NSCA’s Performance Training Journal: A free publication of the NSCA.
Lactic Acid: Understanding the "Burn" During Exercise
By Travis Triplett-McBride, PhD, CSCS,*D
Everyone has experienced the burning sensation that accompanies intense exercise, such as a fast lap around the track or the last few repetitions of a high-repetition set of leg presses. The cause of this type of discomfort is different from the muscle soreness and tenderness that occurs a couple of days after a hard exercise session. The “burn,” as it is commonly known, is from a build-up of a substance called lactic acid, which is a by-product of the breakdown of carbohydrate sources for energy to perform exercise, a process known as glycolysis.
Glycolysis is the breakdown of glucose from the blood or of glycogen, a stored form of glucose, from the muscle and liver. The purpose of glycolysis is to supply energy for the body’s cells to operate. The process of glycolysis involves several enzymes that control a series of chemical reactions. Along the way there are various by-products that are either used as energy, used in other chemical reactions, or are excreted as waste3.
The process of glycolysis may advance at different rates, labeled fast glycolysis and slow glycolysis. The end-product of fast glycolysis is a substance called pyruvic acid, which is converted to lactic acid when pyruvic acid starts to accumulate. This pace of glycolysis provides energy for the cells at a faster rate compared with slow glycolysis, in which pyruvic acid is transported to another part of the cell for energy production through the oxidative, or aerobic system. The outcome of the end products is controlled by the energy demands within the cell. If energy needs to be supplied very quickly, such as during sprinting or heavy resistance training, fast glycolysis is primarily used. If the energy demand is not as high and there is enough oxygen is present in the cells, slow glycolysis is primarily used3.
Fast glycolysis also occurs during the very beginning of exercise or later in an exercise session when exercise intensity is high enough that the oxidative system cannot keep pace with the muscular demands for energy. Muscular fatigue experienced during exercise is often associated with high concentrations of lactic acid in the muscle6. Lactic acid accumulates when the body cannot clear it out of the muscle and other tissues quickly enough. The problem with lactic acid accumulation is that there is a corresponding increase in hydrogen ion concentration. High concentrations of hydrogen ions are believed to inhibit the reactions of glycolysis and to directly interfere with muscle contraction9. Also, the decrease in pH levels from the increased hydrogen ion concentration, which makes the muscle cell environment more acidic, inhibits the activity of other enzymes of the cells. The overall effect is a decrease in available energy and the force of muscle contraction during exercise6.
The terms lactic acid and lactate are often used interchangeably, but this is not entirely correct. Lactic acid is eventually converted to the salt form lactate, by buffering systems in the muscle and blood. Unlike lactic acid in the muscle, lactate is not believed to be a fatigue-producing substance2. Instead, lactate is often used indirectly as an energy source itself, especially in slow twitch skeletal and cardiac muscle fibers1. It is also used to form glucose by combining lactate and other non-carbohydrate sources, which occurs during prolonged exercise and during recovery2. However, blood lactate concentrations do reflect lactic acid production and clearance. It is difficult to measure muscle lactic acid levels but it is very simple to measure lactate levels in the blood. The clearance of lactate from the blood is an indicator of a person’s ability to recover from exercise. Lactate can be cleared by breakdown within the muscle fiber in which it was produced, or it can be transported in the blood to other muscle fibers to be broken down. Lactate can also be transported in the blood to the liver, where it is converted to glucose and is often stored as glycogen2. (See Figure 1).
Normally there is a low concentration of lactate in blood and muscle. The normal range of lactate concentration in the blood is 0.5 to 2.2 mmol/L at rest5. As previously mentioned, lactic acid production increases with increasing exercise intensity. However, lactic acid production is also related to muscle fiber type. The faster-contracting muscle fibers, also labeled fast-glycolytic (FG) and fast oxidative-glycolytic (FOG), show a higher rate of lactic acid production. This is mainly due to the fact that these muscle fibers are preferentially called upon for intense physical activity requiring a large amount of strength, power, and speed. In addition, the FG and FOG muscle fibers generally reflect a higher concentration or activity of glycolytic enzymes than that of the SO, or slow oxidative, muscle fibers1. Although the highest possible concentration of lactate accumulation is not known, complete fatigue can occur at blood concentrations between 20 and 25 mmol/L. The highest reported concentration of blood lactate is >30 mmol/L, which was measured after multiple bouts of dynamic exercise6. Along with exercise intensity and muscle fiber type, exercise duration, level of training, and initial glycogen levels can also influence lactate accumulation. For example, lactate tends to build up more with longer duration exercise, in untrained individuals, and when the muscle has high initial glycogen levels5.
Blood lactate accumulation is greater following high-intensity, intermittent exercise (e.g., resistance training and sprints) than following lower-intensity, continuous exercise, where it does not accumulate until >55% VO2 max6. Most studies have reported the highest blood lactate concentrations after maximal bouts of anaerobic exercise (1 – 3 min). One investigation8 observed that multiple sets of the squat exercise to failure with increases in resistance resulted in higher blood lactate concentrations in trained individuals than in untrained individuals, because the time to failure and total work accomplished were greater in trained people than in untrained people. However, trained people experienced lower blood lactate concentrations than untrained people when exercising at the same absolute workload (the same resistance)(see Figure 2). This indicates that resistance training results in alterations in the lactate response similar to those from higher-intensity aerobic training5. These alterations include a lower blood lactate concentration at a given workload in trained individuals and higher blood lactate concentrations in trained individuals during maximal exercise7.
Most studies have reported that blood lactate concentrations return to pre-exercise values within an hour after the exercise session is over. Light activity, known as an active recovery, during the post-exercise period has also been shown to increase blood lactate clearance rates, and aerobically trained and anaerobically trained individuals also have faster lactate clearance rates than untrained people5. Peak blood lactate concentrations occur approximately five minutes after the cessation of exercise, mainly due to the time required to buffer and transport lactic acid from the tissue into the blood5.
The point of build-up, or lactate threshold, is used as an estimate of anaerobic effort in exercise. This is because anaerobic systems increase energy production when exercise intensity increases past the point where the body can supply the needed energy oxidatively. The lactate threshold is marked by a significant increase in blood lactate, but can be inaccurate because the measured blood levels also may be from reduced clearance, not just increased production. To try and account for this, an arbitrary value of 4 mmol/L is commonly used and is known is the onset of blood lactate accumulation (OBLA). The lactate threshold is used more to determine at what percent of max VO2 the threshold occurs since it usually occurs in trained individuals at 70 – 80% of max VO2 and at 50 – 60% of max VO2 in untrained individuals. It is beneficial to increase the lactate threshold, which means one can exercise longer at a given intensity before lactate accumulation (from the corresponding lactic acid buildup) occurs and fatigue sets in4. (See Figure 3).
Training to Improve Your Lactic Acid Tolerance
Any athlete who needs to be able to maintain a high level of intensity for 1 – 3 minutes can benefit from training specifically designed to increase the lactate threshold. Improving lactic acid tolerance and the lactate threshold is generally best accomplished by interval training. Intervals should typically be in-line with the event that one is training for, although some workouts can consist of longer or shorter intervals to focus more on pure speed or speed-endurance, for example. Intervals that are approximately 30 seconds to 1.5 minutes in duration will focus more on fast glycolysis while intervals of 1.5 to 3 minutes in duration will focus more on slow glycolysis, although fast glycolysis is still a major part of the effort. The rest periods between the intervals should be approximately 2 minutes for the shorter intervals and 3 – 6 minutes for the longer intervals if the intervals are performed at maximal effort. Coaches sometimes choose to shorten the rest period so that full recovery is not achieved even though this means not being able to perform every interval at top pace. This is dependent on the goal of that training session and where the athlete is in the training year. Intervals are usually set up so that a certain total distance is covered, i.e. 8 x 400 m intervals for a total of approximately 2 miles. Interval training is a great alternative to long, slow distance training where VO2 is not diminished yet lactic acid tolerance can be improved, which will potentially result in a better athlete.
Figures
About the Author
Travis Triplett-McBride, PhD, CSCS,*D, is currently the Director of the Neuromuscular Laboratory and the Strength and Conditioning Concentrations for the BS and MS degrees in Exercise Science at Appalachian State University. After receiving a BS in Health and Sport Science from Wake Forest and an MS in Exercise Science from Appalachian State, Dr. McBride completed a research assistantship in Sports Physiology at the Olympic Training Center in Colorado Springs. Dr. McBride then completed her PhD in Physiology of Exercise at Penn State and a postdoctoral research fellowship at Southern Cross University in Australia. Dr. McBride is an associate editor for the Journal of Strength and Conditioning Research, and is on a NASA review board for developing resistance exercise countermeasures to micro-gravity for the International Space Station.
References
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- Davis JA, Frank MH, Whipp BJ, Wasserman K. (1979). Anaerobic threshold alterations caused by endurance training in middle-aged men. Journal of Applied Physiology, 46: 1039 – 1046.
- Gollnick PD, Bayly WM, Hodgson DR. (1986). Exercise intensity, training, diet, and lactate concentration in muscle and blood. Medicine and Science in Sports and Exercise, 18: 334 – 340.
- Hermansen L, Stenvold I. (1972). Production and removal of lactate in man. Acta Physiologica Scandinavica, 86: 191 – 201.
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- Tesch P. (1980). Muscle fatigue in man, with special reference to lactate accumulation during short intense exercise. Acta Physiologica Scandinavica, 480: 1 – 40.
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Figures
1Lactate can be transported in the blood to the liver, where it is converted to glucose and is often stored as glycogen.
2A generalized graph showing the relationship of blood lactate to exercise intensity in trained and untrained individuals.
3A generalized graph showing the relationship of blood lactate to oxygen consumption before and after a training program designed to increase lactate threshold.
