You know the feeling, it’s the last 100 meters of the race, your lungs are aching and your thighs are burning … the pain and effort invariably makes you slow down and the next day your quads are sore and you can barely walk down the stairs. Inevitably, you blame the dreaded lactic acid, the bane of every runner! While the strain to keep running at a fast pace and post workout soreness are real experiences, a myth has pervaded the training of the endurance runner and lactic acid has received an unfair reputation.
The Lactic Acid Myth Defined
As our bodies perform prolonged duration, fast paced running (i.e. 800m to 5k), we begin to breathe faster as our working muscles demand more oxygen. The human body prefers to generate the majority of its energy aerobically (from oxygen) which occurs in the mitochondria of our cells, but as the runner tries to maintain a fast pace for a longer period of time, our bodies demand energy production faster than our bodies can optimally provide oxygen. Under this circumstance, the working muscles generate energy anaerobically, or without oxygen, which occurs in the cytoplasm of our cells. The energy to keep running comes from glucose, broken down from ingested carbohydrates, in most instances, through a process called glycolysis. During glycolysis, glucose is metabolized, through a series of chemical reactions, into two molecules of a substance called pyruvic acid. When running aerobically, pyruvic acid is further broken down and the energy in its molecule is used to form high-energy compounds such as NADH, ultimately leading to more energy for the runner. When running in an anaerobic state, NADH, cannot be reoxidized to NAD+, which needs to occur for important metabolic functions, due to the lack of adequate oxygen. Failure to regenerate NAD+ would force the energy yielding reactions of glycolysis to stop. Therefore, in the anaerobic state, NAD+ is regenerated when pyruvate releases a hydrogen ion to form lactate.
Ultimately, this reaction is part of a process that allows the creation of a molecule called adenosine triphosphate, or ATP, (consisting of one adenosine and three phosphate groups) which is the primary compound, when metabolized (through a process called hydrolysis in which ATP is split into a compound called adenosine diphosphate or ADP), that provides the energy for biochemical reactions involved in every muscle contraction necessary for running as well as most other cellular functions in the body.
The prevailing myth within the athletic community and general public is that lactic acid, or the more accurate term lactate, is a waste product of glycolysis that accumulates in the blood and muscles during anaerobic running, due to increased dissociation of lactic acid into lactate and hydrogen ions along with the release of a phosphate proton from the breakdown of ATP, thereby creating an acidic environment.
This common assertion claims that the acidic environment disrupts the cross-bridge cycle (contraction) of working muscles thus contributing to the inability to preserve a fast running pace.
As myths typically go, none of the detrimental beliefs about lactate that appear as common knowledge in the athletic community are true. In fact, exercise physiologists have known, without controversy, since the mid-1980s, about the falsehood of lactate’s negative effects
Note – runners typically use the terms “lactate” and “lactic acid” interchangeably, although they are not the exact same chemical compound. In the interest of accuracy, lactate is lactic acid that has lost a hydrogen ion and gained a sodium or potassium ion. Lactic acid must first be converted to lactate before it can leave the muscles because muscle cell membranes will not allow lactic acid to pass through or be pumped from them. The chemical differences between lactate and lactic acid are not relevant to this discussion and will be used interchangeably
Lactate and Acidosis
The term lactate is not a new concept and can be traced back to its initial discovery in sour milk in the 1780’s, hence the name (lactic or lactate = of or relating to milk). Lactic acid as a component of biological metabolic activity was identified in the late 1800’s. Pioneering research of skeletal muscle biochemistry occurred in the 1920’s when physiologists found that the exposure of frog legs to high levels of lactic acid interfered with the ability of the muscles to contract in response to electrical stimulation. As a result, it was concluded that the reason for muscular fatigue during exercise was the accumulation of lactic acid. It was suggested that lactate was formed in the body by the removal of a proton from lactic acid and when protons accumulate in living tissues, tissues become more acidic which then interfered with muscles contractility.
This was the prevailing belief as followed among the athletic community for many decades.
However, no experimental evidence has ever revealed a cause-effect relationship between lactate production and acidosis. Past studies supporting the lactic acidosis concept are entirely based on indirect evidence, meaning that since lactate increased in volume in muscle tissue as acidosis progressed, followed by a decline in muscle performance, a correlation was made that lactate caused acidosis.
Hence, lactate is associated with fatigue, without in itself causing fatigue
While it is clear that lactate is not responsible for muscle failure causing acidosis, lactate production does result in the release of a hydrogen ion which can cause a drop in tissue pH. But, the hydrogen ion is quickly buffered by bicarbonate within the blood stream which is quickly converted into water and carbon dioxide which is excreted by the body as sweat and exhalation to preserve the acid-base balance.
However, it was not until 1977 that lactate’s view as a harbinger of fatigue during intense running began to evolve into our current view. Biochemist, Wieland Gevers, showed that:
lactate in the body actually slows the progression of muscle acidosis;
it was found that this reaction actually consumes versus produces a pair of acid environment causing free protons, namely hydrogen ions. However, these findings sat idle until 1983 when researchers Hochachka and Mommsen rediscovered and wrote an extensive review on this topic. These findings were further supported by other researchers ultimately claiming the following:
the hydrolysis of ATP into ADP, with the accumulation of potassium and phosphate molecules inhibit muscle contraction and present as the dominant source of fatigue while running anaerobically.
The question remains that if the truth about lactate has been known for years, then why does the running world continue to follow this fallacy? That question remains to be answered, however the purpose of this treatise is to facilitate the dismissal of this misguided information so as to facilitate optimal training and education of the endurance runner.
The accumulation of lactate is now linked with counteracting the negative effects of muscle contraction including the buffering of metabolites, acting as a substrate for fuel production, providing a pathway to preserve neuronal and cognitive function during exercise and facilitating the development of mitochondria, ultimately promoting the growth and performance of the endurance runner.
Lactate as Fuel
Lactate is continually produced whenever glycolysis occurs. During low to moderate intensity (i.e. aerobic) running, the volume of lactate that is produced is equally metabolized with no accumulation. But at faster, prolonged duration paces, as lactate production begins to exceed its metabolic capabilities, an anaerobic pathway initiates in muscle tissue called the Lactate-Shuttle. This process gives working muscle two parallel pathways that release energy quickly to keep up with the muscle’s energy demands. In this process, lactate can stay in the working muscle cells (under anaerobic conditions) to contribute to energy production or be transported from the muscle to surrounding muscles that have oxygen available and be metabolized into fuel or travel (via the bloodstream) to the liver where it can be converted back to pyruvate, then to glucose (via the Cori cycle) thru a process known as gluconeogenesis for continued running at a fast pace.
The use of lactate as fuel within the muscle itself varies with how well a person’s endurance muscle fibers are aerobically trained; the greater one is aerobically trained, the more efficient the metabolism of lactate. Research on untrained individuals, during running, shows that approximately 75% of the available lactate is directly oxidized in comparison to about 90% in trained runners. So, as one can see, lactate does not contribute to fatigue, but actually helps the runner to keep running at a given pace as it is noted that approximately one third of total energy contribution comes from lactate while the remainder of energy contribution is from circulating blood glucose and stored muscle glycogen.
Lactate and Endurance Development
Mitochondria are cell organelles, the powerhouses of the cell, responsible for aerobic respiration and production of energy through the breakdown of ATP. A fundamental biochemical adaptation induced by endurance training is an increase in the mitochondrial volume and size within trained muscle fibers. Enhanced mitochondrial content and size increases the capacity for aerobic energy production from glycolysis and can be found in both slow-twitch (endurance based muscles) and fast-twitch fibers (speed based muscles) when they are stimulated by an appropriate training program.
While lactate has been shown to act as a substrate for oxidation in the Lactate Shuttle, increased lactate levels are also believed to act as a signalling hormone thus inducing changes in gene expression sugesting that lactate stimulates mitochondrial biogenesis. Intracellular lactate accumulation during intense running stimulates the muscle cell to produce more mitochondria, thus enhancing its ability to burn lactate (and other fuels) in future workouts and race events. As a result, this increases the proportion of type I (slow-twitch) fibers which further enhances the endurance runners performance.
Lactate the Buffer
When a runners muscle demand for ATP is met by aerobic respiration (during low to moderate intensity aerobic running) there is no phosphate proton accumulation (as a byproduct from the breakdown of ATP to ADP) in the cell because mitochondria metabolize the protons in other chemical processes to preserve what is termed a proton gradient within the intermembranous space. A proton gradient occurs when there is a higher concentration of protons outside the mitochondria versus inside; this is a driving force behind ATP synthesis. During anaerobic running, phosphate accumulation exceeds metabolism capabilities thus causing a progressive lessening of the difference in charge strength between intracellular and intercellular spaces, a dysfunction of the proton gradient. This results in weaker and less efficient muscle contractions, hence the runner slows down. Lactate can also act as a medium to buffer the accumulation of phosphate. As lactate is metabolized either in the working muscle or surrounding muscle cell or organs (i.e. liver) , lactate is converted back to pyruvate. From this point, further ATP is produced by attaching a free phosphate to ADP. Lactic acid allows the continued production of ATP by buffering the excess phosphate accumulation thus allowing the runner to continue their pace for a longer period of time.
Muscle contractions are stimulated by neurological impulses that flow through the body via minerals including sodium and potassium. During muscle contraction, potassium molecules, inside the muscle cell, exchange place with sodium ions located outside the cell which occurs most efficiently when a high degree of polarization (a difference in electrical charge strength) exists between intra and extra cellular spaces. At the initiation of fast running the the charge strength inside the muscle cell is much stronger than outside the cell thus facilitating the transfer of sodium and potassium across the cell membrane As fast paced, sustained running continues, potassium accumulates outside the cell membrane because a special potassium pump within the cell membrane is unable to keep up with its production. This accumulation causes a progressive decline of the difference in charge strength between the intracellular and intercellular spaces, thus causing weaker and less efficient muscle contractions causing the runner to slow down. High levels of lactate have been shown to partially restore muscle cell function in a depolarized state. The presence of lactic acid reduces the threshold for muscle excitation thus allowing depleted muscles to keep contracting, while fatigued, and allowing the runner to preserve their pace for a longer period of time. Lactic acid counters this fatigue by interfering with the flow of chlorine ions which essentially lowers the amount of sodium required for muscle contraction.
Lactate Facilitates Brain Function During Exercise
Lactate is also regarded as a valuable metabolite for brain function as well as it being a significant substrate for energy for neurons during exercise . Additionally, lactate optimizes GABA, the chief inhibitory neurotransmitter in the central nervous system, ensuring that inhibitory signals from the central nervous system, caused by a drop in cell pH, are effectively detected. Lactate can therefore be regarded as important to the maintenance of cognitive function, protecting neurons from damage by acidosis. Also, lactate may be shuttled between astrocytes and neurons (both showing the ability to metabolize lactate) referred to as the astrocyte-neuron-lactate shuttle which is responsible for contributing up to 33% of total energy substrate utilized by the brain during exercise.
So, Why Are My Muscles Sore The Next Day?
The dreaded delayed onset muscle soreness (DOMS) is caused by eccentric exercise, that is, exercise consisting of eccentric (lengthening) contractions of the muscle (i.e. bending of the knee while weightbearing as seen with squatting or downhill running). The former theory, yet still present myth among poorly informed coaches, athletes and the general public proposes that DOMS is caused by the build-up of lactic acid in the blood, whose production was believed to continue following exercise. However, this theory has been wholly discarded, as concentric (shortening) contractions (i.e. bending of the knee while not weightbearing as seen with a standing hamstring curl) which also produce lactic acid has not been shown to cause DOMS. In addition, lactate has been shown to be restored to resting levels within 60 minutes of completing a running activity, therefore being incapable of causing pain that occurs 24 to 72 hours after activity completion. One study had subjects run on a treadmill for 45 min on two separate days, one day on a level grade and the other day on a 10% downhill grade. Level running produced no muscle soreness while the downhill running, which required extensive eccentric action, resulted in considerable soreness within 24 to 48 h, even though blood lactate concentrations were much higher with level running. An important, additional, point attacks the often proposed claim by coaches to stretch after running to reduce the onset of DOMS. But, a review of systematic reviews on the effects of stretching before or after exercise on the development of delayed-onset muscle soreness found that pre- and post-workout stretching did not reduce the effects of DOMS in healthy adults.
Biochemically, there is no support for the common claim that lactic acid causes muscle acidosis. In addition, lactate accumulation does not cause the runner to slow down. Acidosis is directly related to ATP synthesis occurring outside cell mitochondria and is a primary component for the regeneration of NAD+ in order to promote continued ATP production during glycolysis. while also consuming protons to reduce acidosis. While the accumulation of blood lactate serves as an indirect marker of heightened proton release and increased tissue acidity, this does not indicate a cause-effect relationship.
The concept that lactic acid causes tissue acidosis with imminent running performance decline is a vestige of research from the 1920’s. The truth about lactic acid shows that:
- Lactate is an important substrate for energy production that is used by the muscles during submaximal running to promote continued performance levels, while lactate is the preferred source of fuel for the heart and brain
- Lactic acid is not the cause of delayed onset muscle soreness, plain and simple; eccentric exercise causes micro-trauma to muscle tissue thus inducing post workout soreness
- Training accelerates the body’s ability to process lactate thus providing a continued source of energy substrate to promote continued running performance; training above the lactate threshold promotes the biogenesis of mitochondria thus promoting greater endurance and facilitates the buffering of muscle contraction metabolites thus promoting continue running.