Setting the Record Straight on Lactate
Lactate is a bad guy in the running world. It’s blamed for lots of bad things including fatigue, muscle soreness, and preventing you from running faster. There is even a well known and widely followed training method – tempo runs – that was originated specifically to help you overcome all the bad things lactate was believed to be doing in your body, therefore helping you run faster.
The problem is that none of the bad things you’ve heard about lactate are true. None of them! In fact, exercise physiologists have known for 20 years – yes, 20 years…really – that all the bad things previously believed about lactate are not true. Indeed, quite a bit of the updated information about lactate has been known since the mid-1980s, meaning that some of the updated information on lactate has been known for quite a bit more than 20 years. It’s not even a case of controversy amongst exercise physiologists about the negative effects of lactate – it is widely accepted in the exercise physiology world that lactate is NOT responsible for any of the bad things you’ve heard about it.
If the information about lactate is known to be false, and the true nature of lactate has been known and accepted for many years by the exercise physiology world, then why do runners continue to believe all those horrible things about lactate? Why do the negative beliefs about lactate persist in the running community in the face of incontrovertible information to the contrary? I won’t speculate why the long updated information about lactate hasn’t been widely disseminated within the running community. Instead, the purpose of this article is to bring you updated information about lactate and its role in your body. My goal is to set the record straight on lactate so that at the end of this article any negative beliefs you’ve held about lactate are dispelled, replaced with accurate information that gives appropriate credit for the important energy role lactate plays in performance. Considering the depth and width of the negative beliefs about lactate that permeate the running community, this is a big task, so let’s get started.
Note – runners generally use the terms “lactate” and “lactic acid” interchangeably, even though they are not the exact same chemical compound. Though there are chemical differences between lactate and lactic acid these differences are not significant to our discussion. For our purposes we will use the term lactate and lactic acid interchangeably.
In order to properly tackle the various negative beliefs about lactate we begin with a review of the origin of these beliefs about lactate. Why has lactate been considered so important in terms of running performance and just how did lactate become such a villain in the first place? To answer this question requires us to first review the beliefs about the limits of exercise – i.e. why can’t you run faster?
You have probably been exposed to the terms “aerobic” and “anaerobic”. Well, these two terms are key to understanding the origin of the villainous beliefs about lactate. In basic terms, aerobic simply means with oxygen and anaerobic means in the absence of oxygen. These terms are talking about the two ways your body has of producing energy. Your body can produce energy with oxygen, aerobically, or without oxygen, anaerobically.
These methods of producing energy – with and without oxygen – are central to the theory of endurance performance. In the 1920s British physiologist and Nobel Prize winner A.V. Hill first proposed the exercise theory that has since been termed the cardiovascular/anaerobic model and has been a foundation belief of the running community for more than 90 years. In essence, Hill’s theory was that the reason you can’t run faster is because you can’t get enough oxygen to your working muscles. He suggested that as the intensity of exercise increased the runner reached a point where he was unable to take in and use more oxygen. You have likely heard this belief expressed as the term VO2max. “V” means the volume of flow of oxygen to the body, O2 (correctly written O2) is the chemical symbol for oxygen, and max is the abbreviation for maximum. So, the term VO2max simply means the maximum volume of oxygen being taken in and used by the body. At VO2max, the runner is unable to absorb and use more oxygen. However, and this is key, Hills’ belief was that at VO2max the runner was not running as fast as possible. The runner could run a little bit faster even though he could not take in and use more oxygen.
What happens when a runner can’t get enough oxygen to meet the aerobic energy needs of his muscles? When this happens, the body must meet its energy needs via anaerobic methods. As the runner gets closer and closer to VO2max, more and more of his energy is met via anaerobic metabolism. Now we come to the genesis of the negative beliefs about lactate. The cardiovascular/anaerobic model preached that lactate was produced as a result of anaerobic energy production. In accordance with this model, as the intensity of exercise increased oxygen becomes increasingly in short supply, forcing the body to rely more and more on anaerobic metabolism, resulting in an increasing higher level of lactate within the body. This model further suggested that lactate interfered with the muscles’ ability to contract, thus causing fatigue.
Here is a basic summary of the cardiovascular/anaerobic model, which explains why lactate has been considered so important by the running community for so many years. The cardiovascular/anaerobic model believes:
- As exercise intensity increases, the body’s energy needs cannot be met entirely through aerobic metabolism – i.e. there is insufficient oxygen available to the working muscles.
- Due to the increasingly insufficient oxygen supply, the energy needs of the body are instead increasingly met via anaerobic metabolism – i.e. the muscles have become anaerobic.
- Anaerobic metabolism produces lactate as a by-product.
- Increasing levels of lactate interfere with muscle contractions, causing fatigue within the muscles.
Now you know the basics of why lactate has been considered important to the running community – it was believed to cause fatigue. This brings us to the concept of lactate threshold.
When scientists first starting measuring changes in blood lactate levels with increasing exercise intensity they noticed something interesting. Lactate seemed to rise very slowly at first, then all of sudden it began to rise very quickly. The traditional explanation for this sudden rise in lactate levels was that the muscles had become “anaerobic” – meaning that anaerobic energy production had become the primary source of energy within the muscle. The point where lactate levels began increasing rapidly is usually called the lactate threshold, but has also been called the anaerobic threshold and the ventilation threshold.
The Real Facts About Lactate
Now that you understand why lactate has been considered important by the running community and the origins of the negative beliefs about lactate we turn our attention to the updated information about lactate.
Muscles don’t become anaerobic during exercise
The first thing we need to address is the foundation belief that at high exercise intensity there is insufficient oxygen to meet the energy needs of the body. Despite the widespread belief by many that there is insufficient oxygen to working muscles at high exercise intensity, this has never been proven. In fact, it has always been assumed there is insufficient oxygen, but has never been proven despite years of efforts by physiologists.
McArdle, Katch, and Katch, writing in their well respected exercise physiology textbook have this to say about limited oxygen supply during exercise. “The usual explanation for a lactate increase is based on an assumed relative tissue hypoxia during heavy exercise.”(1) They clearly state that the belief that there is limited oxygen to working muscle (relative tissue hypoxia) is an assumption. It has never been proven.
Despite the fact that this belief has never been proven, it is important to know that it has been treated as a fact for many years by many, and perhaps most, in the scientific community and, consequently, by the lay public.
However, more recent efforts by experts using new techniques to determine if muscles become anaerobic during heavy exercise have shown the opposite to be the case: “these data demonstrate that, during incremental exercise, skeletal muscle cells do not become anaerobic…since intracellular PO2 (the oxygen pressure in the muscles) is well preserved at a constant level, even at maximal exercise.”(2)
So, you now know that muscles do not become anaerobic during exercise.
Why lactate levels increase with exercise intensity
If muscles don’t become anaerobic, then why do lactate levels increase during exercise of increasing intensity? After all, isn’t lactate produced through anaerobic energy production? The short answer to these questions is that lactate is produced during carbohydrate metabolism, irrespective of the availability of oxygen. Here is what Prof. Tim Noakes has to say on this topic in the most recent edition of Lore of Running:
“As the exercise intensity increases, so does the rate of carbohydrate use. When high exercise intensities (greater than 85% to 95% VO2max) are achieved, virtually all the energy comes from carbohydrate oxidation (G.A. Brooks and Mercier 1994; Brooks 1998). This means that the rate of energy flow through the glycolytic pathways increases steeply with increasing exercise intensity. The result is that the rate of lactate production increases inside the muscles.”(3)
In essence, then, lactate is a by-product of carbohydrate metabolism. It is not a matter of the body becoming anaerobic. Instead, as the intensity of exercise increases the body relies increasingly more on carbohydrates to provide the needed energy. More carbohydrates being burned results in a greater volume of lactate being produced and an increase in blood lactate levels. The muscles have not become “anaerobic” – lactate is increasing because the body is burning more and more carbohydrates.
There is NO lactate threshold
Okay, now we know that the muscles don’t go anaerobic during heavy exercise and lactate production is due to carbohydrate being burned to produce energy. This brings us to the topic of “lactate threshold”. Recall that the theory of lactate threshold was that at some exercise intensity blood lactate levels increase dramatically, i.e. crosses a threshold, due to anaerobic metabolism. We already know that lactate is being produced in increasing high amounts for reasons other than the muscles becoming “anaerobic”, but is lactate increasing after crossing some “threshold”? Again, the answer is no.
Lactate increases exponentially with increases in exercise intensity and does NOT exhibit a threshold. This being the case, why did exercise physiologists believe there was a lactate threshold? Going back to Prof. Noakes again:
“This mistaken conclusion resulted from at least 2 errors. First, too few blood samples were measured. For example, if only 4 blood samples had been drawn at running speeds of 10, 14, 16, and 20 km per hour, then a fictitious anaerobic threshold would have been identified at 15.5 km per hour. But measuring blood lactate concentrations repeatedly – for example every km per hour – shows that blood lactate concentrations rise exponentially without any evidence of a threshold phenomenon.”
“It is clear that the blood lactate concentrations do not show a clearly defined, abrupt threshold response during exercise of progressively increasing intensity. Rather, blood lactate concentrations begin to rise as soon as progressive exercise commences. However, at low intensities, the rate of the increase is so low that it is barely noticeable. Only when the exercise becomes more intense does the rise become apparent, which perhaps explains the erroneous impression that blood lactate concentrations increase abruptly when the lactate threshold is reached.”
“For these reasons, the term anaerobic threshold, lactate threshold, and lactate turnpoint are no longer justifiable”(4)
So, you see, there is not a lactate threshold. Lactate increases exponentially with increases in exercise intensity and exhibits no evidence of a “threshold”.
Lactate doesn’t cause fatigue – it helps prevent fatigue
You might say at this point that whether lactate is produced by anaerobic metabolism or not, or increases in a “threshold” manner or not is immaterial if increasing amounts of lactate cause fatigue. After all, it doesn’t really matter how the level of lactate increases if lactate is the cause of fatigue. (Recall that it has long been believed by the running community that lactate causes fatigue.) It is this core belief that has caused runners to focus so intently on lactate threshold – lactate causes fatigue and the lactate threshold is the point where there is suddenly enough lactate in the body to cause fatigue to increase rapidly. There is no doubt that blood lactate levels increase with increasing exercise intensity. If lactate causes fatigue then it wouldn’t matter if muscles become anaerobic or how lactate increases in the body – these points do not negate the idea that lactate causes fatigue. Lactate does increase with increasing exercise intensity and if it causes fatigue, then the other points are ancillary. Therefore, the most important question to ask is, Does lactate cause fatigue? The answer is, Absolutely not!
“Lactate is a totally innocuous substance that, if infused into the bloodstream, has no noticeable effects.”(5)
That’s right – you could inject your muscles with lactate and you would experience NO additional fatigue because lactate does not cause fatigue.
Topping off the facts about lactate is this kicker – lactate not only does not cause fatigue as it has long been believed to, but there is reason to believe it actually helps prevent fatigue. How’s that for a complete turnaround of everything you ever believed about lactate?
Researchers examining muscle fatigue in rats caused by a reduced pH and loss of potassium found that the “subsequent addition of…lactic acid led, however, to an almost complete force recovery.” These researchers write:
“In contrast to the often suggested role for acidosis as a cause of muscle fatigue, it is shown that in muscles where force was depressed by high (potassium), acidification by lactic acid produced a pronounced recovery of force. Since intense exercise is associated with increased (potassium), this indicates that acidosis may protect against fatigue rather than being a cause of fatigue.”(6)
What they are saying in the above quote is that lactic acid in the muscles is likely to protect against fatigue, allowing the muscle to work longer and/or harder before fatigue sets in.
Hydrogen Ions & Muscle Acidity
Some physiologists, knowing that lactate does not cause fatigue, have suggested an alternate theory for muscle fatigue. They suggest that hydrogen ions (H+), which are produced during the conversion of lactic acid to lactate, are the true cause of muscle fatigue. This theory holds that the H+ changes the pH within the muscle, increasing muscle acidity, which interferes with the muscles’ ability to contract. As more and more lactate is produced, so too are more H+ produced, leading to an increasing acidic muscle and an increasing level of fatigue. This theory explains why increases in lactate correlate with increased fatigue. H+ is produced as a result of lactate metabolism, the H+ makes the muscle cell acidic, and the acidity interferes with muscle contraction (in effect, causes fatigue) – more lactate means more H+, producing greater acidity, resulting in more fatigue.
However, this theory has been challenged. Dr. Bruce Gladden, in his 2004 review of lactate metabolism writes,
“…lactic acid is more than 99% dissociated at physiological pH. This has led to the incorrect notion that the donation of a proton by each lactic acid molecule causes a decreased pH during conditions such as exercise.(7)
A research update by Stackhouse, et al addresses this topic:
“In addition, many textbooks report that muscle fatigue is mainly the result of a decrease in pH within the muscle cell due to a rise in hydrogen ion concentration ([H+]) resulting from anaerobic metabolism and the accumulation of lactic acid. Recent literature, however, contradicts this assertion.”(8)
These two quotes mean that lactate derived H+ does not play a major role in changing muscle pH levels. H+ does increase in the muscles, but it is not a primary player in creating muscle acidity.
Finally, a research paper by Westerblad et al says this:
“…the increase in H+ (i.e. reduced pH or acidosis) is the classic cause of skeletal muscle fatigue. However, the role of reduced pH as an important cause of fatigue is now being challenged, and several recent studies show that reduced pH may have little effect on contraction in mammalian muscle at physiological temperatures.”(9)
What Westerblad is saying here is that recent research indicates that increased muscle acidity is NOT a cause of fatigue. Though it is too soon to dismiss the idea that muscle acidity contributes to fatigue, the theory is certainly being challenged and recent evidence on this topic suggests the H+ are not the primary cause of muscle acidity.
Lactate is Actually A Potent Energy Source
Instead of being a source of fatigue, exercise physiologists now know that lactate is a potent fuel source for the body, and some have suggested it may be the most important fuel available to the muscle. Research shows that about 75-80% of lactate is used to produce energy through oxidation, with the remainder converted to glucose and glycogen. Working muscles oxidize the lactate for fuel. Blood lactate is absorbed by the liver, the heart, and inactive muscle. The liver converts the lactate to produce glucose and glycogen, the heart uses lactate as a preferred fuel, and inactive muscle stores lactate.
More recently leading lactate researcher George Brooks has pioneered the concept of a “lactate shuttle”. The importance of the lactate shuttle is that it is the mechanism that allows carbohydrates to be moved from one muscle group to another. Muscles do not have the ability to send their stored carbohydrates (glycogen) to other parts of the body, so, for example, a resting group of muscles can’t send their stored glycogen to working muscles that may be low on glycogen. Dr. Brooks has shown that the lactate shuttle is the way in which the body’s store of carbohydrates can be transferred to working muscles during and after exercise. For example, during a run workout glycogen stores in your inactive arm muscles can be converted to lactate and shuttled to your leg muscles, providing an additional and important source of energy for your working leg muscles.
In summary, it has long been held by the running community that lactate was the primary culprit in lots of metabolic “crimes”. These beliefs are now known to be false. Muscles do not become anaerobic during exercise, lactate does not cause fatigue, and there is NO lactate threshold. Instead lactate is produced as a result of carbohydrate metabolism and may actually delay fatigue. Lactate is now accepted as an important and potent source of fuel for working muscles. In his 2004 review of the current state of knowledge about lactate Prof. Bruce Gladden sums it up best. He writes:
“For much of the 20th Century, lactate was largely considered a dead-end waste product of glycolysis due to hypoxia, the primary cause of the O2 debt following exercise, a major cause of muscle fatigue, and a key factor in acidosis-induced tissue damage…
The bulk of the evidence suggests that lactate is an important intermediary in numerous metabolic processes, a particularly mobile fuel for aerobic metabolism, and perhaps a mediator of redox state among various compartments both within and between cells. Lactate can no longer be considered the usual suspect for metabolic ‘crimes’, but is instead a central player in cellular, regional, and whole body metabolism.”(6)
- McArdle, Katch, Katch, Exercise Physiology: energy, nutrition, and human performance, 4th edition, 1996, pg. 123
- Richardson R, Noyszewski E, Leigh J, Wagner P. Lactate efflux from exercising human skeletal muscle: role of intracellular PO2, J Appl Phsiol 1998, 85(2), 627-634
- Noakes, T Lore of Running, 4th edition, 2004, pg 160
- Noakes, T Lore of Running, 4th edition, 2004, pg 158-159
- Noakes, T Lore of Running, 4th edition, 2004, pg 163
- Nielsen O, Paoli F, Overgaard K. Protective Effects of lactic acid on force production in rat skeletal muscle J of Physiol 2001, 536.1, 161-166
- Gladden L. B., Lactate Metabolism: a new paradigm for the third millennium J Physiol 2004 558(1), 5-30
- Stackhouse SK, Reisman DS, Binder-Macleod SA., Challenging the role of pH in skeletal muscle, Phys Ther 2001, 81(12), 1897-903
- Westerblad H, Allen D, Jannergren J. Muscle Fatigue: Lactic Acid or Inorganic Phosphate the Major Cause? News Physiol Sci 2002, 17, 17-21