Lactic Acid and Exercise Performance: Friend or Foe?

Among athletes and exercisers alike there is a distinct belief that lactic acid is the cause of fatigue within working skeletal muscle. However, this is simply a convenient explanation for a complicated sequence of biochemical processes. Blood lactate is not the cause of fatigue, in fact it can be used as a highly efficient and useful energy source¹ – and this is why.

In order to understand blood lactate and how it behaves, a basic understanding of exercise metabolism is firstly required. The body utilizes three metabolic pathways to serve energy to the active muscles during exercise, each pathway converts a certain chemical or macronutrient substrate into ATP. ATP is regarded as a high-energy phosphagen that enables the contraction of skeletal muscle fibres.

Immediate energy, as soon as any physical activity commences, is provided by the ATP-PCr (phosphocreatine) system. It has the ability to provide immediate energy since very few reactions and enzymes are involved in the pathway, this is of great advantage to high intensity, explosive sports such as weight lifting and shot put. However, the body only stores 15 mmol of the pathway’s substrate (phosphocreatine) within each kilogram of skeletal muscle. As a consequence, during intense exercise intramuscular stored glycogen must provide the means to resynthesize ATP in the second of the metabolic pathways, anaerobic glycolysis. This pathway also has the ability to rapidly produce ATP due to only a few short steps being necessary. Yet, it is this anaerobic production of ATP via glycolysis (glucose breakdown) that leads to the formation of lactate and hydrogen ions. Although these two products result from the same reaction to give lactic acid, they dissociate very quickly and so it is highly unlikely any lactic acid will be found in the blood.

It is in the last of our metabolic systems that lactate realises its full potential. Lactate has the ability to circulate from the fast twitch muscle fibres where it is produced, to the slow switch muscle fibres where it undergoes conversion into the compound pyruvate during aerobic energy metabolism. Pyruvate then undergoes conversion into acetylCoA and enters the Krebs cycle, a cyclical chain of reactions whereby aerobic ATP production takes place. Skeletal muscles oxidize much of the lactate they produce before it is even released into the blood, meaning that a capacity to generate increased lactate levels enhances maximal power output.

Alternatively, the liver possesses the ability to accept skeletal muscle born lactate for synthesis into glucose via the Cori Cycle. This lactate derived glucose can either return to the blood for energy metabolism within active skeletal muscle or it can be synthesized into glycogen for storage and future energy use by the liver. These uses of lactate make it a valuable source of energy for skeletal and cardiac muscle, whilst also being a fundamental contributor to the making of glucose within the liver². The picture below illustrates the relationship between lactate and energy production. 

Since lactic acid is in fact a myth in the domain of sport and exercise and since lactate can be used as an energy substrate, it is the presence of hydrogen ions (H⁺) that are responsible for muscle fatigue during intense bouts of physical activity.  H⁺ ions that result from anaerobic glycolysis lower the intracellular pH within the muscle, increasing acidity and interfering with muscle contractions. This increased acidity denatures various metabolic enzymes that are key to energy transfer and reduces skeletal muscles contractility due to the progressive loss of intracellular potassium³.

While the notion of lactic acid is easily relatable to athletes and exercisers, its presence has hindered the knowledge we now have regarding skeletal muscle fatigue for the last two decades. So to summarise, appreciable amounts of lactic acid are not found in the blood and so is not the direct cause of skeletal muscle fatigue. It is in fact a valued and necessary source of energy, whilst also being fundamental in the biochemical process of gluconeogenesis⁴.

References

1.  Brooks G. A, 1986. The lactate shuttle during exercise and recovery. Medicine and Science in Sports and Exercise. 18, p. 360-368.
2. Consoli et al, 1990. Contribution of liver and skeletal muscle to alanine and lactate metabolism in humans. American Journal of Physiology. 259, p. 677-684.
3. Nielsen et al, 2004. Effects of high-intensity intermittent training on potassium kinetics and performance in human skeletal muscle. Journal of Physiology. 554, p. 857-870. 
4. Miller et al, 2002. Metabolic and cardiorespiratory responses to "the lactate clamp". American Journal of Physiology – Endocrinology and Metabolism. 283, p. 889-898.