The Science of Lactate Threshold

The Science of Lactate Threshold

Lactate Threshold

Article Difficulty: Advanced

In this article we are going to look at 

  • Exactly what lactate threshold is 
  • Why lactate threshold causes fatigue
  • How endurance training improves lactate threshold
  • How to train to improve lactate threshold

In a previous article, we looked at VO2 max and I mentioned that if you had two athletes and one had a much higher VO2 max, they would normally outperform the other in endurance competition, and while this is true, there is more to endurance performance than just VO2 max. What if two endurance athletes have a similar VO2 max? Well, this is where a high lactate threshold can make a big difference. A high lactate threshold means you can utilize a large proportion of your VO2 max without the byproducts of anaerobic metabolism rising too high and causing fatigue. You know that feeling when you’ve been giving it hard for minutes and your legs start to burn and feel heavy and you are forced to slow down? Well this is what happens when we exercise above our lactate threshold. If we can increase the intensity/pace at which lactate threshold occurs, then we can run faster (generate greater power output) without having to slow down due to fatigue. In this article, we are going to take a deep dive into what lactate threshold is, the basic science of why it occurs, and finish with how we go about improving it through running training. Although running is used as an example, the information within this article is applicable to any kind of endurance sport.

What is lactate threshold?

Lactate threshold has two commonly used definitions:

  • Lactate threshold represents the point in which exercise intensity is so high that the aerobic energy production system can no longer keep up with the energy demand and instead anaerobic metabolism must supply a significant amount of ATP (energy) to allow the desired work output to continue. This rapid ATP production and breakdown causes an increase in hydrogen ions within the muscle that cause fatigue, while simultaneously lactate production increases and accumulates within the blood which is commonly measured to define when lactate threshold occurs.
  • The point in which blood lactate begins to rapidly accumulate in the blood.

  • Another way to conceptualize lactate threshold is the % of VO2 Max that can be utilized without lactate threshold induced fatigue. Trained athletes have a lactate threshold that occurs at a higher percentage of their VO2 Max, which means they can train at a higher intensity without lactate threshold induced fatigue. 

    You could essentially stop reading here, but if you are interested in learning more about why lactate threshold occurs, read on.

    Many names, and multiple definitions

    Onset of blood lactate accumulation (OBLA), Anaerobic threshold, Maximum lactate steady state (MLSS), Lactate turn point, Lactate threshold and LT2 are all used interchangeably with lactate threshold. And with no consistency or general consensus amongst the scientific community on the exact definition, lactate threshold can be fairly confusing! But we will clear all of this up shortly.

    Lactate threshold can be measured in two ways:

    1. Maximum sustainable prolonged work output / training intensity
    2. Rapidly rising blood lactate level (generally above 4.0 mmol/L)

    Both of these two things coincide at the same time, and because lactate threshold can be measured in these two ways, this has led to many different names and no definitive definition and there is little consistency amongst researchers. What all of these different names have in common is that they represent the point that is the maximum work rate we can maintain for an extended period of time and any intensity higher than this, metabolic byproducts begin to rise exponentially and we become fatigued. This is also the same point in which lactate begins to accumulate in the blood. Therefore, at the same time we become fatigued, there is a rise in blood lactate.

    To understand a bit more about why lactate threshold occurs and why it causes fatigue, we have to look at how energy is produced in the muscle. 

    Anaerobic and aerobic metabolism, the cause of lactate threshold

    During exercise, our muscles produce energy (in the form of the molecule ATP) in two ways:

    • With oxygen (aerobic metabolism)
    • Without oxygen (anaerobic metabolism)

    (Within anaerobic metabolism there are two pathways, glycolysis and the phosphagen system, but we are just focusing on glycolysis in this article)

    Both aerobic metabolism and anaerobic metabolism start the same way with the breakdown of a glucose molecule through a process known as glycolysis ("glyco" referring to glucose and "lysis" meaning the breaking of). At rest, almost all of the energy is produced aerobically, while at maximal exercise levels, a very large proportion is produced anaerobically. Everything in-between lies on this continuum.

    You may be wondering, why does our body need to do this rather than just using oxygen to produce all of the energy? The reason is because it takes time for our oxygen distribution systems to meet the oxygen demand of the muscle. This oxygen debt occurs at the onset of exercise, as it takes time for our oxygen delivery systems to catch up with the muscular demand, and during high exercise intensities. It is this high level of exercise intensity and large amount of anaerobic metabolism that causes lactate threshold to occur. In the next section, we will look at how lactate threshold causes fatigue.  

    Fatigue mechanism 1, glycogen depletion

    Anaerobic glycolysis allows higher rates of ATP resynthesis than can be achieved by aerobic metabolism, but the capacity of the system is limited and fatigue follows rapidly. Aerobic metabolism can produce far more energy per glucose molecule than anaerobic metabolism (32 ATP Vs. 2 ATP) and can continue for much longer, but it's rate of energy production is slower which is why when we need to exercise very intensely, we require the support of anaerobic metabolism. Because anaerobic metabolism is inefficient in turning glucose into ATP, it requires a lot more glucose. Therefore, the first reason why we become fatigued when we train above lactate threshold is a rapid depletion of muscle glycogen (stored glucose), due to the rapid rates of anaerobic metabolism. So the first fatigue mechanism when exercising above lactate threshold is glycogen depletion.

    Fatigue mechanism number 2, muscle acidity and increased metabolic byproducts

    Both energy production pathways (aerobic and anaerobic) produce energy in the form of ATP. When ATP is broken down within a muscle cell, it powers muscle contraction. During this ATP breakdown, there is a release of a hydrogen proton (H+). When ATP breakdown is high, hydrogen protons are build up in the muscle. This H+ build up causes acidity, and the acidic environment causes fatigue via a reduction in muscle force output. 

    Our muscle does it’s best to clear the H+, and this takes place via three primary mechanisms:

    • Transfer into the blood (where the H+ is buffered and dispelled via respiration as CO2)
    • During the formation of lactate (lactate accepts 1 H+ when it is formed from pyruvate)
    • H+ is in the mitochondria for energy production (in the electron transport chain)  

    During aerobic conditions, when oxygen supply is plentiful, H+ production and utilization are equal, so there is no net H+ accumulation and no net pH decrease. However, during anaerobic respiration, H+ production is very high due to very rapid ATP breakdown (and resynthesis). The H+ can’t be dispersed into the blood fast enough, and the mitochondria can not accept it due to lack of oxygen, so the H+ begins to accumulate in the muscle causing acidity. The rapid rate of ATP breakdown also causes other byproducts (ADP and Pi) to accumulate which further contribute to muscle fatigue. Therefore, the second fatigue mechanism when exercising above lactate threshold is an accumulation of ADP, Pi and H+ which reduce the muscle cell's ability to contract, causing reduced power output.

    Summary of aerobic and anaerobic metabolism

    Why do we see increased blood lactate?

    You may wonder that if lactate doesn’t cause fatigue, why is blood lactate measured to define lactate threshold? And the reason a blood lactate test is used is because lactate formation occurs due to anaerobic glycolysis, and this coincides with rising levels of H+ in the muscle. Therefore, blood lactate acts as a marker for increasing rates of anaerobic metabolism. The significant increase in blood lactate (above 4 mmol/L) is what is commonly measured in a lab to define lactate threshold. 

    Fats and proteins

    You may be wondering, what about the metabolism of fats and proteins? Well these are first broken down into smaller components which then enter the mitochondria and are metabolized through the Krebs cycle; this is the same place where the pyruvate produced from glycolysis enters. Why is this important? Well simply put, you need glucose in order to exercise at high intensities because without ample glucose availability, we are limited to aerobic metabolism of fats and proteins which is much slower at producing energy. 

    How training improves lactate threshold

    Training has been shown to increase lactate and hydrogen buffering by 65% (1), and as a result lactate threshold occurs at a higher % of VO2 max in trained vs. untrained individuals. Active muscle accounts for a large proportion of lactate disposal during exercise (7, 15), therefore improvements in lactate clearance are partially due to an increased ability for working muscles to use lactate as a fuel. Specifically, this clearance is from our oxidative fibres using lactate as a fuel, and the increased ability comes about through an increase in mitochondrial size and density, as well as an increase in mLDH, which converts lactate to pyruvate and back, and an increase in lactate transporters for (MCT-1) that shuttle the lactate to the oxidative fibre's mitochondria. 

    Another major reason why training improves lactate threshold is simply an increased ability and efficiency of using oxygen to produce energy. By improving the efficiency and capacity to utilize oxygen, the higher the speed/intensity at which we can run while our aerobic system provides most of the energy and therefore, the higher the lactate threshold. Further improvements at the muscle level include, decreased reliance on lactate producing muscle fibers as well as improved muscle capillarization which allows for greater clearance.  Many of these same aerobic improvement systems also improve VO2 max, and here is the link to the previous VO2 max article which discusses these mechanisms in more detail. 

    Training specificity

    Improving lactate threshold must be accomplished with various training intensities to improve the various mechanisms.

    1. Slow base training to improve oxidative capacity, remember we need greater mitochondria to utilize more lactate and H+.
    2. Some threshold work to stress the lactate clearance and buffering systems
    3. And some VO2 max length intervals to increase total aerobic capacity, as it can also increase VO2 max, then lactate threshold will occur at a higher absolute work intensity. 

    The relationship between lactate threshold and ventilation rate

    Imagine when you are going really hard, such as during an 800m or a 1 mile running interval, and at a certain point you notice you begin breathing much faster; this occurs around the same time as lactate threshold and is a result of our body trying to buffer (remove) the H+ ions from our blood. Our body must work to remove H+ from the muscle and the blood to prevent significant changes in pH so that ATP production can continue. When most of our energy production is powered aerobically, ventilation rate and oxygen supply/demand have a linear relationship, meaning ventilation increases proportionally to oxygen demand. However, when we begin crossing lactate threshold due to high amounts of aerobic metabolism, ventilation rate begins to increase disproportionately to oxygen demand, and this is termed ventilatory threshold. The reason this occurs is due to the way that H+ is removed from the blood. This takes place through a system of reaction known as the bicarbonate buffer system. The bicarbonate buffer system uses bicarbonate to turn H+ into carbon dioxide and dispel it through respiration. Increasing levels of H+ and carbon dioxide within trigger receptors increase our respiration rate so that our body can clear it from the blood and this is why we have an exponential rise in respiration rate when we have high levels of aerobic metabolism. 

    LT1, LT2, VT1, VT2

    In this article, we have been discussing lactate threshold as a single point, however there are actually two lactate threshold points (LT1 and  LT2). The one we have been talking about is known as LT2, but there is another one that occurs earlier on at lower exercise intensity levels, known as LT1; this is the first distinguishable rise in blood lactate above resting levels. Again, because lactate and H+ are produced together and H+ causes increased respiration, both LT1 and LT2 also closely correspond to respiratory thresholds, VT1 and VT2. You can essentially think of LT1/VT1 as your long easy run pace, 68%-72% HR max the top of zone 2, when you can still easily have a conversation, and LT2/VT2 is the top end of what you could sustain, such as during a tempo run.

    Why we need lactate

    When oxygen is available, NADH’s electrons can be quickly used by the electron-transport chain in the mitochondria, thereby yielding valuable energy. When oxygen is not available, however, mitochondria can no longer effectively clear electrons. Thus, under anaerobic conditions, fermentation is the only metabolic option. Even when oxygen is available, ATP production by oxidative phosphorylation can be limited by the oxygen uptake rate. Thus, under high-demand conditions, such as intense exercise, fermentation provides a way to accelerate energy generation. Accordingly, when muscle is pushed beyond the aerobic threshold, such as during a short sprint or toward the end of a long hard run, lactate is released as metabolic waste. Without lactate formation, we would be limited to aerobic metabolism. Lactate is used as a fuel by the heart, liver, kidney and brain, and can travel to the liver to be used to form glucose through gluconeogenesis. Thus lactate is not a waste product, but a valuable interconvertible energy source.

    Final note, lactic acid doesn’t really exist

    Throughout the article, I have not used the term Lactic acid and I’ll explain why. The term ‘lactic acid’ refers to lactate and hydrogen in one single compound, however, more recent research has proved that this compound does not really exist in the human body. So it’s best to consider lactate and hydrogen as two entirely different products of anaerobic metabolism that occur at the same time. This is also useful as their buffering and metabolism occurs in different ways. It’s worth mentioning here that lactate itself is not the culprit of fatigue. It's production is actually what allows anaerobic glycolysis to happen when pyruvate production exceeds oxygen supply. Lactate acts as a useful compound allowing glycolysis to continue, and can be reused at a later date to produce energy by various tissues (heart, liver, muscle), as well as being converted back into glucose in the liver


    2. Ghosh A. K. (2004). Anaerobic threshold: its concept and role in endurance sport. The Malaysian journal of medical sciences : MJMS, 11(1), 24–36.
    3. Kravitz, L. (2005). Lactate: Not guilty as charged. IDEA Fitness Journal, 2(6), 23-25. (shows lactate actually retards acidosis)
    4. Robergs, R. A., Ghiasvand, F., & Parker, D. (2004). Biochemistry of exercise-induced metabolic acidosis. American journal of physiology. Regulatory, integrative and comparative physiology, 287(3), R502–R516.
    5. McLester J. R., Jr (1997). Muscle contraction and fatigue. The role of adenosine 5'-diphosphate and inorganic phosphate. Sports medicine (Auckland, N.Z.), 23(5), 287–305.
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