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
- Brooks G. A, 1986. The lactate shuttle during exercise and recovery. Medicine and Science in Sports and Exercise. 18, p. 360-368.
- 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.
- 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.
- Miller et al, 2002. Metabolic and cardiorespiratory responses to "the lactate clamp". American Journal of Physiology – Endocrinology and Metabolism. 283, p. 889-898.
