal of General Physiology, 99(5), 795-816.
- Melzer, W., Rios, E., & Schneider, M. F. (1984). Time course of calcium release and removal in skeletal muscle fibers. Biophysical Journal, 45(3), 637.
- Millar, N. C., & Homsher, E. (1990). The effect of phosphate and calcium on force generation in glycerinated rabbit skeletal muscle fibers. A steady-state and transient kinetic study. Journal of Biological Chemistry, 265(33), 20234-20240.
- Nielsen, O. B., de Paoli, F., & Overgaard, K. (2001). Protective effects of lactic acid on force production in rat skeletal muscle. The Journal of Physiology, 536(1), 161-166.
- Pate, E., Bhimani, M., Franks-Skiba, K., & Cooke, R. (1995). Reduced effect of pH on skinned rabbit psoas muscle mechanics at high temperatures: implications for fatigue. The Journal of Physiology, 486(3), 689-694.
- Pathare, N., Walter, G. A., Stevens, J. E., Yang, Z., Okerke, E., Gibbs, J. D., … & Vandenborne, K. (2005). Changes in inorganic phosphate and force production in human skeletal muscle after cast immobilization. Journal of Applied Physiology, 98(1), 307-314.
- Phillips, S. K., Wiseman, R. W., Woledge, R. C., & Kushmerick, M. J. (1993). The effect of metabolic fuel on force production and resting inorganic phosphate levels in mouse skeletal muscle. The Journal of Physiology, 462(1), 135-146.
- Posterino, G. S., & Lamb, G. D. (2003). Effect of sarcoplasmic reticulum Ca2+ content on action potential‐induced Ca2+ release in rat skeletal muscle fibres. The Journal of Physiology, 551(1), 219-237.
- Robergs, R. A., Ghiasvand, F., & Parker, D. (2004). Biochemistry of exercise-induced metabolic acidosis. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 287(3), R502-R516.
- Ruff, R. L. (1996). Single-channel basis of slow inactivation of Na+ channels in rat skeletal muscle. American Journal of Physiology-Cell Physiology, 271(3), C971-C981.
- Ruff, R. L. (1996). Sodium channel slow inactivation and the distribution of sodium channels on skeletal muscle fibres enable the performance properties of different skeletal muscle fibre types. Acta Physiologica Scandinavica, 156(3), 159-168.
- Ríos, E., & Pizarro, G. (1991). Voltage sensor of excitation-contraction coupling in skeletal muscle. Physiological Reviews, 71(3), 849-908.
- Sahlin, K., Harris, R. C., Nylind, B., & Hultman, E. (1976). Lactate content and pH in muscle samples obtained after dynamic exercise. Pflügers Archiv, 367(2), 143-149.
- Spriet, L. L., Lindinger, M. I., McKelvie, R. S., Heigenhauser, G. J., & Jones, N. L. (1989). Muscle glycogenolysis and H+ concentration during maximal intermittent cycling. Journal of Applied Physiology, 66(1), 8-13.
- Steeghs, K., et. al. (1997). Altered Ca2+ responses in muscles with combined mitochondrial and cytosolic creatine kinase deficiencies. Cell, 89(1), 93-103.
- Westerblad, H., Allen, D. G., & Lannergren, J. (2002). Muscle fatigue: lactic acid or inorganic phosphate the major cause?. Physiology, 17(1), 17-21.
- Wiseman, R. W., Beck, T. W., & Chase, P. B. (1996). Effect of intracellular pH on force development depends on temperature in intact skeletal muscle from mouse. American Journal of Physiology-Cell Physiology, 271(3), C878-C886.
Last Updated on