The anaerobic threshold (AT) concept was first introduced by Wasserman and McIllroy in 1964 (1) in a study of cardiac patients. The aim was to determine the point at which anaerobic metabolism begins to dominate for energy production, a state related to the rapid onset of fatigue, or AT. Their findings revealed that ventilatory data could detect the AT from submaximal exercise intensities, thus reducing the risk of adverse cardiac events associated with maximal exercise in cardiac patients. This enabled the development of submaximal exercise protocols in clinical populations that could be at or close to the AT and sustained for extended periods of time (≤60 minutes).
In the early 1960s, studies primarily used ventilatory measures to determine AT due to ease of use. However, later that decade saw the development of capillary blood lactate analysis, which was easier still for measuring AT. Blood lactate is a known marker of the AT, as it accumulates at greater rates than it can be cleared during anaerobic glycolysis, which is the predominant energy source beyond the AT, thereby indicating when the AT occurs (2). This understanding has enabled the application of the AT to improve endurance performance and is now widely used for exercise prescription for athletes wanting to sustain high-performance aerobic exercise for as long as possible (3).
At present, the gold standard measure of aerobic fitness is the assessment of maximal oxygen consumption (V˙O2max), which among other uses enables gender and age-based categorization of individuals. However, limitations of V˙O2max testing include poor discrimination between endurance capacity in highly trained individuals, resulting in low sensitivity to detect small changes in endurance. In addition, V˙O2max testing requires a true maximum effort, which if not given may affect the accuracy of the V˙O2 measure (4). Thus, the use of ventilatory and blood lactate measurements during submaximal incremental exercise can provide a valid and safe approach to determine AT (5).
DEFINING THE KEY TERMS
Several terms, including lactate threshold (LT), ventilatory threshold (VT), gas exchange threshold, respiratory compensation threshold, lactate turn point, lactate minimum, and onset of blood lactate accumulation (OBLA) set to 4 mmol·L−1, are often used interchangeably to describe AT (6). In addition, the interpretation of the physiological changes, such as the initial increase in blood lactate levels above resting values, might be termed AT by some (1) and aerobic threshold by others (7). The use of different terminology arose from the variety of test modes used to determine AT, but coaches and practitioners should be aware that these terms reflect distinct physiological mechanisms and metabolic processes that can occur at different exercise intensities (Table).
Terminology used to describe AT
||The exercise stage at which there is a significant and exponential increase in lactate during an incremental exercise test.
|Maximum lactate steady state
||Occurs at the stage before the exponential increase in lactate, where lactate production and clearance are optimally balanced.
||The accumulation of blood lactate up to a specific amount (usually 4 mmol·L−1) during incremental exercise. It is thought this critical value reflects the shift to higher exercise intensities.
|Ventilatory threshold (also termed VT1)
||The exercise intensity at which ventilation increases disproportionately to oxygen consumption, primarily to breathe out excess carbon dioxide produced during anaerobic glycolysis.
|Respiratory compensation point (also termed VT2)
||A period of hyperventilation during very intense exercise, mediated by several physiological factors.
||The exercise/training zone between VT1 and VT2 that reflects optimized bicarbonate buffering, which along with hyperpnea, are enough to prevent acidosis. It can be used as a measure of performance in the aerobic-to-anaerobic zone.
Another unique point about the AT is to clarify that while the term “threshold” is commonly used, it may be more accurate to use terms akin to “transition,” as the change from aerobic to anaerobic energy pathways is not binary (i.e., low to high) but occurring via several interrelated stages and simultaneous physiological mechanisms (4). However, it is acknowledged that the threshold does represent a critical point of distinction between aerobic and anaerobic metabolism for changes in blood lactate and ventilation.
PHYSIOLOGICAL BASIS OF AT
The physiological events occurring at the AT are complex and multifactorial. Ventilation, V˙O2, and VCO2 (exhaled carbon dioxide) can be determined from expired gases collected during an incremental lab-based exercise test. These collected gases provide information about the amount of O2 being consumed and CO2 produced in the mitochondria. Regardless, ventilation must closely match not only oxygen consumption but also, more importantly, the CO2 being produced. In addition, although considerable debate has persisted over time as to whether lactate and VTs are interrelated or not (8), the strong relationships and shared physiological mechanisms are indicators that both can be used to determine the AT.
Ultimately, it is the exercise intensity that determines the ventilatory and lactate response. Running at a low exercise intensity will predominantly use oxidative phosphorylation to produce energy, in the form of adenosine triphosphate (ATP); lactate production will be low, and ventilation increases will be linear with O2 consumption. This stage of exercise has been referred to as the aerobic threshold because it encompasses a predominantly aerobic energy component and is a suitable intensity for deconditioned and/or clinical patients. As the running progresses toward moderate-intensity exercise, recruitment of type II muscle fibers increases the active muscle mass, which in turn requires greater ATP production, and the relative contributions of the energy systems begin changing, with anaerobic glycolysis providing some of the ATP. This transition of energy sources results in the accumulation of some lactate, but the clearance rate is enough to prevent an exponential rise in lactate. At moderate intensity, ventilation still closely matches O2 consumption and is enough to expel the greater CO2 produced from the increasing contribution of anaerobic glycolysis.
Once the running progresses to high intensity (e.g., sprinting or encountering a steep hill), the ATP requirement will increase to a rate greater than which can be provided by aerobic energy pathways, and anaerobic glycolysis will become the primary energy source. Once this occurs, there will be a concomitant increase in lactate production, which will exceed muscle–lactate clearance capacity, leading to an exponential rise in blood lactate, that is, the LT (9).
The term maximum lactate steady state is also used to reflect AT and occurs at the stage before the exponential increase in lactate, where lactate production and clearance are optimally balanced (7). At high exercise intensities, the ventilatory response also undergoes changes resulting from an increase in the partial pressure of CO2 (PCO2) and the presence of excess hydrogen (H+) ions. At the tissue level, the increased production of CO2 combines with water (H2O) to form carbonic acid (H2CO3), which is unstable and quickly forms H+ and a bicarbonate ion. The H+ subsequently combines with hemoglobin, allowing for an earlier unloading of O2 to the nearby muscle tissue, also known as the Bohr effect. The hemoglobin also keeps hold of the H+, acting as a buffer to prevent acidosis.
Despite the lay perception that all lactate is bad, one of the mechanisms involved in lactate clearance is the shuttling from fast twitch fibers in active muscles to slow-twitch fibers contained within the same muscle belly, thus enabling the lactate to be used for aerobic metabolism. Similarly, lactate also can be shuttled to the brain, heart, liver, and kidneys to be used in aerobic metabolism (10). Importantly, the shuttling of lactate from anaerobic glycolysis to aid aerobic metabolism illustrates the close overlap of these energy pathways at differing exercise intensities (10), emphasizing the true nature of the “transition” between the two.
The production of exercise metabolites (e.g., CO2 and H+), sometimes called “waste” products, stimulates chemoreceptors in the carotid bodies to signal to the respiratory center in the medulla oblongata to increase ventilation (causing hyperpnea), thus enabling excess CO2 to be breathed out (11). This helps to prevent the buildup of CO2 and H+ and delays the occurrence of metabolic acidosis—a state which quickly causes fatigue. During gas exchange analysis in an exercise testing lab, these physiological processes can be mapped, and this point of deflection has been referred to as AT by some (1) or VT1 by others (4).
A second threshold also can be observed during prolonged exercise and is called VT2 or respiratory compensation point (12). This primarily reflects a period of hyperventilation during very intense exercise. The physiological mechanism relating to the increased ventilation is not clear, as several factors might stimulate this, including a limit for bicarbonate buffering, changes in core body temperature, and responses sent from metaboreceptors and mechanical receptors in the muscle to the respiratory center in the medulla (13). The zone between VT1 and VT2 is often referred to as the isocapnic buffering phase because hyperpnea and bicarbonate buffering are enough to prevent acidosis. As such, it is a good measure of performance in the aerobic to anaerobic zone.
APPLICATION OF THRESHOLDS FOR PERFORMANCE
VT1 and VT2 appear to better discriminate small changes in aerobic capacity between trained and highly trained amateur cyclists, when compared to V˙O2max (14). In particular, while V˙O2max is similar between groups of cyclists, the work that could be sustained at both thresholds differs between groups, with the highest workloads achieved in the highly trained cyclists, likely reflecting their ability to work beyond the zone of isocapnic buffering for long periods of time (14). Studies comparing elite runners with nonelite runners and sedentary individuals reveal that elite runners have longer buffering capacity than nonelites or sedentary controls, indicating that training-based improvements in physiological buffering capacity might explain differences in sustaining high performance in elite sport (15).
The findings are similar for LT, which can predict running performance across a range of distances (e.g., 800 m–3000 m) in female distance runners (16). When using fixed lactate levels of 4.0 mmol·L−1 (defined as OBLA), running velocity at this lactate concentration strongly related to running velocity during a marathon race (17). Further, maximum lactate steady state shows strong relationships with a range of different endurance activities, including 5k and 8k running, as well as 40-km cycling time trial (9).
Practitioners with limited access to an exercise laboratory may use field tests to determine AT. One such test is the functional threshold power (FTP), which reflects the highest power that can be sustained over 60 minutes by a cyclist (18). A less daunting 20-minute test also can be used, as it involves shorter time at maximum intensity. In this test, the athlete uses a bike equipped with a power meter and starts pedaling at the hardest intensity that can be maintained for 20 minutes. Average power can be derived from the power meter, and 5% is then subtracted from the value to obtain the FTP. The FTP number is expressed as watts per kilogram of body mass and equates to maximum lactate steady state. A higher FTP number reveals greater aerobic capacity and can be used to set training zones to improve AT and ultimately endurance performance (18). Other field tests include the 3-minute critical power/speed test, which can be specialized for runners. The test requires maximum effort for 3 minutes, with the average pace (or power if cycling) of the last 30 seconds representing the FTP/AT. GPS devices can be used to log the speed obtained in the last 30 seconds. Finally, in a study of 2,560 individuals, ratings of perceived exertion between 11 and 14 associated with AT (19). This simple tool could be useful to practitioners in a range of clinical and performance environments.
AT is an important determinant of endurance performance, which can be reliably determined using gas exchange analysis and capillary blood lactate measurements. However, the exercise physiologist must develop a sound understanding of the underlying physiology of each threshold to correctly identify when they occur. Both thresholds are useful for developing exercise prescriptions, which help the athlete train in the zone of isocapnic buffering, which subsequently enable adaptations that can increase endurance performance.
1. Wasserman K, McIlroy MB. Detecting the threshold of anaerobic metabolism in cardiac patients during exercise. Am J Cardiol
2. Gladden LB. Lactate metabolism: a new paradigm for the third millennium. J Physiol
. 2004;558(1):5–30. doi: https://doi.org/10.1113/jphysiol.2003.058701
3. Atkinson G, Davison R, Jeukendrup A, Passfield L. Science and cycling: current knowledge and future directions for research. J Sports Sci
. 2003;21:767–87. doi:10.1080/0264041031000102097.
4. Meyer T, Lucía A, Earnest CP, Kindermann W. A conceptual framework for performance diagnosis and training prescription from submaximal gas exchange parameters—theory and application. Int J Sports Med
. 2005;26:S38–48. doi:10.1055/s-2004-830514.
5. Londeree BR. Effect of training on lactate/ventilatory thresholds: a meta-analysis. Med Sci Sports Exerc
. 1997;29(6):837–43. doi:10.1097/00005768-199706000-00016.
6. Jones AM, Vanhatalo A, Doust J. Kinanthropometry and Exercise Physiology Laboratory Manual: Exercise Physiology
. 2009. p. 271–306.
7. Kindermann W, Simon G, Keul J. The significance of the aerobic-anaerobic transition for the determination of work load intensities during endurance training. Eur J Appl Physiol Occup Physiol
. 1979;42:25–34. doi:10.1007/BF00421101.
8. Loat CE, Rhodes EC. Relationship between the lactate and ventilatory thresholds during prolonged exercise. Sport Med
. 1993;15:104–15. doi:10.2165/00007256-199315020-00004.
9. Faude O, Kindermann W, Meyer T. Lactate threshold concepts: How valid are they?Sports Med
. 2009;39(6):469–90. doi:10.2165/00007256-200939060-00003.
10. Brooks GA. Cell-cell and intracellular lactate shuttles. J Physiol
. 2009;587(Pt 23):5591–600. doi:10.1113/jphysiol.2009.178350.
11. Wasserman K, Whipp BJ, Koyal SN, Cleary MG. Effect of carotid body resection on ventilatory and acid–base control during exercise. J Appl Physiol
. 1975;39(3):354–8. doi:10.1152/jappl.1922.214.171.1244.
12. Beaver WL, Wasserman K, Whipp BJ. A new method for detecting anaerobic threshold by gas exchange. J Appl Physiol (1985)
13. Sales MM, Sousa CV, da Silva Aguiar S, et al. An integrative perspective of the anaerobic threshold. Physiol Behav
. 2019;205:29–32. doi:10.1016/j.physbeh.2017.12.015.
14. Lucía A, Pardo J, Durántez A, Hoyos J, Chicharro JL. Physiological differences between professional and elite road cyclists. Int J Sports Med
. 1998;19(5):342–8. doi:10.1055/s-2007-971928.
15. Röcker K, Striegel H, Freund T, Dickhuth HH. Relative functional buffering capacity in 400-meter runners, long-distance runners and untrained individuals. Eur J Appl Physiol Occup Physiol
. 1994;68(5):430–4. doi:10.1007/BF00843741.
16. Yoshida T, Udo M, Iwai K, et al. Significance of the contribution of aerobic and anaerobic components to several distance running performances in female athletes. Eur J Appl Physiol Occup Physiol
. 1990;60(4):249–53. doi:10.1007/BF00379391.
17. Sjödin B, Jacobs I. Onset of blood lactate accumulation and marathon running performance. Int J Sports Med
. 1981;2(1):23–6. doi:10.1055/s-2008-1034579.
19. Scherr J, Wolfarth B, Christle JW, Pressler A, Wagenpfeil S, Halle M. Associations between Borg’s rating of perceived exertion and physiological measures of exercise intensity. Eur J Appl Physiol
. 2013;113(1):147–55. doi:10.1007/s00421-012-2421-x.