Lactic Acid: Friend or Foe?

Dan Vannatta

In the arena of exercise, reference to lactic acid has commonly evoked the most negative of responses. For years, lactic acid has been considered an exercise evil whose presence was believed to induce muscle soreness, fatigue, oxygen debt, and anaerobic threshold. No longer can such an all-encompassing and destructive label be placed on this metabolite. While lactic acid may play a role in fatigue (3, 6), its supposed role in muscle soreness has been disproved (9), and it is now being recognized as more of a positive player in metabolism. George A. Brooks has described lactic acid as a key substance used to provide energy, dispose of dietary carbohydrate, produce blood glucose and liver glycogen, and promote survival in stressful situations (3). This paper briefly describes the metabolic functions of lactic acid and relates the functions to recovery from exercise.

Muscle glycogen is one of the main energy sources for exercise. In order to be utilized, stored muscle glycogen must be broken down into glucose, a process known as glycolysis. During glycolysis, each glucose molecule is cleaved into two pyruvic acid molecules, and energy is released to form adenosine triphosphate (ATP). Normally, the pyruvic acid enters the mitochondria (the principal cell sites where energy is generated) and undergoes the oxidative stage of glycolysis to produce yet more ATP. However, when there is not enough oxygen present for this reaction to take place, the pyruvic acid transforms into lactic acid. From this point, lactic acid can diffuse out of the muscle cell into the blood. It is by this process (known as anaerobic glycolysis) that muscle glycogen can be converted into energy without the presence of oxygen as opposed to ATP production via aerobic glycolysis (6). Such a conversion allows glycolysis to proceed for minutes, when it could otherwise last only seconds (6). Thus, energy is supplied to promote survival in stressful times.

Once sufficient oxygen is restored, the lactic acid produced via anaerobic glycolysis can be utilized for energy or reconverted into glucose by the liver and other tissues (a process known as oxidation). This brings us full circle, and the rest of the metabolic functions as quoted earlier from Brooks have been met. This process also applies to the world of exercise.

In exercise, human bodies use energy for the purpose of muscle contraction. To accomplish this, both aerobic and anaerobic energy-producing systems need to function. Regardless of the system, lactic acid is continuously being formed and removed, even at rest (2). Studies show that during aerobic glycolysis lactate production seems to increase in proportion to our metabolic rate (2, 5). At some point, depending on exercise duration and intensity, a workload will be reached in which lactate concentration is greatly magnified. This is known as the lactate threshold and can usually be elicited between 50-80 percent of a person’s maximal oxygen consumption, VO2max (10). It is at this point in which the rate of lactic acid appearance becomes greater than the rate of disappearance (1, 10). This manifestation will often occur in anaerobic activities such as the 400 meter dash, 100 meter swim, tennis, or soccer (6, 7). What is the significance of this fact?

When lactic acid accumulates in the cell following anaerobic glycolysis, there is potential for problems. It is necessary to maintain the proper degree of acidity in the cell because when acidity increases important contractile and metabolic functions are hindered. In the case that acidity is not regulated, the accumulation of lactic acid may be a factor in fatigue.

Coaches, teachers, and athletes can address both training regimen (including warm down) and diet to successfully combat excessive lactate formation, glycogen depletion, and the consequent fatigue that may result. According to Brooks, “a major goal of training should be to minimize lactic acid production and to enhance lactic acid removal during competition”(5). He suggests a combination of high intensity interval training and prolonged submaximal training. Interval training will help to maximize cardiovascular adaptation and increase VO2max. The more oxygen consumed, the less reliance on the anaerobic breakdown of carbohydrate to lactic acid. Prolonged submaximal training can help to induce muscular adaptations such as increases in capillary and mitochondrial functional capacity. These adaptations will help to reduce lactic acid formation by increased utilization of fatty acids as a mitochondrial fuel source and will facilitate lactic acid removal (5).

Many athletes incorporate a warm down period into their training for the purpose of decreasing blood lactate concentration. In recent times, questions have emerged regarding the benefits of active versus passive recovery. Here, active recovery implies light exercise while passive refers to rest. In a study by Choi et al. (4), this question was addressed. They found that blood lactate levels decreased more rapidly during active recovery than during rest. However, the difference was not found to be very significant. Attention thus focuses on glycogen depletion.

Although active recovery decreased lactic acid levels faster, it may also further deplete the glycogen stores that need replenishment. Therefore, a combination has been suggested whereby active and passive recovery are utilized together to decrease lactic acid levels while promoting maximal glycogen resynthesis (4). In other words, the athlete should warm down until normal rates of breathing return and then rest. At this time, a high carbohydrate meal should be consumed to help replace the glycogen stores, which have been depleted through exercise.

In summary, lactic acid is not a useless metabolic by-product. It can serve as a very important and useful energy source. However, if the lactate threshold is reached during exercise, excessive lactic acid can accumulate, causing fatigue. Fortunately, this negative effect can be partially offset by proper training, warm down, and a high carbohydrate diet.


(1) Brooks, G. A. (1985). Anaerobic threshold: review of the concept and directions for future research. Medicine and Science in Sports and Exercise 17:1, 22-31.
(2) Brooks, G. A. (1986). The lactate shuttle during exercise and recovery. Medicine and Science in Sports and Exercise 18:3, 360-368.
(3) Brooks, G. A. (1988). Blood lactic acid: sports bad boys turns good. Gatorade Sports Science Institute, Sports Science Exchange 1: 2.
(4) Choi, D., Cole, K. J., Goodpaster, B. H., Fink, W. J., & Costill, D. L. (1994) . Effect of passive and active recovery on the resynthisis of muscle glycogen. Medicine and Science in Sports and Exercise 26:8, 992-996.
(5) Donovan, C. M., & Brooks, G. A. (1983). Endurance training affects lactate clearance, not lactate production. American Journal of Physiology 244, E83-E92.
(6) Guyton, A. C. (1991). Metabolism of carbohydrates and formation of adenosine triphosphate. In M. J. Wonsiewicz (Ed.), Textbook of medical physiology (8th ed., pp. 743-752). Philadelphia, PA.: W. B. Saunders and Company.
(7) Guyton, A. C. (1991). Sports physiology. In M. J. Wonsiewicz (Ed.), Textbook of medical physiology (8th ed., pp. 939-949). Philadelphia, PA.: W. B. Saunders and Company.
(8) Lieber, R. L. (1992). Skeletal muscle physiology. In J. P. Butler (Ed.), Skeletal muscle structure and function (pp. 49-108). Baltimore: Williams and Wilkins.
(9) Schwane, J. A., Watrous, B. G., Johnson, S. R., & Armstrong, R. B. (1983). Is lactic acid related to delayed-onset muscle soreness? The Physician and Sportsmedicine 11:3, 124-129.
(10) Stanley, W. C., Gertz, E. W., Wisneski, J. A., Morris, L. D., Neese, R. A., & Brooks, G. A. (1985). Systemic lactate kinetics during graded exercise in man. American Journal of Physiology 249, E595-E602.

Originally published in the Student Newsletter, Health and Wellness, for the Exercise and Movement Science Department in the College of Arts and Sciences at the University of Oregon.