There is NO Lactate Threshold

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.

Lactate History

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:

  1. 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.
  2. 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.
  3. Anaerobic metabolism produces lactate as a by-product.
  4. 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.

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)


  1. McArdle, Katch, Katch, Exercise Physiology: energy, nutrition, and human performance, 4th edition, 1996, pg. 123
  2. 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
  3. Noakes, T Lore of Running, 4th edition, 2004, pg 160
  4. Noakes, T Lore of Running, 4th edition, 2004, pg 158-159
  5. Noakes, T Lore of Running, 4th edition, 2004, pg 163
  6. 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
  7. Gladden L. B., Lactate Metabolism: a new paradigm for the third millennium  J Physiol 2004 558(1), 5-30
  8. Stackhouse SK, Reisman DS, Binder-Macleod SA., Challenging the role of pH in skeletal muscle, Phys Ther 2001, 81(12), 1897-903
  9. Westerblad H, Allen D, Jannergren J. Muscle Fatigue: Lactic Acid or Inorganic Phosphate the Major Cause?  News Physiol Sci 2002, 17, 17-21


There is NO Lactate Threshold — 26 Comments

  1. Interesting article, thank you and like your site.
    One point to clarify, although I don’t think it changes the conclusions: by definition H+ is the cause of muscle acidity, as the definition of acidity is a measure of the concentration of H+ ions in aqueous solution.

    Whether these are generated from Lactic Acid or not or whether they cause or prevent fatigue are separate questions, as you say.

  2. Great article and thanks for educating me on the latest science.

    I would like to ask if the lactic acid / carbohydrate consumption relationship is linked to what all marathon runners have probably encountered as “the wall” or “bonking”.

    Would I be correct in thinking that if I run at a high lactate level, my body is consuming higher blood glycogen, until it eventually depletes and and I hit “the wall” and have to change to consuming fat stores?

    If this understanding is correct, would it be right to say that we have a ‘carbohydrate consumption threshold’ that is the real limit? and that training to lift the misconstrued ‘Lactate threshold’ will have benefit in delaying this effect?

    (Sorry for the long one, but I want to get my head around this)

    • Ben,

      Your body stores carbohydrates, as a substance called glycogen, inside your muscles. Glycogen is an energy source for working muscles. Whether you are running at high levels of lactate or not, working muscles use their stored glycogen to meet their energy needs. There is also glycogen stored inside your liver, which is where glycogen in the blood comes from. The term “hitting the wall” usually means that the glycogen inside working muscles has been depleted. With no glycogen for energy the muscles become dependent on fat to meet their energy needs. Converting fat into energy is a slower process than converting glycogen into energy and, typically, it becomes very difficult for a runner to maintain the same pace.

      The typical training method for increasing the “lactate threshold” doesn’t seem to be the best training to maximize glycogen storage. To help delay hitting the wall, athletes will often train and eat so that glycogen stores are maximized. Long distance running causes muscles to adapt by storing more glycogen. (Versus shorter, faster runs used to train the “lactate threshold”). Eating a high carb diet, especially in the days leading up to an event, is believed to cause glycogen stores to increase (this is called carbo-loading).

      Finally, at the end of a marathon, runners don’t typically exhibit high lactate levels, nor are they at their “lactate threshold”. Lactate levels rise once the race commences and then stabilize for the remainder of the race so the exhaustion one typically experiences near the end of long race, such as a marathon, doesn’t really have anything to do with high lactate levels.

      • Hi rgibbens,
        I think your response reiterates my (and probably conventional) understanding of how we run, train and eat for marathons, but I guess my question is more to do with the context of the article and this revised view of Lactic acid.

        Before reading the article, I had the following understanding:
        – Run marathon below “Lactate Threshold” by controlling pace and HR
        – Avoid muscles becoming hypoxic and having to payback ‘the oxygen debt’ at some point during race
        – Avoid muscle fatigue from excess lactic acid in muscles

        Now after reading article I wonder if I can:
        – Run marathon at a higher Lactate level, which from what I read above, only causes excess consumption of carbohydrate, does not make muscles hypoxic and all other effects seem to be benefits, but the higher lactate level would likely reduce to time to hit ‘the wall’
        – Fuel carbohydrates more intensively during race to counteract greater consumption
        – thereby run faster over long periods?

        I should note that I doubt that this is a good strategy for a marathon but it has got me wondering if I can increase consumption or train my body to digest higher rates of carbohydrates during running and thereby cope with a higher lactate rate.

        This would go against my current training strategies that you have mentioned such as increasing glycogen stores and improving fat consumption.


        • Ben,

          My advice is to ignore blood lactate levels as I believe the evidence supports the idea that they are not causative in performance (i.e. lactate levels don’t predict or control performance). My personal bias is that the #1 factor that ultimately determines performance is the contractile properties of your muscle fibers. The better you train the muscle fibers the better your performance will be. Certainly other factors, such as pre-race glycogen levels, your body’s ability to burn fat, your hydration strategy, and so on, influence performance but to a significantly lesser degree than muscle contractile properties.



  3. It’s interesting that you didn’t cite Coyle/Costill’s published article from which the tie-in between blood lactate levels and running performance primarily originates.

    It’s a free download, here:

    The relationship between blood lactate levels and performance is well documented but very few people with knowledge of running physiology consider it a cause/effect relationship. Whether lactate is considered ‘good’ or ‘bad’ is irrelevant, and this is mainly because it’s measured in the bloodstream outside of muscle tissue, not within. The measurement or view at blood level is after the fact, which is why the relationship between blood lactate levels and running performance are of interest. While lactate within muscle tissue may very well be utilized and potentially even necessary for performance, the rate at which lactate leaves muscles and enters the blood stream is indicative of a change in intracellular metabolism.

    There are very good reasons to train at levels that push blood lactate levels up and also good reasons to keep them down. But that’s training. Try to race a marathon and see how well you hold up maxing your blood lactate levels 2 miles in.

    Coyle’s research led to the term ‘lactate threshold’ not based on whether lactate is good or bad, but based on the testing protocol that identified it and it’s relationship to running performance. It doesn’t exist because lactate is ‘bad’, But also it isn’t non-existent because it’s ‘good’ which is what you are implying in your article.

    • This is good. We are arguing semantics here mostly. Most training methods have developed through trial and error. The science to rationalize the way we train often comes later.

  4. Are endurance athletes simply training the glycolic pathways to be better carb shuttles? More tolerant of acidosis? Better aware of HR effects? Individually advanced by dailing in optimized fueling?

    I am also curious about the relationship between oxygen pressure and oxygen absorption. Can they be improved aside from training at higher altitudes? Do the new altitude sim masks work? Would training to have better max time under water time / distance improve the O2 variables for endurance? Improving my O2 Shuttle?

    Ben – Great article. Great puzzle!! Thanks for the research.

  5. Hi

    Ok there is no threshold, I agree. But: WHAT in your muscles is then the limiting factor. WHY can’t you maintain speed at some point. E.g. running at 5k pace why can’t sustain for longer. What fails? You mention what is not the cause (lactate, H+) but what is? Do you have an article or pointer on that?

    • Paul,

      Unfortunately, science does not know the answer to what causes muscle fatigue. My personal bias is that there is no one single cause of fatigue for all muscle fibers. Instead, I hypothesize that different types of fibers fatigue for different reasons at different times.

      The good news is that whatever the cause of fatigue we know that training fibers to or near the point of failure causes those fibers to adapt and improve.


    • The threshold is the point where there is no longer steady state and the production becomes higher than the removal of lactate. Over that point, lactate levels keeps going up with time. In addition, what matters is not the pH inside the muscle cell. It seems that the acidity alter the capacity of the nervous system to recruit the muscle fiber (that would be the reason why it makes sense to train tolerance, mainly below 2 minutes).
      Also remember that When you consider long distances glycogen depletion and temperature control play an important role. That might create confusion.

    • First, I would ask that you clarify what kind of fatigue you are asking about – Central or peripheral fatigue. Many would argue that most of us quit exercising due to central fatigue rather than peripheral fatigue. But my guess is that you are curious about peripheral fatigue (i.e. muscle fiber fatigue).

      I would agree with Rich that there is no one single cause of peripheral fatigue. Most recently, scientists have discovered that an increase in extra-cellular potassium caused muscle fiber fatigue. The excess potassium causes hyper polarization of the muscle cell membrane, making it more difficult to depolarize the membrane and initiate cross bridge cycling (i.e. muscle shortening). Where does the potassium come from? It accumulates when the motor nerve is firing at very high rates (high action potential frequency). Action potentials cause potassium that is normally in higher concentration on the inside of the cell to diffuse out of the cell and then be re-sequestered back into the cell. When action potential frequency is very high, there is not enough time for the muscle cell to re-sequester all the potassium, so it begins to accumulate on the outside of the cell.

      Take a look at: Lindinger and Sogaard. Potassium regulation during exercise and recovery. Sports Med. 11(6): 382-401, 1991; or Clausen. Excitation-induced exchange of N+, K+, and Cl- in rat EDL muscle in vitro and in vivo: physiology and pathophysiology. J General Physiol. 2013. DOI: 10.1085/jgp.201210892.

  6. Not sure I would consider points of failure as something significant. Fatigue is mainly descriptive in nature. Similar to ‘strength’, ‘power’, ‘performance’, I cringe a bit when I see these terms used and swapped between disciplines in physiological discussions. Not only can they have different affecting factors but they can simply have very different meanings. Even the most demanding workouts you would do for endurance training are far below the points of actual muscle failure. You may slow down, but actual failure would be truly rare.

    More correctly, endurance training targets sustained energy/ATP production, bound to glycolysis, lipolysis, and making the most effective and efficient use of that energy. A typical runner in a 10k will repeat an action more than 5000 times per leg. A typical marathoner more than 20,000 times per leg. This requires a very different approach than just training near some point of failure like that of a bench press.

  7. The acidity in the blood does not really alter the capacity of nervous system to recruit muscle cells. Because in a repeat training of e.g. 8×300 at high intensity, the last repeats are with astronomic lactate levels, however still running speed is not much influenced.

    I think the ATP resynthesis within the muscle cell is the limiting factor. At some moment these processes don’t go quick enough any more. Maybe hindered by H+ ions, or maybe because other biochemical processes just can’t produce the necessary ATP quick enough. It’s not a blood issue but a muscle issue.

  8. What a load of twaddle, the blind leading the blind. Firstly, Noakes isnt a true biochemist or expert in metabolism…….you have cherry picked statements from cited articles and unfortunately misconstrued the information to convince others of your beliefs, some of which give an impartial balance of evidence particularly between the myth of lactic acid and the role of lactate which is almost irrelevant to your discussion.

    This clearly suits your biased conclusions, which are clearly not of an earnt scientific credibility (or any substantial biochemical background?), of which trained individuals have sound skills of objective appraisal.

    One of your statements is worrying….”Despite the widespread belief by many that there is insufficient oxygen to working muscles at high exercise intensity, this has never been proven.”

    So you have based your objection on evidence which has proven there is sufficient oxygen to working muscles at all times? Do you know what SmO2 represents? Perhaps you care to investigate and cite all the studies looking into muscle hypoxia/ insufficiency and glycolytic activity.

    While I dont have the inclination to posit the many flaws in your reasoning, I will supply the reference for a solid article you managed to leave off your list.

    Will leave you with the the following excerpt from Gladden which you should read carefully over and over and then go and put it in context of whole body metabolism and oxidative phosphorylation (respiration)…..before commenting, I beg.

    There is no disagreement that PO2 values in the range of ∼0.5 Torr or less result in O2-limited cytochrome turnover, and therefore O2-limited oxidative phosphorylation, a condition termed dysoxia (Connett et al. 1990). However, problems have arisen because of the application of the converse of this construct, i.e. that elevated HLa production and accumulation necessarily indicate the presence of dysoxia. This supposition formed the groundwork for the anaerobic threshold concept, which was introduced and detailed by Wasserman and colleagues in the 1960s and early 1970s (see Wasserman, 1984). The basic anaerobic threshold paradigm is that elevated HLa production and concentration during muscular contractions or exercise are the result of O2-limited oxidative phosphoryation. Similarly, standard medical practice has accepted an elevated blood La− concentration ([La−]) as the herald of O2 insufficiency (Mizock & Falk, 1992).

    ps. I do hope you post my comment, otherwise you would have confirmed my belief of your biased appraisal and critical analysis of the ‘science’, and are not open to debate as many non-scientific types often use as defence.

  9. Simon is fairly direct in his post, but I have to agree with part of what he has said. To be honest I think the author here, Richard, has spent a lot of time formatting his blog to reflect the style of published peer reviewed studies and articles, but it really seems little more than a very elaborately written opinion piece. The science doesn’t appear to extend beyond links to articles found through keyword searches. The handful of items I’ve checked out makes it clear the author here decided the outcome before doing whatever research he undertook.

    I was originally drawn here by the layout and presentation. Substance though, despite being quite wordy and peppered with terminology, is highly lacking and too biased to be useful.

    • I have several hundred full text research studies in my personal library. Additionally, I’ve had access to the University of Texas library system for many years (which is how I stocked my personal library) and have access to an incredible amount of published research. The majority of articles I’ve written and posted to this site are reviews of published, peer-reviewed research studies. I attempt to take the facts, figures, findings, and conclusions from published research and discuss them in lay terms as they apply to endurance or strength athletes as appropriate. I cite all the research studies in my articles.

      Over the past 15 or so years, I’ve encountered a number of people. like Simon, who disagree with the findings of one or more of the research studies that I’ve written about and attempt to dismiss it by claiming things such as a) the research is invalid for one or more reasons, b) my interpretation of the research is flawed, c)I’m cherry picking the research I write about (ignoring research that doesn’t support a pre-determined conclusion) and d) I’m expressing an opinion disguised as a scientific review.

      Despite the criticisms above, in all these years I can’t recall a single person who has taken the time to review the research on a particular subject (such as lactate threshold) and then written a counter-argument showing errors in my reviews or evidence of cherry-picking. As an example, a review of Simon’s post reveals no credible evidence supporting his opinions. He claims numerous flaws in my lactate threshold article but provides no evidence supporting his claim. His one source of “proof” is a link to a lactate threshold study. It is left to the reader to read the linked study. closely compare it to the body of research cited in my article, and then draw his/her own conclusions as to whether there are errors, flaws, or serious omissions from my article. In effect, damnation by inference, not actual fact or research.

      For the record, in my articles I always attempt to distinguish between research supported claims and my opinion.

      • I more or less agree with Simon… you mix up several concepts in your reasoning. You say, for instance, that muscles don’t become anaerobic during exercise. On the one hand, this isn’t true since there IS a VO2max and if you run faster than a certain speed you definitely can’t suck in enough oxygen to meet demands. On the other hand, the aerobic/not aerobic during exercise is not that important for your story.
        Being still in an aerobic state or not, the lactic acid is produced in small or larger quantities. Your point is that these quantities don’t CAUSE fatique and certainly not at some threshold (which I agree with). But the whole story about aerobic etc, complicates the whole thing.

        • Hi, Paul.

          Would you please cite the research supporting the belief that muscles become anaerobic during exercise. More specifically, that a limited supply of oxygen to muscles during exercise causes muscles to be come anaerobic and, therefore, fatigue.

          Also, would you please cite current research demonstrating that there IS a VO2max and it is the primary cause of fatigue during exercise. The most recent research I’ve read showed that fully 70% of tested subjects do not exhibit a VO2max during fatiguing exercise.

          When I was earning my degree in exercise physiology I was taught, and accepted as truth, the traditional aerobic/anaerobic model that you have alluded to in your comments. Things like VO2max and muscles going anaerobic during exercise. My belief in the aerobic/anaerobic model changed as more and more research has been done demonstrating significant flaws in the aerobic/anaerobic model.

          The scientific model demands that when a theory is shown to be false that the theory must then be abandoned or modified to fit the new evidence. “My story” as you call it, is simply a result of following the research – I abandoned the aerobic/anaerobic model because the research shows it to be false and I suggest an alternate theory based on the current body of scientific research. Those who continue to believe the aerobic/anaerobic model have the burden of proof for explaining why the model remains valid despite a significant and growing body of evidence against it.

  10. what can I say…
    When running at 18km/h for 5 minutes my HF is max and I can’t suck in more oxygen than about 61 ml/kg/min. I don’t see how that can rise more than a few percentage points further. My point: there IS “some” upper limit on oxygen uptake. You can’t argue that theoretically this can get arbitrarily higher as there is a ceiling for every one of us (denying that fact that is valid for 100% of people would be silly).
    Ofcourse the muscles get this oxygen delivered so they are surrounded by oxygen. Maybe that’s what you mean when you say the muscles don’t get anaerobic. But there IS a limited supply of oxygen (you can’t deny that. My VO2max is not going to be 70). For the muscles to keep producing energy they then revert to glycolysis, producing lactate. This is all good and fine and lactate production (i agree) does not cause the fatigue and yes, even prevents it by keeping the energy production going.

    So: no, muscles don’t “go anaerobic” during exercise and no, lactate does not cause fatique (rather, calcium transport issues etc may do that). But yes: there IS a de facto VO2max (what’s yours? I assume it’s not infinite). And yes: it may not be reached by 70% of subjects (e.g. because they don’t have the muscular power to do so or because they can’t produce lactate at an enough fast rate) but these 70% DO tire (not because of lack of oxygen but because of things like calcium or lack of enzymes and lack of ability to produce lactate (!) etc in their muscles etc etc).

    hope this clarifies my point

    • Paul,

      Yes, of course there is an upper limit on how much oxygen the lungs can take in, the blood can absorb, and the heart can transport to the body. The issue is not whether there is an upper limit, the issue is whether that limit is what is limiting endurance exercise performance. The research is clear – VO2max is not the limiting factor in endurance exercise performance. A limited supply of oxygen to working muscles is not the cause of fatigue during endurance exercise.

      But, clearly, people do fatigue during endurance exercise. Something (or, as I suggest, many somethings) causes that fatigue. My bias is that there is no single cause of fatigue. I suggest that fatigue primarily originates in the muscle fibers themselves but that multiple other elements can, and do, cause fatigue depending on the circumstances and environment.

  11. Ok yes then we seem to agree to some degree. There is no single cause of fatigue and certainly not lactate.

    However: the (VO2max) limit can be limiting in exercise performance.
    Not for everybody: 70% of people have too weak muscles etc to even reach VO2max (as you state)
    And not directly. But indirectly yes. Lactate is produced because further breakdown of metabolites is not possible because there is only a limited supply of oxygen (you don’t deny that, do you?). Then via a chain reaction some other resources (calcium etc etc) get depleted an then fatigue comes in. So not ‘directly’ but certainly via backpressure the limit in oxygen uptake leads to fatigue (i purposely don’t say ‘lack of oxygen’ because you seem to interpret that as ‘muscle going anaerobic’).

    • Paul,

      Yes, we agree that there is no single cause of fatigue.

      It is not correct to assume that only untrained adults with weak muscles comprise the 70% category. The 70% figure includes trained endurance athletes.

      The research that reveled this data is one piece of a significant and growing body of research that contradicts the traditional aerobic/anaerobic model. It is difficult to claim that an insufficient or limited supply of oxygen causes, or leads to, fatigue, when the aerobic system is not operating at max. In other words, we know there is capacity for additional oxygen to be absorbed, transported, and used by working muscles yet the muscles are fatigued/fatiguing.

      I don’t accept that a limited supply of oxygen is limiting metabolite breakdown and causing the chain reaction you are referring to.

      What I suggest is that different muscle fibers have varying capabilities to produce energy aerobically. Slow twitch fibers have the greatest aerobic energy production capability while fast twitch B fibers have the least. And across all fiber types there is a continuum of oxygen processing capability (i.e. not all slow twitch fibers have the same aerobic energy production capability). As exercise intensity increases, more and more muscle fibers are activated. The size principle tells us that higher exercise intensities increasingly activate fibers with lesser aerobic energy production capabilities, leading to more anaerobic production of energy, driving lactate levels higher. But note that lactate levels aren’t increasing due to limited oxygen, it is increasing due to greater carbohydrate usage via anaerobic production. There is no evidence of limited oxygen to working muscles. There is evidence of limited oxygen utilization by faster twitch muscle fibers due to the physiological characteristics of those faster twitch muscle fibers.

      My personal bias is that a change in the potassium/calcium levels at the cell wall level is the primary source of muscle fiber fatigue.

      For example: marathoners do not race at VO2max

  12. Ok, I see what you mean.
    Marathon running is under vO2max, intense tests don’t elicit vO2max. Still the athletes can’t run faster. So the conclusion is that oxygen is not limiting because it can get higher, the limit may be muscular in nature (ca/ka etc). I also see that at heavy workloads more fast twitch fibres are utilised that produce lactate even if there is sufficient oxygen.

    A nice thought experiment: it is a known fact in professional cyclists that they have such a large amount of slow twitch muscle that they can ride at a high percentage of vO2max while producing small amounts of lactate, very efficient.

    These cyclists cannot get much faster. Suppose (theoretically) they had ONLY slowtwitch fibers that could ONLY produce energy via oxygen (via fat oxidation or via lactate which is metabolised further in their very efficient mitochondria). In such a perfect situation their aerobic power is still capped at 100% VO2max.

    However for less accomplished athletes (you, me, the majority of people) there are all kinds of inefficiencies: muscle cells can’t use oxygen very efficiently; not enough capillaries so some cells don’t get the (abundance of) oxygen, other cells are fast twitch as you rightly state etc etc. For this group of people it makes not much sense to ‘increase vo2max’, it is more a matter of training a lot to increase quality of muscle cells. And yes, agree, for this group the supply of oxygen is not limiting.

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