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The Science of Performance |
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Do High Lactate Concentrations Actually Improve Performance? If you read popular running books or magazines you have most likely been exposed to the term lactate threshold. Additionally, these same sources would have advised you that in order to improve your distance running performance that you need to improve your lactate threshold. What is lactate and what is the lactate threshold? Why are you advised that improving your lactate threshold is important in running performance? In this article we will discuss the traditional role that lactate has believed to have played in endurance performance, explain the concept of lactate threshold, and then review the latest research on lactate’s influence on endurance performance. We begin with a history lesson. (Even though they are slightly different chemical compounds, for discussion purposes I will use the terms lactic acid and lactate interchangeably.) The History of Lactate One of the long held beliefs of modern training theory and the cardiovascular/anaerobic model of endurance performance is that lactate is a primary source of muscle fatigue. The cardiovascular/anaerobic theory proposes that when the energy demands of working muscles cannot be met aerobically (due to either lack of oxygen or insufficient aerobic development of the muscles) that the working muscles are forced to rely increasingly on anaerobic energy production. The model further proposes that a by-product of anaerobic energy production is lactic acid. In this model lactic acid is believed to be a metabolic waste product and a primary source of muscle fatigue. The model asserts that as exercise intensity increases, the body’s energy needs are increasingly met by anaerobic metabolism resulting in more and more lactic acid being produced. Eventually the amount of lactic acid in the body exceeds the body’s tolerance level and fatigue sets in, causing a slowing of the running pace. This belief in the role of lactic acid continues to be held by many even today and lactic acid continues to play a central role in the cardiovascular/anaerobic model of endurance physiology. Along with the belief in lactic acid as a primary source of fatigue, scientists also noted that there seemed to be an association between blood lactate levels and endurance performance. The first research studies that measured blood lactate during increasing intensity exercise found what was believed to be a “lactate threshold”. The lactate threshold theory held that as exercise intensity increased, so too did blood lactate levels. However, it was believed that lactate levels did not increase in a linear fashion; instead it was proposed that they increased slowly at first as exercise intensity increased and then suddenly increased dramatically at some intensity level or threshold. This sudden increase in lactate levels was termed the “lactate threshold”. The threshold effect was believed to be caused by the inability of the body to meet its energy needs via aerobic means. In popular terms, the muscles became “anaerobic”. Remember that lactic acid was supposed to be produced by anaerobic metabolism. With insufficient oxygen available to the working muscles, they were forced to produce energy anaerobically, thus producing large volumes of lactate. The lactate in turn caused muscle fatigue, resulting in a slowing of the running pace. Further research showed that the lactate threshold was a very accurate predictor of endurance performance – in fact it was shown to be a better predictor of performance than even VO2max, reinforcing the cardiovascular/anaerobic model and the role of lactate in that model. Scientists also noted that increases in the lactate threshold accompanied improvements in endurance performance, leading many to adopt the belief that improved performance was caused by an improved lactate threshold. Armed with the above beliefs coaches and runners devised training programs designed to improve lactate threshold in the belief that it would result in improved performance. Updated Research The general beliefs above about the fatigue causing role of lactate were formed between about 1900 and 1970. Since the 1970s a large amount of additional research has been conducted examining the role of lactate in performance and has generally refuted every negative claim made against it. Most important 30 years of additional research has shown that lactic acid does not cause fatigue. Instead lactate has shown to be a potent source of energy, perhaps even more important than carbohydrates in endurance performance! How’s that for a turn around - from fatigue causing metabolic waste product to energy product rivaling carbohydrates in importance. Modern research has also demonstrated that the muscles do not go “anaerobic” during intense exercise. Despite 30 years of effort to prove it, lack of oxygen to exercising muscles has always been an assumption – it has never been proven. Instead, more recent research indicates that at all exercise intensities sufficient oxygen is available to working muscles. Newer research has also shown that there is no “lactate threshold”. Instead, lactate rises exponentially as a result of increasing exercise intensity and does not suddenly rise precipitously at some level of intensity. Previous research that indicated a “lactate threshold” made two mistakes. First, most simply failed to measure lactate levels at frequent enough intervals – too few blood samples were taken. Later research that took blood samples at closer intervals revealed that lactate rises exponentially without any evidence of a threshold. Second, it was not originally understood that lactate is both produced and used by exercising muscles. Lactate is a by-product of carbohydrate metabolism, not necessarily just anaerobic metabolism as first suggested. The more carbohydrates the body burns, the more lactate that is produced. As exercise intensity increases the body burns more and more carbohydrates and produces more and more lactate. In addition to producing lactate during carbohydrate metabolism, the body also burns lactate as a source of energy. Without going into all the physiological details, blood lactate is absorbed by the heart, liver, and exercising muscles, sparing further carbohydrate use. It is also important to know that oxygen is required for the body to burn lactate. The exponential rise in lactate production during increasing exercise intensity is a result of a progressively greater increase in rate of production than in rate of use, resulting in a progressive accumulation in the blood. Not only is lactate production highest at the fastest running speed, but lactate use is also highest at the fastest running speed. Since lactate is metabolized via aerobic metabolism, the fact that its use is highest at the fastest running speed means that the muscles couldn’t be “anaerobic”. In summary, despite the things you’ve been told about lactate and the importance of the lactate threshold, we now know that 1) lactate does not cause fatigue – instead lactate is a potent source of energy 2) muscles do not become “anaerobic”, even during maximum exercise 3) there is no lactate threshold – lactate rises exponentially as a function of exercise intensity 4) lactate is a by-product of carbohydrate metabolism – higher exercise intensity burns more carbohydrates and produces more lactate In contrast to the volume of evidence supporting the above points and its wide acceptance by many scientists, these updated views of lactate’s role have not been widely adopted by runners and other endurance athletes. I believe the primary reason the above evidence has been so widely ignored by athletes is that no other comprehensive model of endurance performance has been widely promoted. Even with all the evident flaws of the cardiovascular/anaerobic model, the lack of a comprehensive, competing model of endurance performance has resulted in runners maintaining their belief in both the cardiovascular/anaerobic model and the role of lactate in that model. Updated Lactate Theory - H+ In the face of the above data, especially the research demonstrating that lactate does not cause fatigue, some scientists that support the cardiovascular/anaerobic model now suggest that the hydrogen ions (H+) associated with lactic acid are the primary cause of fatigue. This updated lactate theory proposes that the H+ that are produced during the same glycolytic process that produces lactic acid cause a significant change in body pH. The increased acidity level is believed to cause muscle fatigue by interfering with muscle contractility. As exercise intensity increases so to does the production of both lactate and H+, resulting in an increasingly acidic muscle environment. Therefore, even though lactate is now generally accepted by scientists to not cause fatigue within the body, its close association with H+, which is suggested by some as a primary cause of fatigue, allows the belief in the importance of lactate levels to be retained and its predictive powers to be explained. With H+ now seen as a primary fatigue causing agent, this still remains only a side step from the belief in lactate as a fatigue agent. Since H+ is produced during the same process that produces lactate, then lactate levels are an indirect measure of H+ levels. The belief that H+ is a primary cause of fatigue allows a continued belief in the cardiovascular/anaerobic model of performance Research Does increasing muscle acidity cause muscle fatigue? Many scientists consider it to be an important contributor to muscle fatigue. However, its role in causing fatigue has been questioned by other scientists. Two recent studies on muscle acidity levels and lactic acid examined this very question. Let’s take a look at what they found. When muscles contract they lose potassium (K). During contractions the potassium within a muscle cell is transported outside the cell into the surrounding interstitial fluid. The reduced intramuscular potassium and, specifically, the increased extracellular potassium has been suggested by some researchers to be a primary cause of fatigue; research has shown a decrease in muscle fiber contractility due to high interstitial potassium levels. Knowing that the role of lactic acid in causing fatigue was in question, in 2001 a group of researchers in Denmark wanted to examine the interaction between increasing lactic acid levels in combination with increasing interstitial potassium levels (1). To study the combined effects of these changes on muscle function, they isolated rat soleus muscles and incubated them at an elevated potassium level. Sure enough, muscle force was reduced by 75% with the increase in potassium levels. After they had established that the increased potassium levels had indeed reduced muscle function, they then introduced lactic acid into the mix. With the addition of the lactic acid (which caused acidity) there was “…an almost complete recovery of force that was maintained for at least 50 minutes. Moreover, adding lactic acid at the same time as potassium was increased completely prevented the reduction in force.” In this experiment, not only did lactic acid not contribute to muscular fatigue, it actually reversed already existing fatigue. The researchers concluded with the following. “…the present data indicate that when muscles are placed in a milieu that with respect to (interstitial potassium levels) mimics the milieu seen by the muscle fibers during intensive exercise, lactic acid acidosis not only does not cause a reduction in force but actually increases force by counteracting the force-depressing effects of high (interstitial potassium levels). The present study therefore suggests that instead of being a cause of muscle fatigue, accumulation of lactic acid during intensive work actually protects muscles against fatigue.” How about that? Instead of lactic acid induced acidity causing fatigue, this study demonstrates that it actually prevents fatigue. Quite a difference from the view of conventional training wisdom and the cardiovascular/anaerobic model isn’t it? As interesting as the above study may be, in isolation it is insufficient to change a century of thinking on the fatiguing effect of lactate. In 2003 another group of researchers, also from Denmark, wanted to evaluate the effects temperature might have on muscle sensitivity to potassium. However, they also wanted to study the interaction between potassium and lactic acid and confirm some of the earlier research (2). During intense exercise muscle heat production and muscle temperature rise. The researchers hypothesized that an increased muscle temperature would provide some protection from the fatiguing effects of high potassium levels. Their working hypothesis was that the combination of increased temperature and lactic acidosis would protect against the loss of force induced by increasing potassium levels. Using incubated rat soleus or extensor digitorum longus muscles, the researchers evaluated the effect changing temperature had on muscle force in the presence of high potassium levels. First, using different temperatures as their starting point, they measured the drop in muscle force caused by increasing potassium levels. No matter what the starting temperature, when potassium levels were increased, muscle force decreased. After carefully assessing the drop in force, muscle temperatures were then raised in the presence of a high potassium level. Sure enough, just as they hypothesized, when muscle temperature was increased muscle force increased, though it was not fully restored. Then the researchers repeated the experiment but added lactic acid to the mix. Muscle fibers were again exposed to an elevated potassium level and muscle force was measured. Temperature was again raised, inducing an increase in muscle force output. Lactic acid and salbutamol (a catecholamine) were then added to the milieu. The result? “If lactic acid and salbutamol were added simultaneously with temperature elevation, a rapid and complete force recovery was observed.” The researchers stated that, “…the present study suggests an exercise scenario in which the loss of excitability and force by increased (interstitial potassium levels) is counteracted by the simultaneous elevation of muscle temperature, lactic acidosis and the presence of catecholamines.” Just as in the previous study, this group of researchers concluded that not only does lactic acidosis not cause fatigue it actually counteracts the fatigue causing effects of other compounds and bodily environments. (By the way, I have only reviewed two research studies in this article. There are several other studies supporting the conclusions here, but I believe these two serve to sufficiently make the point.) Summary Where does this leave us? The evidence is compelling that the traditional view of lactate as a cause of fatigue and the more recent view of H+ induced muscle acidity as a cause of fatigue is flawed. 30 years of research have shown that lactate does not cause fatigue and now we have more recent evidence that H+ induced acidity is also not a factor in muscle fatigue. Instead, new research has revealed that lactic acid acidosis provides protection against other fatigue causing compounds and environments. The training implication of this conclusion is not yet fully known. My own bias is that while “lactate threshold” training is known to be effective, the physiological explanation for it will have to be modified. Additionally, it is also possible that with the demise of the “lactate threshold” theory, other training methods may very well be devised that prove to be more effective. Reference: 1. Nielsen O., Paoli F., Overgaard K. Protective effects of lactic acid on force production in rat skeletal muscle Journal of Physiology 2001, 536 (1), 161-166 2. Pedersen T., Clausen T., Nielsen O. Loss of force induced by high extracellular [K+] in rat muscle: effect of temperature, lactic acid and b2-agonist Journal of Physiology 2003, 551(1), 277–286
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