Lactate and threshold concepts in performance diagnostics -Lactate part 3

Lactate plays a central role in the energy supply and performance of athletes. Lactate measurement is used, among other things, in sports performance diagnostics. However, the existing concepts of the so-called lactate threshold for monitoring training progress need to be reconsidered. The first two articles on the subject of lactate can be found here: Part1 Part2

Performance diagnostics with lactate measurement

In performance diagnostics, conclusions about the athlete’s performance are drawn by measuring blood lactate. However, misinterpretations can easily occur here. Performance diagnostics in cycling usually takes place on an ergometer under controlled conditions. The athlete pedals on the ergometer while the resistance is increased – e.g. gradually. This increases the energy demand of the body. Lactate is also produced by the body at rest, so this is referred to as resting lactate, which is measured as the baseline value. With increasing resistance and increasing power, a measurement of blood lactate levels shows an increase. As soon as the first increase in lactate appears in the blood measurement data with increasing power on the ergometer, this point is set as the “aerobic threshold” (see below). The body always produces only as much lactate as necessary and tries to break down the lactate that is produced more frequently during exercise. The rate of decomposition is not constant, but increases with increasing lactate production. Thus, the body keeps the lactate concentration in the blood at an approximately constant level for a certain period of time as the load increases, before the lactate concentration also rises to a new level as the load continues to increase. The level with the highest blood lactate concentration at which this succeeds is called the maximum lactate threshold, maxLass or MLSS (maximum lactate steady state). Usually people like to talk about the “lactate threshold” or “threshold” for short, but it does not correspond to the actual “aerobic threshold”. The athlete can perform at “the threshold” for a longer period of time. Above this level, the lactate curve of the measurement in the blood continues to rise steadily. Another common threshold term is that of the so-called “individual anaerobic threshold” IAS (e.g. according to Stegmann et al. 1981). A correlation between the lactate threshold and the IAS was shown in studies for about 95 percent of the test subjects. Even today, unfortunately, the mistake is made to use absolute values of lactate for the interpretation of performance. The application of lactate-based threshold concepts dates back to a scientific publication by Mader et al. in 1976. On the lactate performance curve during a test, the “aerobic-anaerobic threshold” was defined as a point and was intended to serve as a criterion for assessing endurance performance. Intensity ranges for training control were classified on the basis of lactate measurements and the resulting lactate performance curve. The lactate threshold defined the transition area between the area with aerobic, partly anaerobic energy supply to the area with anaerobic energy supply in the loaded muscle. The threshold was set at a blood lactate value of 4 mmol/l, since this value was most frequently found in the underlying investigations. Even today, reference is made to this value, although in practice individual values of 2 to 8 mmol/l are found in exercise tests. The level of the lactate values at threshold does not necessarily say anything about the absolute performance capacity, as measured, for example, in watts by means of a power meter. As the aerobic capacity of an athlete increases, the lactate concentration at the maximum lactate threshold MLSS decreases. The absolute lactate concentration at the MLSS varies within a range, which underlines the necessity of an individual assessment. To estimate endurance performance, the so-called functional threshold power (FTP) was introduced. FTP is the maximum power that can be delivered over 60 minutes and coincides well with the lactate threshold in trained athletes. Glycolysis and formation of lactate occurs even at rest and our body always has a low concentration of lactate. Lack of oxygen is not the cause of lactate formation. Numerous threshold concepts exist for lactate, with two thresholds in particular being frequently used. To summarize: At the first threshold, lactate concentration begins to rise above the lactate resting value due to higher energy demand. The second threshold is supposed to mark the transition between the partially still aerobic and anaerobic energy supply, whereby the latter, however, does not exist in this form at all. There is no pure anaerobic range! Even at the threshold (MLSS), the energy supply takes place predominantly with the use of oxygen (aerobic). Just above threshold, anaerobic-lactacid energy provision is about 2 percent. The elimination of lactate depends on the lactate concentration as well as on the turnover of the aerobic metabolism. The higher the concentration of lactate and/or the higher the aerobic energy turnover the higher the elimination. Under increased load, more than 80 percent of the lactate formed is used in aerobic energy provision. Thus, an athlete may have experienced an increase in performance in two consecutive performance tests despite unchanged lactate values in the meantime.

Performance diagnostics via respiratory gases and previously ignored criticism

In recent years, the so-called spiroergometry has become established in addition to or even instead of performance diagnostics via the measurement of blood lactate. Spiroergometry is a non-invasive method based on the continuous measurement of respiratory gases. Indicators of endurance performance include maximal oxygen uptake VO2max (highest amount of oxygen metabolized), respiratory equivalents (e.g., volume ratio of O2 or CO2 to breath), or ventilatory thresholds (VT). However, lactate also has an impact on spiroergometry. Spiroergometry dates back to a work by Wasserman et al (1964). The original method uses, among other things, the ratio of exhaled CO2 to inhaled O2 – the respiratory exchange ratio (RER). The CO2 output per O2 intake via the respiratory air is often referred to by the term respiratory quotient (RQ). The RQ is used, among other things, to provide information about the proportion of fat or carbohydrate that is used to provide energy. This is called indirect calorimetry. Theoretically, pure energy production from fatty acids would result in an RQ of about 0.71. Pure metabolism of carbohydrates would result in an RQ of 1.0. Proteins or amino acids would result in a value of 0.8 (except in the case of glycogen depletion). However, proteins for energy production are neglected and only fatty acids and carbohydrates are included. Protein, along with fat and carbohydrates, is used to a not inconsiderable extent for energy production during endurance training and accounts for about five percent of the converted energy. When glycogen stores are depleted, the proportion of energy gained from protein can easily double. Therefore, neglecting this leads to inaccurate statements regarding substrate utilization. Glucose and glycogen also show differences as an energy substrate in their metabolism, but this is also neglected. In practice, a mixed ratio of energy substrates is usually present under load. According to the “inventor” Wassermann (Wasserman et al. 1964), the estimation of energy substrates by respiratory gas analysis (fat and carbohydrates) only works as long as no additional CO2 source is present. However, the body buffers H+ ions produced with a rise in lactate via bicarbonate in the blood to maintain a constant blood pH. Buffering when lactate rises in the blood with bicarbonate releases additional CO2, which is exhaled and RQ rises even though the ratio of energy substrates fat/carbohydrate need not have changed. Therefore, according to Wasserman et al., the buffering via bicarbonate must be included in the calculation of the RQ/RER or the RQ measurement must be performed at constant lactate values. If the blood lactate increases during exercise – as is the case above the 2nd threshold – the RQ/RER without taking lactate buffering into account cannot, by definition (!), be used to make any statement about the energy substrates. Therefore, a determination of the energy substrates fat and carbohydrates based on RQ is initially subject to a small error at low exercise intensities without a significant increase in blood lactate, but this error becomes larger as lactate increases, which is why substrate determination should only be used at most up to an exercise load corresponding to 75 percent of VO2max. Furthermore, the athlete’s diet influences the values of the RER. Increased fat burning due to a low-carbohydrate diet or due to depletion of glycogen stores result in a lower RQ. Hyperventilation results in a higher RER than would result from energy substrate use alone. The aerobic threshold (1st lactate threshold) is established at the point at which RQ begins to rise from rest. The second “anaerobic threshold” is often defined at RQ=1. The ventilatory threshold VTs are described by the RQ. While the two lactate thresholds mentioned above describe metabolic changes, the two ventilatory thresholds (VT1 and VT2) are quasi the response of the respiratory tract to these metabolic changes. Due to an increase in lactate with increasing exertion, CO2 must be increasingly exhaled for the necessary buffering and respiration is thus increased: this is the first ventilatory threshold VT1. The second ventilatory threshold VT2 (at the respiratory compensation point RCP) is reached when the maximum lactate steady state MLSS is exceeded with sharply rising lactate and is manifested in a disproportionate increase in respiration, whereby the 2nd threshold is somewhat overestimated by VT2. This method is now increasingly criticized and considered inaccurate. A combination of spiroergometry and lactate measurement provides a more comprehensive overall picture in performance diagnostics.

Conclusion: Lactate is not a culprit and not the main driver of muscle fatigue. Lack of oxygen during exercise does not trigger lactate production. Rather, under exercise, lactate is an important signaling molecule and a potent energy carrier. Both the main site of production and the main site of elimination for lactate is the musculature. The respective muscle fiber types show differences in lactate uptake and breakdown. Fast-twitch muscle fibers produce the most lactate. In endurance muscle fiber types, more lactate can sometimes be broken down than is produced. A decisive role is played by the different lactate transporters MCTs, whose function and number influence the performance of an athlete. The lactate values in the blood are the result of numerous influences. The measured values of blood lactate remain important parameters in performance diagnostics. Above the “2nd threshold”, no statement can be made about energy substrates with the RER without taking lactate buffering into account, by definition. One goal of training should be to optimize the redistribution and utilization of lactate in the body and thus increase performance.

Blood lactate concentration depends on a wide variety of factors (Wahl et al. 2009):

  • Lactate production rate: greater in fast-twitch than slow-twitch muscle fibers.
  • Isoforms of the enzyme LDH: lactate production versus lactate oxidation.
  • Blood flow velocity: breakdown of lactate gradient
  • Metabolic capacity: lactate elimination higher in type 1 muscle fibers
  • pH: influence on transport via MCTs
  • Lactate transport rates via MCT transporters


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