- Lactic Acidosis: Symptoms, Causes, Treatment, and More
- Heart disease
- Severe infection (sepsis)
- Short bowel syndrome (short gut)
- Acetaminophen use
- Chronic alcoholism
- Intense exercise or physical activity
- What Is Blood Lactate?
- The ATP-PCr system
- The Glycolytic System
- The Oxidative system
- What is Blood Lactate?
- How can we use the measurement of Blood Lactate to improve endurance performance?
- Creating a Blood Lactate Curve
- Share this article
- What is lactic acid? (And where does it come from?)
- How muscles produce lactic acid
- Other sources of lactic acid
- Your body on lactic acid
- Lactate Profile
- Lactate: valuable for physical performance and maintenance of brain function during exercise
- Lactate-induced acidosis
- Noxious metabolites
- Why Does Lactic Acid Build Up in Muscles? And Why Does It Cause Soreness?
- How to get rid of lactic acid
- Drinking plenty of water
- Taking deep breaths
- Decreasing exercise intensity
- Stretching after a workout
- Calcium lactate Uses, Side Effects & Warnings – Drugs.com
- What is calcium lactate?
- What other drugs will affect calcium lactate?
Lactic Acidosis: Symptoms, Causes, Treatment, and More
Lactic acidosis is a form of metabolic acidosis that begins when a person overproduces or underutilizes lactic acid, and their body is not able to adjust to these changes.
People with lactic acidosis have problems with their liver (and sometimes their kidneys) being able to remove excess acid from their body. If lactic acid builds up in the body more quickly than it can be removed, acidity levels in bodily fluids — such as blood — spike.
This buildup of acid causes an imbalance in the body’s pH level, which should always be slightly alkaline instead of acidic. There are a few different types of acidosis.
Lactic acid buildup occurs when there’s not enough oxygen in the muscles to break down glucose and glycogen. This is called anaerobic metabolism.
There are two types of lactic acid: L-lactate and D-lactate. Most forms of lactic acidosis are caused by too much L-lactate.
There are two types of lactic acidosis, Type A and Type B:
- Type A lactic acidosis is caused by tissue hypoperfusion resulting from hypovolemia, cardiac failure, sepsis, or cardiopulmonary arrest.
- Type B lactic acidosis is caused by impairment of cellular functioning and localized areas of tissue hypoperfusion.
Lactic acidosis has many causes and can often be treated. But if left untreated, it may be life-threatening.
The symptoms of lactic acidosis are typical of many health issues. If you experience any of these symptoms, you should contact your doctor immediately. Your doctor can help determine the root cause.
Several symptoms of lactic acidosis represent a medical emergency:
- fruity-smelling breath (a possible indication of a serious complication of diabetes, called ketoacidosis)
- jaundice (yellowing of the skin or the whites of the eyes)
- trouble breathing or shallow, rapid breathing
If you know or suspect that you have lactic acidosis and have any of these symptoms, call 911 or go to an emergency room right away.
Other lactic acidosis symptoms include:
- exhaustion or extreme fatigue
- muscle cramps or pain
- body weakness
- overall feelings of physical discomfort
- abdominal pain or discomfort
- decrease in appetite
- rapid heart rate
Lactic acidosis has a wide range of underlying causes, including carbon monoxide poisoning, cholera, malaria, and asphyxiation. Some common causes include:
Conditions such as cardiac arrest and congestive heart failure may reduce the flow of blood and oxygen throughout the body. This can increase lactic acid levels.
Severe infection (sepsis)
Any type of severe viral or bacterial infection can cause sepsis. People with sepsis may experience a spike in lactic acid, caused by reduced oxygen flow.
HIV medications, such as nucleoside reverse transcriptase inhibitors, can spike lactic acid levels. They also may cause liver damage. This makes it harder for the body to process lactate.
Cancer cells create lactic acid. This buildup of lactic acid may accelerate as a person loses weight and the disease progresses.
Short bowel syndrome (short gut)
While rare, people with short gut may experience a buildup of D-lactic acid, caused by bacterial overgrowth in the small bowel. People who’ve had gastric bypass surgery may also get D-lactic acidosis.
Regular, frequent use of acetaminophen (Tylenol) can cause lactic acidosis, even when taken in the correct dosage. This is because it can cause an accumulation of pyroglutamic acid in the blood.
Drinking alcohol to excess over an extended period of time can lead to lactic acidosis and alcoholic ketoacidosis. Alcoholic ketoacidosis is a potentially fatal condition if left untreated, but it can be combated with intravenous (IV) hydration and glucose.
Alcohol increases phosphate levels, which negatively impact the kidneys. This makes the body’s pH more acidic. If you’re having trouble reducing your alcohol intake, support groups can help.
Intense exercise or physical activity
A temporary buildup of lactic acid can be caused by vigorous exercise if your body doesn’t have enough available oxygen to break down glucose in the blood. This can cause a burning feeling in the muscle groups you’re using. It can also cause nausea and weakness.
A specific class of oral diabetes medication, called biguanides, can cause a buildup of lactic acid levels.
Metformin (Glucophage) is one of these drugs. It’s used to treat diabetes and may also be prescribed for other conditions, such as renal insufficiency. Metformin is also used off-label to treat polycystic ovarian syndrome.
In people with diabetes, lactic acidosis may be more of a concern if kidney disease is also present. If you have diabetes and experience any symptoms of lactic acidosis, call 911 or go to an emergency room immediately.
Lactic acidosis is diagnosed through a fasting blood test. Your doctor may instruct you to not eat or drink anything for 8 to 10 hours before taking the test. You may also be instructed to curb your activity level in the hours leading up to the test.
During the test, your doctor may tell you not to clench your fist, as this may artificially spike acid levels. Tying an elastic band around the arm may also have this result.
For these reasons, the lactic acidosis blood test is sometimes done by finding a vein on the back of the hand instead of the arm.
the root cause, treatments for lactic acidosis often result in full recovery, particularly if treatment is immediate. Sometimes, kidney failure or respiratory failure may result. When left untreated, lactic acidosis can be fatal.
Lactic acidosis prevention is also determined by its potential cause. If you have diabetes, HIV, or cancer, discuss your condition and the medications you need with your doctor.
Lactic acidosis from exercise can be prevented by remaining hydrated and providing yourself with long resting periods between exercise sessions.
It’s vitally important to avoid misusing alcohol. Discuss rehabilitation and 12-step program options with your doctor or counselor.
What Is Blood Lactate?
To understand what blood lactate is and how it is produced during exercise, it is useful to have a basic understanding of the systems the body uses to produce energy.
Whether you’re running a marathon or performing an Olympic lift, skeletal muscle is powered by one important compound; adenosine triphosphate (ATP).
The body only stores small amounts of ATP in the muscles so it has to replace and resynthesize this energy compound on an ongoing basis. Understanding how it does this is the key to understanding energy systems.
There are 3 separate energy systems through which the body produces ATP. Describing each of these systems in detail goes beyond the aim of this article. Instead it is intended that the brief outlines provided will assist in describing the role of blood lactate during energy production for exercise, and how this knowledge can be used to help with training for improved endurance performance.
The ATP-PCr system
This system produces energy during the first 5-8 seconds of exercise using ATP stored in the muscles and through the breakdown of phosphocreatine (PCr). This system can operate with or without the presence of oxygen but since it doesn’t rely on oxygen to work it is said to be anaerobic. When activity continues beyond this period the body relies on other ways to produce ATP.
The Glycolytic System
This system produces ATP through the breakdown of glucose in a series on enzymatic reactions. The end product of glycolysis is pyruvic acid. This either gets funneled through a process called the Kreb’s cycle (slow glycolysis) or gets converted into lactic acid (fast glycolysis).
The fast glycolytic system produces energy more quickly than slow glycolysis but the end product of lactic acid can accumulate and is thought to lead to muscular fatigue. The contribution of the fast glycolytic energy system rapidly increases after the first 10 seconds and activity lasting up to 45 seconds is supplied by energy mainly from this system.
Anything longer than this and there is a growing reliance on the Oxidative system.
The Oxidative system
This is where pyruvic acid from slow glycolysis is converted into a substance called acetyl coenzyme A rather than lactic acid. This substance is then used to produce ATP by funneling it through the Krebs cycle. As it is broken down it produces ATP but also leads to the production of hydrogen and carbon dioxide.
This can lead to the blood becoming more acidic. However, when oxygen is present it combines with the hydrogen molecules in series of reactions known as the electron transport chain to form water thus preventing acidification. This chain, which requires the presence oxygen, also leads to the production of ATP.
The Krebs cycle and the electron transport chain also metabolise fat for ATP production but this again requires the presence of oxygen so that the fats can be broken down. More ATP can be liberated from the breakdown of fats but because of the increased oxygen demand exercise intensities must be reduced.
This is also the most sustainable way of producing ATP.
It is important to remember that these systems are all constantly working to produce energy for all bodily functions and one system is never working exclusively over the others.
When it comes to energy production for exercise one system will play a more dominant role (this will be dictated by the type of activity being performed) but all 3 systems will still be working to provide adequate amounts of ATP.
What is Blood Lactate?
It is through the Glycolytic System that the role and production of blood lactate becomes apparent. Recall the end product of glycolysis is pyruvic acid. When this is converted into lactic acid it quickly dissociates and releases hydrogen ions.
The remaining compound then combines with sodium or potassium ions to form a salt called lactate. Far from being a waste product, the formation of lactate allows for the continued metabolism of glucose through glycolysis.
As long as the clearance of lactate is matched by its production it becomes an important source of fuel.
Clearance of lactate from the blood can occur either through oxidation within the muscle fibre in which it was produced or it can be transported to other muscle fibres for oxidation. Lactate that is not oxidized in this way diffuses from the exercising muscle into the capillaries and it is transported via the blood to the liver.
Lactate can then be converted to pyruvate in the presence of oxygen, which can then be converted into glucose. This glucose can either be metabolized by working muscles (as an additional substrate) or stored in the muscles as glycogen for later use. So lactate should be viewed as a useful form of potential energy.
Lactic acid and lactate do not cause fatigue per se.
In fact, it is a common misinterpretation that blood lactate or even lactic acid has a direct negative effect on muscle performance.
It is now generally accepted that any decrease in muscle performance associated with blood lactate accumulation is due to an increase in hydrogen ions, leading to an increased acidity of the inter-cellular environment.
This acidosis is thought to have an unfavourable effect on muscle contraction, and contributes to a feeling of heavy or ‘jelly’ legs.
The term ‘accumulation’ is therefore the key, as an increased production of hydrogen ions (due to an increase production of lactic acid) will have no detrimental effect if clearance is just as fast. During low intensity exercise blood lactate levels will remain at near resting levels as clearance matches production.
As exercise intensity increases there comes a break point where blood lactate levels will start to rise (production starts to exceed clearance). This is often referred to as the lactate threshold (LT). If exercise intensity continues to increase a second and often more obvious increase in lactate accumulation is seen.
This is referred to as the lactate turn point (LTP).
How can we use the measurement of Blood Lactate to improve endurance performance?
The physiological processes discussed above can’t be over ruled when it comes to the limiting factors of endurance performance i.e. you can’t run a marathon once lactate is significantly increasing. An individual’s LT and LTP are therefore powerful predictors of endurance performance.
Knowing the exercise intensity that represents these two points can prove to be a valuable tool in assessing a person’s current performance capabilities. In addition it can also help with the construction of an effective training program. With the right kind of training i.e.
appropriate volume, intensity and frequency an individual should see a shift in their LT and LTP, whereby the exercise intensity is higher at these two points. This would then be reflected in improved endurance performance as the limiting effects of lactate accumulation don’t occur at the intensity or pace that was observed prior to training.
The prescription of training zones to achieve this type of adaptation is the heart rate ranges that represent an individual’s original LT and LTP.
Using these heart rate zones, a specific training program can be created to make sure that an appropriate amount of time is spent training at intensities above, below or equivalent to LT and LTP.
The main goal is to raise the intensity at which LT and LTP occur and this would in turn be reflected in an ability to work at higher intensities for longer periods of time i.e. the clearance of lactate matches production at a higher intensity and muscle fatigue due to acidosis is delayed.
Other benefits of using these specific heart rate zones include making training more specific to a particular event as some events will require more work in certain zones than others. It is also possible to protect glycogen stores and therefore enable a higher training volume whilst avoiding over doing it.
Pace judgement can improve as the ability to hold training intensities gets better and doing the right amount of work by following a targeted program can give an athlete confidence and reduce anxiety. Figure 1. Shows what a blood lactate profile may look before and after a period of appropriate training.
Creating a Blood Lactate Curve
Thanks to the development of blood lactate testing equipment, ascertaining this type of information is relatively easy and can be done outside of a laboratory with a high degree of accuracy.
Blood samples can be taken from the ear lobe at various stages during a short sub-maximal incremental test procedure (normally on a treadmill, bike or rowing machine).
Instantaneous blood lactate readings can be produced during the test, graphed against intensity and correlated with heart rate, all within a relatively short time frame.
This is not something that is reserved only for the elite population. In fact recreational runners, cyclists and rowers stand to gain more from this type of information as they potentially have more room for improvement.
It is for this reason that Matt Roberts Personal Training has added this type of testing to its battery of training focused services.
All recreational endurance enthusiasts stand to gain valuable and usable insights into their own physiology with this type of testing and when used in conjunction with a well-structured training program performance is guaranteed to improve.
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What is lactic acid? (And where does it come from?)
Lactic acid, or lactate, is a chemical byproduct of anaerobic respiration — the process by which cells produce energy without oxygen around. Bacteria produce it in yogurt and our guts. Lactic acid is also in our blood, where it's deposited by muscle and red blood cells.
It was long thought that lactic acid was the cause of muscle soreness during and after an intense period of exercise, but recent research suggests that's not true, said Michael Gleeson, an exercise biochemist at Loughborough University in the U.K., and author of “Eat, Move, Sleep, Repeat” (Meyer & Meyer Sport, 2020).
“Lactate has always been thought of as the bad boy of exercise,” Gleeson told Live Science.
Contrary to that reputation, lactic acid is a constant, harmless presence in our bodies. While it does increase in concentration when we exercise hard, it returns to normal levels as soon as we're able to rest — and even gets recycled back into energy our body can use later on, Gleeson said.
How muscles produce lactic acid
Throughout most of the day, our body burns energy aerobically — that is, in the presence of oxygen. Part of that energy comes from sugar, which our muscle cells break down in a series of chemical reactions called glycolysis.
(We also get energy from fat, but that involves a whole other chemical process). The end product of glycolysis is pyruvate, a chemical that the body uses to produce even more energy. But energy can be harvested from pyruvate only in the presence of oxygen.
That changes during hard exercise.
Related: Muscle spasms and cramps: Causes and treatments
When you break into an all-out sprint your muscles start working overtime. The harder you work, the more energy your muscles need to sustain your pace. Luckily, our muscles have built-in turbo-boosters, called fast-twitch muscle.
Un slow-twitch muscle, which we use for most of the day, fast-twitch muscle is super-effective at producing lots of energy quickly and does so anaerobically, Gleeson said. Fast-twitch muscle also uses glycolysis to produce energy, but it skips harvesting energy from pyruvate, a process that takes oxygen.
Instead, pyruvate gets converted into a waste product, lactic acid, and released into the bloodstream.
It's a common misconception that muscle cells produce lactic acid when they can't get enough oxygen, Gleeson said. “That's not the case. Your muscles are getting plenty of oxygen,” he said. But in times of intense energy needs, muscles switch to anaerobic respiration simply because it's a much quicker way to produce energy.
Other sources of lactic acid
Muscle cells aren't the only sources of lactic acid. Red blood cells also produce lactic acid as they roam the body, according to the online text Anatomy and Physiology published by Oregon State University. Red blood cells don't have mitochondria — the part of the cell responsible for aerobic respiration — so they only respire anaerobically.
Many species of bacteria also respire anaerobically and produce lactic acid as a waste product. In fact, these species make up between 0.01-1.8% of the human gut, according to a review published in the Journal of Applied Microbiology. The more sugar these little guys eat, the more lactic acid they produce.
Slightly more insidious are the lactic acid bacteria that live in our mouths. Because of the acidifying effect they have on saliva, these bacteria are bad news for tooth enamel, according to a study published in Microbiology.
Finally, lactic acid is commonly found in fermented dairy products, buttermilk, yogurt and kefir. Bacteria in these foods use anaerobic respiration to break lactose — milk sugar — into lactic acid.
That doesn't mean that lactic acid itself is a dairy product, however — it's 100% vegan.
It happens to get its name from dairy simply because Carl Wilhelm, the first scientist to isolate lactic acid, did so from some spoiled milk, according to a study published in the American Journal of Physiology.
Lactic acid is found in fermented dairy products, yogurt, but lactic acid itself isn't dairy — it's 100% vegan. (Image credit: Shutterstock)
Your body on lactic acid
It's common to feel a burning in your legs after you squat with heavy weights, or complete a hard workout. But contrary to popular belief, it's not lactic acid that causes the soreness, Gleeson said.
Lactic acid is processed by the liver and the heart. The liver converts it back into sugar; the heart converts it into pyruvate.
During exercise, concentrations of lactic acid in the body do spike because the heart and liver can't deal with the waste product as quickly as it's produced.
But as soon as we're done exercising, lactic acid concentrations go back to normal, Gleeson said.
Related: Feel the pain? Don't blame lactic acid.
Muscle soreness after exercise most ly has more to do with tissue damage and inflammation, Gleeson said. Hard exercise physically breaks down your muscles, and it can take days for them to recover.
Lactic acid can build up to life-threatening levels in the body, according to a review published in the Mayo Clinic Proceedings. But this condition, called acute lactic acidosis, happens because of acute illness or injury, not exercise. When tissues are deprived of blood due to a heart attack or sepsis, for example, they tend to go into anaerobic respiration, producing lactic acid.
“They get starved of oxygen,” Gleeson said.
But Gleeson said he's never heard of a case of life-threatening lactic acidosis because of exercise. “That would be most unusual.”
Lactate is a bi-product constantly produced in the body during normal metabolism and exercise. It does not increase in concentration until the rate of lactate production exceeds the rate of lactate removal which is governed by a number of factors.
The concentration of blood lactate is usually 1-2 mmol/L at rest, but can rise to greater than 20 mmol/L during intense exertion. Blood lactate levels essentially serve as an indirect marker for biochemical events such as fatigue within exercising muscle.
Lactate levels are assessed for several different reasons such as determining sustainable threshold, peak, tolerance and clearance values. The reason to assess is relative to the desired performance outcome and the lactate levels are often related to speed, power or heart rate.
Sustainable threshold values are the most common assessment outcome and are used by endurance athletes primarily. To determine sustainable lactate levels, subjects perform exercise at incremental loads, for 12 to 15 minutes, while having blood drawn in droplets either from a finger or earlobe.
A stationary bicycle, a personalized bike and Computrainer or a treadmill are typically used. The test starts with an easy-moderate work load which is maintained for a 3-5 minutes. The load is increased gradually every 3-5 minutes until reaching 1 testing stage above when lactate levels reach 4 mmol/L blood.
This is done by increasing the cycling resistance or the speed and/or grade of the treadmill. The lactate levels, heart rate, speed and/or watts are measured at the lactate threshold and maximal load.
The most significant value obtained from this assessment is the Onset of Blood Lactate Accumulation (OBLA) value. OBLA is the point at which lactate begins to accumulate in the blood at an accelerated rate.
This is the point at which the body can sustain a particular effort for 20-60 minutes on average and can be a good guide to one’s performance abilities.
At this point, HR, speed and/or watts are also calculated and it is from this data that training parameters can be developed.
To determine peak, tolerated or clearance lactate levels involves other maximal effort tests and will not be reviewed in this document.
Lactate values cannot be used in every-day training but follow-up lactate values can be used as a measure of progress.
However, since heart rate, speed and/or power is typically measured during a lactate test, these training parameters can then applied to everyday training.
Other information such as lactate endurance levels (lactate values at a given heart rate or power output) can also be tested and compared to subsequent tests.
One of the better ways to incorporate this information into training is to use the OBLA data to establish field time trail parameters. Once those are established the time trails can be re-assessed periodically to determine improvements in the field with lab reassessments used to establish new training parameters.
After training you can perform at a higher rate of work without raising your blood lactate levels above initially tested levels.
In other words, blood lactate concentrations at various training intensities are lower and your speed or power at OBLA is faster or greater respectively.
This is in part due to the fact that, training results in a decrease in lactate production and an increase of lactate re-uptake within the body.
How often an OBLA value at a certain power or speed will change significantly, will depend in part on an individual's training history and habits – for example, someone who is just beginning in and/or returning to cycling or running for instance, may see large and rapid changes in their threshold power or speed, whereas an experienced rider or runner who has been training for many years and/or an athlete who maintains a high level of conditioning year round will probably experience much less variation.
There is limited research regarding health status and lactate. McArdle’s disease is a condition involving lactate production and the individuals who suffer from this condition cannot produce lactate during exercise.
In general, a high lactate level also represents a high H+ concentration, which can lead to metabolic acidosis, a serious condition and is to be avoided as all costs.
Metabolic acidosis is typically is seen in conditions such as in the kidney and chronic renal failure.
Lactate: valuable for physical performance and maintenance of brain function during exercise
Lactate accumulation has long been associated with impaired sports performance, with many supporting the lactate acidosis hypothesis. However, due to advances in experimental design and research, numerous beneficial roles of lactate have been established that may impact upon sports performance.
Recent studies highlight lactate as a biomarker of fatigue rather than as a direct cause. The lactate-shuttle mechanism facilitates the utilization of lactate as an energy substrate in both type I and type II skeletal muscle fibres, promoting energy sufficiency during exercise.
Recent literature also supports a role for lactate in enhancing human oxidative capacity by up-regulating skeletal muscle mitochondrial biogenesis. In addition, lactate-neuron and lactate-astrocyte shuttles enable lactate to supply energy to support cognitive function, during periods of low blood glucose such as prolonged aerobic exercise.
This review aims to clarify the role of lactate in modulating aerobic performance and critically investigates the mechanisms responsible.
The traditional stance that blood lactate accumulation, during exercise, negatively impacts upon athletic performance arouses from research undertaken in the 1920s by British physiologist A.V. Hill, whose study hypothesized that a decrease in pH depresses cell excitability and consequent muscular contractile force (Hill and Lupton, 1923; Bassett, 2002).
However, with modern technological advances and a greater understanding of the biochemical kinetics of lactate, evidence now strongly indicates that lactate is a valuable energy substrate for various physiological systems, such as the brain, heart and skeletal muscle (Cairns, 2006).
Lactate generation has been identified as advantageous within these systems not only during exercise, but also at rest.
The lactate-induced acidosis theory posits that under hypoxic conditions, such as anaerobic exercise, there is increased dissociation of lactic acid into lactate ions and hydrogen (H+) entering skeletal myocytes (Robergs, 2004).
This process induces acidosis, disrupting the cross-bridge cycle and impairing the contractile capability of such cells (Debold, 2011). Gorostiaga et al.
(2012) demonstrated that once the critical point of lactate, 10–15 mmol per kg−1 wet muscle, had been exceeded a significant decrease in the number of repetitive leg-press exercises was observed, indicative of lactate's involvement in muscular fatigue. In addition, Bonitch-Gongora et al.
(2012) reported an inverse relationship between blood lactate concentration and isometric contractile force during judo bouts. Collectively, these findings suggest that lactate accumulation may contribute to impaired physical performance via disruption to the acid–base balance within skeletal muscle during exercise.
Despite the longstanding hypothesis that lactate-induced acidosis promotes fatigue, lactate can exert a positive effect on aerobic performance.
Its accumulation has been attributed to counteracting the negative effects of noxious metabolites including inorganic phosphate (Pi) and potassium (K+), as well as facilitating removal of muscular proton and also acting synergistically with catecholamines to reduce fatigue (McKenna, Bangsbo and Renaud, 2008).
Greater emphasis has now been placed upon these metabolites as the primary physiological cause of fatigue rather than lactate.
Lactate not only regenerates nicotinamide adenine dinucleotide (NAD+), an essential component for glycolysis and aerobic respiration but its production uses two electrons, promoting a positive pH change as well as providing a chemical gradient for proton removal from anaerobically respiring skeletal muscle (Robergs, 2004). Miller et al. (2002), support this claim, by demonstrating that lactate oxidation increases during moderate-intensity exercise and that this prolongs blood glucose homeostasis.
Lactate is an important component in the multifactorial biochemical response which acts to counteract the muscular fatigue process.
It is capable of counteracting the electrochemical imbalance induced by K+ accumulation during exercise and as a result, lactate indirectly enhances force production, promoting optimal physical performance (Nielsen, de Paoli and Overgaard, 2001; de Paoli et al., 2007). Lindinger et al.
(2006) support this argument and accept lactate as a biomarker of fatigue because it accumulates proportionally in relation to an increase in plasma metabolites, during high-intensity exercise, yet may not cause muscular fatigue.
Hansen, Clausen and Nielsen (2005) identified that lactate is most effective in preserving type II (fast-twitch) muscle fibre function and can exert a greater effect on this subtype due to their low oxidative capacity.
It is plausible to speculate that, due to preferential activity within type II fibres, lactate may expose type I (slow-twitch) muscle fibres to cellular acidosis. However, during exercise, increased circulating plasma-free catecholamines exert protective effects upon slow-twitch muscle fibres via muscular β-2 adrenoceptors.
The accumulating K+ is buffered by β-2 agonist action which consequently up-regulates sodium (Na+)/K+ pump activity within the musculature, facilitating the restoration of an effective propagation pathway and optimal cell excitability, opposing the fatigue process (Hansen, Clausen and Nielsen, 2005). Thus, lactate acts synergistically with catecholamines to ensure that both fast-twitch and slow-twitch muscle fibres are protected from fatigue.
Pi is released via the breakdown of phosphocreatine (PCr) during muscular contraction and an increased Pi concentration is recognized as a factor contributing to muscular fatigue.
It has been suggested that highly concentrated Pi within skeletal muscle may exacerbate sarcoplasmic calcium (Ca2+) efflux, resulting in a series of high frequency impulses and a number of maximal contractions which induce muscular fatigue (see Fig. 1; (Westerblad, Allen and Lannergren, 2001).
Furthermore, Pi may interact with sarcoplasmic Ca2+, impairing Ca2+ efflux and consequent excitation–contraction coupling, see Fig. 1(Fryer et al. 1995; Westerblad and Allen, 1996; Soares et al., 2013). Yet this mechanism only appears relevant for exercise
Why Does Lactic Acid Build Up in Muscles? And Why Does It Cause Soreness?
As our bodies perform strenuous exercise, we begin to breathe faster as we attempt to shuttle more oxygen to our working muscles. The body prefers to generate most of its energy using aerobic methods, meaning with oxygen.
Some circumstances, however—such as evading the historical saber tooth tiger or lifting heavy weights—require energy production faster than our bodies can adequately deliver oxygen. In those cases, the working muscles generate energy anaerobically.
This energy comes from glucose through a process called glycolysis, in which glucose is broken down or metabolized into a substance called pyruvate through a series of steps. When the body has plenty of oxygen, pyruvate is shuttled to an aerobic pathway to be further broken down for more energy.
But when oxygen is limited, the body temporarily converts pyruvate into a substance called lactate, which allows glucose breakdown—and thus energy production—to continue. The working muscle cells can continue this type of anaerobic energy production at high rates for one to three minutes, during which time lactate can accumulate to high levels.
A side effect of high lactate levels is an increase in the acidity of the muscle cells, along with disruptions of other metabolites. The same metabolic pathways that permit the breakdown of glucose to energy perform poorly in this acidic environment.
On the surface, it seems counterproductive that a working muscle would produce something that would slow its capacity for more work. In reality, this is a natural defense mechanism for the body; it prevents permanent damage during extreme exertion by slowing the key systems needed to maintain muscle contraction.
Once the body slows down, oxygen becomes available and lactate reverts back to pyruvate, allowing continued aerobic metabolism and energy for the body’s recovery from the strenuous event.
Contrary to popular opinion, lactate or, as it is often called, lactic acid buildup is not responsible for the muscle soreness felt in the days following strenuous exercise.
Rather, the production of lactate and other metabolites during extreme exertion results in the burning sensation often felt in active muscles, though which exact metabolites are involved remains unclear.
This often painful sensation also gets us to stop overworking the body, thus forcing a recovery period in which the body clears the lactate and other metabolites.
Researchers who have examined lactate levels right after exercise found little correlation with the level of muscle soreness felt a few days later.
This delayed-onset muscle soreness, or DOMS as it is called by exercise physiologists, is characterized by sometimes severe muscle tenderness as well as loss of strength and range of motion, usually reaching a peak 24 to 72 hours after the extreme exercise event.
Though the precise cause of DOMS is still unknown, most research points to actual muscle cell damage and an elevated release of various metabolites into the tissue surrounding the muscle cells.
These responses to extreme exercise result in an inflammatory-repair response, leading to swelling and soreness that peaks a day or two after the event and resolves a few days later, depending on the severity of the damage. In fact, the type of muscle contraction appears to be a key factor in the development of DOMS.
When a muscle lengthens against a load—imagine your flexed arms attempting to catch a thousand pound weight—the muscle contraction is said to be eccentric. In other words, the muscle is actively contracting, attempting to shorten its length, but it is failing.
These eccentric contractions have been shown to result in more muscle cell damage than is seen with typical concentric contractions, in which a muscle successfully shortens during contraction against a load. Thus, exercises that involve many eccentric contractions, such as downhill running, will result in the most severe DOMS, even without any noticeable burning sensations in the muscles during the event.
Given that delayed-onset muscle soreness in response to extreme exercise is so common, exercise physiologists are actively researching the potential role for anti-inflammatory drugs and other supplements in the prevention and treatment of such muscle soreness, but no conclusive recommendations are currently available. Although anti-inflammatory drugs do appear to reduce the muscle soreness—a good thing—they may slow the ability of the muscle to repair the damage, which may have negative consequences for muscle function in the weeks following the strenuous event.
How to get rid of lactic acid
Lactic acid is often the result of normal metabolism. Oxygen in the blood is necessary to convert glucose into energy. However, when there is insufficient oxygen, the body breaks down glucose without oxygen, resulting in lactic acid.
Lactic acid, or lactate, builds up within many tissues, including muscles, and then enters the bloodstream. The body can use small quantities of lactate as energy.
People often experience high levels of lactic acid during or following strenuous exercise. This is called exercise-induced or exercise-related hyperlactatemia.
A buildup of lactic acid can make muscles feel sore or tired. Typically, the liver will break down excess lactate in the blood.
Some health conditions can increase lactic acid production or reduce the body’s ability to clear lactate from the blood. This can result in a more severe buildup of lactate, which doctors refer to as lactic acidosis.
This article provides tips for preventing and reducing exercise-induced hyperlactatemia. We also outline other causes of lactate buildup and lactic acidosis.
Share on PinterestDrinking plenty of water can help the body to break down excess lactic acid.
A buildup of lactic acid in the muscles during or following exercise is not harmful. In fact, some experts believe it can be beneficial. In small amounts, lactic acid can:
- help the body absorb energy
- help the body burn calories
- increase endurance levels
However, many people find that the muscle pain and cramps from lactic acid buildup negatively affects their workouts.
There are several ways to prevent exercise-induced hyperlactatemia, as follows:
Drinking plenty of water
Keeping the body hydrated during exercise gives it the best chance of breaking down any excess lactic acid. People can ensure they stay hydrated by drinking plenty of water.
Taking deep breaths
The body starts to produce lactic acid when it is low in the oxygen necessary to convert glucose into energy. Breathing deeply will help deliver oxygen to the muscles, thereby slowing the production of lactic acid.
Decreasing exercise intensity
When a person feels the effects of lactic acid buildup, they can slow down and reduce the intensity of their workout. This will allow blood oxygen levels to recover.
Stretching after a workout
Lightly stretching the muscles after a workout can help to alleviate any burning sensations or cramps that lactic acid buildup may cause.
In most cases, lactic acid buildup is a harmless response to strenuous exercise and will go away on its own. Once the body has used the resulting lactate for energy, the liver breaks down any excess in the blood.
For a long time, experts thought that lactic acid was responsible for delayed onset muscle soreness (DOMS) following exercise. However, experts no longer believe this is the case. Instead, they now say that DOMS pain and stiffness is the result of microscopic damage to muscle fibers.
DOMS is more ly to occur in the following situations:
- starting a new exercise program
- changing exercise routines
- increasing the duration or intensity of a regular workout
Share on PinterestA person with lactic acidosis may experience pain in the belly, nausea, and sweet smelling breath.
Certain health conditions can lower blood oxygen levels, resulting in increased lactate production. These conditions include:
- heart failure
- severe infection
- poorly controlled diabetes
Also, liver damage and liver disease can affect the liver’s ability to remove lactate from the blood. This can result in high blood lactate levels, which doctors call hyperlactatemia.
In some cases, hyperlactatemia can progress to lactic acidosis. Without treatment, lactic acidosis can alter the PH balance of a person’s blood. This alteration can result in severe health complications.
The symptoms doctors associate with lactic acidosis include:
Lactic acidosis is also a rare side effect of some HIV medications.
Anyone who thinks they have lactic acidosis or nonexercise-induced hyperlactatemia should speak to a doctor straightaway.
A doctor will usually carry out a blood test to check levels of lactate in the blood. In some cases, they may ask the person not to eat, drink, or exercise for several hours before the test.
If the tests detect lactic acidosis, the doctor will work to diagnose and treat its underlying cause. Treatment will allow the body to dispose of the lactic acid in the usual way.
The body makes lactic acid when it is low in the oxygen it needs to convert glucose into energy. Lactic acid buildup can result in muscle pain, cramps, and muscular fatigue.
These symptoms are typical during strenuous exercise and are not usually anything to worry about as the liver breaks down any excess lactate.
Staying hydrated and breathing deeply during exercise can help to prevent exercise-induced hyperlactatemia.
Specific health conditions can increase a person’s risk of developing hyperlactatemia and lactic acidosis. Without treatment, lactic acidosis can result in serious health complications.
Calcium lactate Uses, Side Effects & Warnings – Drugs.com
Generic Name: calcium lactate (KAL see um LAK tate)
Medically reviewed by Drugs.com on Dec 5, 2019 – Written by Cerner Multum
What is calcium lactate?
Calcium is a mineral that is found naturally in foods. Calcium is necessary for many normal functions of your body, especially bone formation and maintenance. Calcium can also bind to other minerals (such as phosphate) and aid in their removal from the body.
Calcium lactate is used to prevent and to treat calcium deficiencies.
Calcium lactate may also be used for other purposes not listed in this medication guide.
Do not take calcium lactate or antacids that contain calcium without first asking your doctor if you also take other medicines. Calcium can make it harder for your body to absorb certain medicines.
Calcium lactate works best if you take it with food.
Before taking this medication, tell your doctor if you have:
a history of kidney stones; or
a parathyroid gland disorder.
If you have any of these conditions, you may not be able to take calcium lactate, or you may need a dose adjustment or special tests during treatment.
Talk to your doctor before taking calcium lactate if you are pregnant.
Talk to your doctor before taking calcium lactate if you are breast-feeding a baby.
Use exactly as directed on the label, or as prescribed by your doctor. Do not use in larger or smaller amounts or for longer than recommended.
Calcium lactate works best if you take it with food.
Take calcium lactate with a full glass of water.
Store at room temperature away from moisture and heat.
Take the missed dose as soon as you remember. Skip the missed dose if it is almost time for your next scheduled dose. Do not take extra medicine to make up the missed dose.
Seek emergency medical attention or call the Poison Help line at 1-800-222-1222.
Overdose symptoms may include nausea, vomiting, decreased appetite, constipation, confusion, delirium, stupor, and coma.
Follow your healthcare provider's instructions about any restrictions on food, beverages, or activity.
Get emergency medical help if you have any of these signs of an allergic reaction: hives; difficulty breathing; swelling of your face, lips, tongue, or throat.
Less serious side effects may include:
nausea or vomiting;
dry mouth or increased thirst; or
This is not a complete list of side effects and others may occur. Call your doctor for medical advice about side effects. You may report side effects to FDA at 1-800-FDA-1088.
Usual Adult Dose for Hypocalcemia:
325 to 650 mg orally 2 to 3 times a day before meals. Treatment may also consist of vitamin D orally.
Usual Adult Dose for Osteomalacia:
325 to 650 mg orally 2 to 3 times a day before meals. Treatment may also consist of vitamin D orally.
Usual Adult Dose for Hypoparathyroidism:
325 mg orally 3 times a day before meals. Treatment may also consist of vitamin D orally.
Usual Adult Dose for Pseudohypoparathyroidism:
325 mg orally once a day before the breakfast meal. Treatment may also consist of vitamin D orally.
Usual Adult Dose for Osteoporosis:
325 to 650 mg orally 3 times a day before meals. Osteoporosis can be affected by increased serum parathyroid hormone, excessive alcohol intake, tobacco use, certain drugs (corticosteroids, anticonvulsants, heparin, thyroid hormone), dietary vitamin D, and weight bearing exercise.
Usual Pediatric Dose for Hypocalcemia:
Hypocalcemia (dose depends on clinical condition and serum calcium level):
Dose expressed in mg of elemental calcium: 50 to 150 mg/kg/day in 4 to 6 divided doses; not to exceed 1 g/day Dose expressed in mg of calcium lactate: 400 to 500 mg/kg/day divided every 4 to 6 hours Oral:Hypocalcemia (dose depends on clinical condition and serum calcium level): Dose expressed in mg of elemental calcium: Children: 45 to 65 mg/kg/day in 4 divided doses Dose expressed in mg of calcium lactate: Infants: 400 to 500 mg/kg/day divided every 4 to 6 hours
Children: 500 mg/kg/day divided every 6 to 8 hours; maximum daily dose: 9 g
What other drugs will affect calcium lactate?
Calcium lactate can make it harder for your body to absorb other medications you take by mouth. Tell your doctor if you are taking:
digoxin (Lanoxin, Lanoxicaps);
antacids or other calcium supplements;
calcitriol (Rocaltrol) or vitamin D supplements; or
doxycycline (Adoxa, Doryx, Oracea, Vibramycin), minocycline (Dynacin, Minocin, Solodyn, Vectrin), or tetracycline (Brodspec, Panmycin, Sumycin, Tetracap).
This list is not complete and other drugs may interact with calcium lactate. Tell your doctor about all medications you use. This includes prescription, over-the-counter, vitamin, and herbal products. Do not start a new medication without telling your doctor.
Remember, keep this and all other medicines the reach of children, never share your medicines with others, and use this medication only for the indication prescribed.
Always consult your healthcare provider to ensure the information displayed on this page applies to your personal circumstances.
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