Brooks, G. A. (1991). Current concepts in lactate exchange. Medicine and Science in Sports and Exercise, 23, 895-906.

Coaches and many sport scientists consider lactate as a representation of oxygen-limited metabolism (anaerobic glycolysis) during exercise. Recent research has shown this to be too simplistic. The formation, exchange, and utilization of lactic acid (lactate) represents an important means of distributing carbohydrate (CHO) energy sources after a carbohydrate meal and during sustained physical exercise. Lactate is now viewed as being a beneficial intermediary metabolite between CHO storage forms (glucose and glycogen) and metabolic end products (CO2 and H2O). The advantage of lactate as an intermediary is that it exchanges rapidly between tissue compartments.

Skeletal muscle, once considered to be the major site of lactate formation, in some circumstances is responsible for significant net lactate removal from the blood. The liver, once thought to be a primary site of lactate removal through its role in the Cori cycle, can contribute in a major way to a rise in arterial lactate, particularly at the onset of strenuous exercise. During exercise, lactate is the predominant fuel for the heart. Other tissues and organs (e.g., skin, intestines) are also involved in blood lactate kinematics during exercise.

Lactate can be formed in fully aerobic tissue, such as the heart, and used within those same tissues.

The finding that lactate can be formed in and released from diverse tissues such as skeletal muscle, liver, and skin under resting conditions of CHO loading and epinephrine stimulation, counters the long-held belief that lactate is formed as the result of oxygen-limited metabolism. There is a lack of evidence that a limitation of oxygen supply causes lactate production, but much evidence to show that it is formed in circumstances of adequate oxygen supply. Factors of substrate supply and mass action are responsible for lactate formation.

Contracting skeletal muscle is not the only contributor to the rise in arterial lactate during exercise. Emotional stimulation, which leads to the release of epinephrine, causes a notable increase in arterial lactate (release from muscles). At high work rates, epinephrine infusion leads to a pattern of accumulation suggesting threshold level.

Arterial blood lactate levels are highly correlated with epinephrine levels. The blood lactate inflection point in graded exercise coincides with the epinephrine inflection point. Moderate exercise intensities result in almost no increase in catecholamine levels (epinephrine and norepinephrine). But beyond 50-70% VO2max, catecholamine levels rise disproportionately. Thus, lactate accumulation largely results from the level of effort and associated hormonal release not oxygen deprivation.

Lactate production has been found in fully oxygenated muscles. Thus, muscle lactate level may not always be a suitable indicator of lack of oxygen (anaerobic work).

Net lactate output from contracting muscle is related to the intensity of stimulation. During prolonged steady-state conditions, contracting muscles can take up lactate on a net basis, especially in the arterial lactate concentration is elevated. Even under conditions of reduced oxygen supply, lactate is increased even if muscle oxygen consumption (VO2) is maintained. That is why lactate is a poor indicator of a lack of oxygen.

During continuous exercise at submaximal levels, lactate rises at first and then declines towards resting levels. When lactate is maintained at an elevated level, it cannot be explained on the basis of net lactate release from the exercising limbs. Exercising muscles can contribute to circulating lactate but active muscle is not the sole contributor to blood lactate concentrations. Exercising skeletal muscle is capable of simultaneously producing and removing lactate. Thus, lactate concentrations cannot be used to quantify lactate production.

1. Approximately one-half of lactate formed during rest is removed through oxidation.
2. The turnover rate of lactate increases during exercise as compared to rest even if there is only a minor change in blood lactate concentration.
3. The fraction of lactate disposed of through oxidation increases to approximately three-quarters during exercise.
4. A minor fraction (one-tenth to one-quarter) of lactate removed during exercise is converted to glucose via the Cori cycle.
5. Lactate concentration measurements offer little information about the rates of blood lactate appearance.
6. Training reduces arterial lactate concentration during exercise mainly by increasing the clearance rate.
7. Improved clearance rates are specific to the exercise of training. Clearance enhancements do not transfer to non-trained activities.
8. During moderate-intensity exercise, lactate turnover ("flux") exceeds glucose turnover. Greater lactate appearance than glucose disappearance is possible because exercise causes a large increase in the rate of muscle glycogenolysis (conversion of glycogen to glucose).

The formation of lactate from endogenous (glycogen) as well as exogenous (dietary) carbohydrates represents a major means by which intermediary metabolism in diverse tissues and cells can be coordinated. The concept of lactate being the by-product of muscle activity under oxygen deprivation is inadequate and largely untrue.

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