Lactic Acid

The expression "lactic acid" is commonly used by athletes to describe the intense pain felt during exhaustive exercise, especially in events like 400 metres and 800 metres. When energy is required to perform an exercise, it is supplied by Adenosine Triphosphate's breakdown (ATP). The body has a limited store of about 85grms of ATP and would use it up very quickly if we did not have ways of resynthesising. Three systems produce energy to resynthesise ATP: ATP-PC, lactic acid and aerobic.

The lactic acid system can release energy to resynthesize ATP without oxygen, which is called anaerobic glycolysis. Glycolysis (the breakdown of carbohydrates) results in pyruvic acid and hydrogen ions (H+). The pyruvic acid molecules undergo oxidation in the mitochondrion, and the Krebs cycle begins. A build-up of H+ will make the muscle cells acidic and interfere with their operation so carrier molecules, called nicotinamide adenine dinucleotide (NAD+), remove the H+. The NAD+ is reduced to NADH that deposits the H+ at the electron transport gate (ETC) in the mitochondria to be combined with oxygen to form water (H2O). Check out this quick difference between nad vs nadh to understand these terms better.

If there is insufficient oxygen, NADH cannot release the H+, building up in the cell. To prevent the rise in acidity, pyruvic acid accepts H+ forming the lactic acid that dissociates into lactate and H+. Some lactate diffuses into the bloodstream and takes some H+ to reduce the H+ concentration in the muscle cell. The muscle cell's normal pH is 7.1, but if the build-up of H+ continues and pH is reduced to around 6.5, muscle contraction may be impaired, and the low pH will stimulate the free nerve endings in the muscle, resulting in the perception of pain (the burn). This point is often measured as the lactic or anaerobic threshold (AT) or onset of blood lactate accumulation (OBLA).

The process of lactic acid removal takes approximately one hour, but this can be accelerated by undertaking an appropriate cool-down that ensures a rapid and continuous supply of oxygen to the muscles.

Astrand et al. (1986)^[1] found that the usual amount of lactic acid circulating in the blood is about 1 to 2 millimoles/litre. The onset of blood lactate accumulation (OBLA) occurs between 2 and 4 millimoles/litre of blood. In non-athletes, this point is about 50% to 60% VO₂ max, and in trained athletes, around 70% to 80% VO₂ max.

Lactic acid - friend or foe?

Lactic acid (lactate) is not:

responsible for the burn in the leg muscles when exercising very fast
responsible for the soreness you experience in the 48 hours following a hard session
a waste product

Lactate, produced by the body all day long, is resynthesized by the liver (Cori Cycle) to form glucose that provides you with more energy.

Lactate Shuttle

Some of the lactate we produce is released into the bloodstream and used directly as fuel by the heart, muscle and liver to make blood glucose and glycogen (Cori Cycle).

The lactate shuttle involves the following series of events:

As we exercise, pyruvate is formed
When insufficient oxygen is available to break down the pyruvate, then lactate is produced
Lactate enters the surrounding muscle cells, tissue and blood
The muscle cells and tissues receiving the lactate either breakdown the lactate to fuel (ATP) for immediate use or use it in the creation of glycogen
The glycogen then remains in the cells until energy is required

65% of lactic acid is converted to carbon dioxide and water, 20% into glycogen, 10% into Protein and 5% into glucose. (Wesson et al. (2004)^[5] p.79)

It has been estimated that about 50% of the lactate produced during intense exercise is used by muscles to form glycogen which acts as a metabolic fuel to sustain exercise.

Krebs Cycle

The Krebs cycle is a series of reactions that occur in the mitochondria and results in ATP formation. The pyruvic acid molecules from glycolysis undergo oxidation in the mitochondrion to produce acetyl coenzyme A, and the Krebs cycle begins.

Three significant events occur during the Krebs cycle. One guanosine triphosphate (GTP) is produced which donates a phosphate group to ADP to form one ATP; three molecules of Nicotinamide adenine dinucleotide (NAD) and one molecule of flavin adenine dinucleotide (FAD) are reduced. Although one molecule of GTP leads to the production of one ATP, the reduced NAD and FAD production are far more significant in the cell's energy-generating process because they donate their electrons to an electron transport system that generates large amounts ATP.

Cori Cycle

The Cori cycle refers to the metabolic pathway in which lactate produced by anaerobic glycolysis in the muscles moves via the bloodstream to the liver, converted to blood glucose and glycogen.

Hydrogen ions

The breakdown of glucose or glycogen produces lactate and hydrogen ions (H+) - for each lactate molecule, one hydrogen ion is formed. The presence of hydrogen ions, not lactate, makes the muscle acidic, eventually stopping muscle function. As hydrogen ion concentrations increase, the blood and muscle become acidic. This acidic environment will slow down enzyme activity, and ultimately the breakdown of glucose itself. Acidic muscles will aggravate associated nerve endings causing pain and increase irritation of the central nervous system. The athlete may become disorientated and feel nauseous.

Aerobic Capacity

Given that high levels of lactate/hydrogen ions will be detrimental to performance, one of the critical reasons for endurance training is to enable the body to perform at a higher pace with minimal lactate. It can be done by long steady runs, which will develop the aerobic capacity using capillarisation (forming more small blood vessels, thus enhancing oxygen transport to the muscles) and creating greater efficiency in the heart and lungs. If the aerobic capacity is more significant, more oxygen will be available to the working muscles, which should delay the onset of lactic acid at a given work intensity.

Anaerobic Threshold

Lactic acid starts accumulating in the muscles once you operate above your anaerobic threshold. It is usually between 80% and 90% of your maximum heart rate (HR_max) in trained athletes.

What a low Lactate Threshold means

If your lactate threshold (LT) is reached at low exercise intensity, it often means that the "oxidative energy systems" in your muscles are not working very well. If they perform at a high level, they will use oxygen to break lactate down to carbon dioxide and water, preventing lactate from pouring into the blood. If your LT is low, it may mean that:

you are not getting enough oxygen inside your muscle cells
you do not have adequate concentrations of the enzymes necessary to oxidize pyruvate at high rates
you do not have enough mitochondria in your muscle cells
your muscles, heart, and other tissues are not very good at extracting lactate from the blood

Improving your Lactate Threshold

The aim is to saturate the muscles in lactic acid to educate the body's buffering mechanism (alkaline) to deal with it more effectively. The accumulation of lactate in working skeletal muscles is associated with this system's fatigue after 50 to 60 seconds of maximal effort. Sessions should comprise one to five repetitions (depending on the athlete's ability) near full recovery.

Training continuously at about 85 to 90% of your maximum heart rate for 20 to 25 minutes will improve your Lactate Threshold (LT).

A session should be conducted weekly and eight weeks before a major competition. It will help the muscle cells retain their alkaline buffering ability. Improving your LT will also enhance your tlimvVO₂ max.

Lactate Tolerance Training Sessions

The following table identifies some possible training sessions that can be used to improve your lactate tolerance:

Distance	Pace	Recovery	Sets x Reps
150 metres	400 metres	90 seconds	3 x 3
300 metres	800 metres	2 minutes	6
150 metres	800 metres	45 seconds	12
150 metres	800 metres	20 seconds	2 x 4
300 metres	1000 metres	90 seconds	9

Sodium Bicarbonate

Energy production via anaerobic glycolysis, particularly essential for events lasting between 30 seconds and 15 minutes, increases the muscle cells' acidity. Soon after, it does the same to the blood. This increase in acidity within the muscle cells is a significant factor in producing fatigue. If there was some way to reduce the acidity within the muscle cells, one could theoretically delay fatigue and continue exercising at a very high intensity for longer.

Sodium bicarbonate is an alkalising agent and therefore reduces the acidity of the blood (known as a buffering action). By buffering acidity in the blood, bicarbonate may draw more of the acid produced within the muscle cells out into the blood and thus reduce acidity within the muscle cells themselves. This could delay the onset of fatigue.

Who might benefit?

The specific athletes who might benefit from bicarb supplementation will typically compete in events that last between one and seven minutes, i.e. 400 metres to 1500 metres running, 100 metres to 400 metres swimming and most rowing competitions.

Van Montfoort et al. (2004)^[2] researched 15 competitive male endurance athletes who performed a run to exhaustion 90 minutes after ingestion of a sodium agent. The mean run times to exhaustion were as follows:

Sodium Bicarbonate - 82.3 seconds
Sodium Lactate - 80.2 seconds
Sodium Citrate - 78.2 seconds
Sodium Chloride - 77.4 seconds

The results suggest that sodium bicarbonate supplementation may be beneficial.

A practical approach

Before using bicarbonate, check with your sport's governing body that the substance is not contrary to doping regulations.

It is essential to experiment with the supplement during training, and Williams (1996)^[4] suggests the following procedure, repeated several times, to determine if bicarbonate supplementation is appropriate for you:

two days of light training
perform a time trial
two days of light training
repeat the time trial in a similar environment after bicarbonate supplementation

The bicarbonate supplementation protocol would be to ingest 0.3grms of sodium bicarbonate per kg body weight approximately one to two hours before the time trial. e.g. for a 66kg runner, consume 20grms of sodium bicarbonate (about four teaspoons).

Side effects

The side effects may be a pain, cramping, diarrhoea or a feeling of being bloated. Drinking up to a litre of water with supplementation is often helpful and should be carried out as standard. Breaking the bicarbonate dose into four equal portions and taking over an hour may also help.

There are potential side effects of taking higher than normal levels of Sodium Bicarbonate, so consult with your doctor first.

Does massage help remove lactic acid?

A study by McMurray (1987)^[3] compared the effects of massage, passive recovery, and mild bicycle riding (about 40% of max oxygen uptake) on lactate metabolism after an exhaustive treadmill run.

The subjects were trained runners who performed a maximal treadmill run to elevate blood lactate levels and induce exhaustion after 4-6 minutes. Researchers sampled the subjects' blood lactate for up to 20 minutes after exercise. They found that passive recovery (lying down supine) and massage did not affect blood lactate levels. At the same time, mild bicycle riding caused a better removal of blood lactate 15-20 minutes after exhaustive exercise.

This does not suggest that massage is of no benefit to athletes; it means that massage does not help remove lactic acid.

References

ASTRAND, P.O. et al. (1986) Disposal of Lactate during and after Strenuous Exercise in Humans. Journal of Applied Physiology, 61(1), p. 338-343
VAN MONTFOORT, M.C.E. et al. (2004) Effects of Ingestion of Bicarbonate, Citrate, Lactate, and Chloride on Sprint Running. Med Sci Sports Exerc, 36 (7), p. 1239-1243
McMURRAY, A.M. (1987) The effect of massage on blood lactate levels following a maximal treadmill run. Thesis (M.A.) University of Northern Iowa
WILLIAMS, A. (1996) Research suggests it may boost performance in short events, but it can have nauseating side effects. Peak Performance, 73, p. 6-7
WESSON, K. et al. (2004) Sport and PE. Great Britain, Hodder & Stoughton Educational

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