The Body in Swimming: The Dogma of Lactic acid

While watching the recent Scottish National Open Championships 2014, held at Tolcross, I couldn’t help but notice the continued use of ‘lactic acid’ testing inflicted on a large number of swimmers immediately after their race. The procedure, used in most national and international competitions, involves a small extraction of blood from, usually, the athlete’s ear. The concentration of the ‘acid’ present in the blood is then calculated using the testing equipment. The results are used to show the ‘anaerobic capacity’ of the swimmer as the acid build up indicates the body’s use of muscles in the absence of oxygen. Well, that’s the belief anyway.

The truth is, there is an enormous amount of misunderstanding and gross overestimation surrounding the area of lactic acid, and it’s testing – starting with the name! Those who refer to lactic acid as the chemical present in your bloodstream have already blundered, it is, in fact, the substance ‘lactate’ which is present in your blood and which is tested for in ‘lactic acid concentration tests’ described above. Lactic acid ‘splits’ into lactate and hydrogen which then enters the blood. The misconceptions go far beyond this, however.

Lactate testing is used to determine the anaerobic capacity of an athlete, as it is believed that increases in lactate correlate with muscles which are working without oxygen. Thus, the higher the levels, the greater the anaerobic capacity of an athlete. Well, the first point to highlight is that lactic acid is not only produced in the working muscles – the liver is a major contributor as well as other tissues such as the skin and intestines. Brooks, et al. (1992), stated, “Lactate measures cannot be inferred to indicate only exercise production”. Another point to note is lactate production is also observed in both fully aerobic tissue – such as the heart, and oxygenated muscles. Lactate production in the muscles merely provides information that an athlete has ‘worked’ at a particular intensity – full stop.

While watching the recent Scottish National Open Championships 2014, held at Tolcross, I couldn’t help but notice the continued use of ‘lactic acid’ testing inflicted on a large number of swimmers immediately after their race. The procedure, used in most national and international competitions, involves a small extraction of blood from, usually, the athlete’s ear. The concentration of the ‘acid’ present in the blood is then calculated using the testing equipment. The results are used to show the ‘anaerobic capacity’ of the swimmer as the acid build up indicates the body’s use of muscles in the absence of oxygen. Well, that’s the belief anyway.

The truth is, there is an enormous amount of misunderstanding and gross overestimation surrounding the area of lactic acid, and it’s testing – starting with the name! Those who refer to lactic acid as the chemical present in your bloodstream have already blundered, it is, in fact, the substance ‘lactate’ which is present in your blood and which is tested for in ‘lactic acid concentration tests’ described above. Lactic acid ‘splits’ into lactate and hydrogen which then enters the blood. The misconceptions go far beyond this, however.

Lactate testing is used to determine the anaerobic capacity of an athlete, as it is believed that increases in lactate correlate with muscles which are working without oxygen. Thus, the higher the levels, the greater the anaerobic capacity of an athlete. Well, the first point to highlight is that lactic acid is not only produced in the working muscles – the liver is a major contributor as well as other tissues such as the skin and intestines. Brooks, et al. (1992), stated, “Lactate measures cannot be inferred to indicate only exercise production”. Another point to note is lactate production is also observed in both fully aerobic tissue – such as the heart, and oxygenated muscles. Lactate production in the muscles merely provides information that an athlete has ‘worked’ at a particular intensity – full stop.

Lactate – the root of all evil…or is it?

Often heard from the mouths of swimmers and other beings who participate in sport are sentences such as, “Ow! My muscles are rather sore today, I must have built up a lot of acid,” or, “Thanks to that darn lactic acid, I can barely move” (or something to that effect). An overwhelming number of coaches will reinforce this blame; however, lactic acid/lactate is in fact, not guilty.

It is a common belief that fatigue, muscle soreness and stiffness are caused by a high accumulation of lactate in the blood which has not cleared, or that the lactate has somehow ‘acidified’ the blood. With regards to fatigue, lactate in the blood does completely the opposite to what is often thought. Lactate prevents the effects of fatigue and is even a useful source of energy in the body. Lactate is converted in two ways, either, into glucose – which will be stored in the liver, or as carbon dioxide and water. The latter two both remove hydrogen (ions) from the blood – hydrogen is a contributor to acidosis and, as a result, fatigue can occur (other factors also contribute). Thus, the presence of lactate can help offset the effects of fatigue in an athlete. Lactate can also remain in the cells it has been produced and be used as fuel. Miller, B. (2002), has shown that lactate can be the preferred source of energy over glucose in cells.

With regards to muscle soreness and that stiff feeling felt by many, this is the result of muscle cell damage due to a level of intensity not usually endured by the athlete. It can also occur when the muscle fibres have been used in an unfamiliar way – likely with a heavier than normal load.

A.T. – Anaerobic threshold or a total waste of time

If you are a swimming coach or athlete, it is highly likely you’ve heard of, or swum an anaerobic threshold set; or indeed you may have written one up for your swimmers. Firstly, what is the anaerobic threshold? The standard explanation is, as the swimmer’s velocity increases, a point or threshold is reached whereby the muscles no longer have a sufficient oxygen supply and the body’s supplies, which can provide energy in the absence of oxygen, are employed – this leads to a spike in lactate. A simpler explanation of the threshold is the point at which the body can no longer equal lactate production with lactate removal, thus, causing an accumulation of lactate.

If you’ve been following the format of this post, you’ll know what is coming next.

The above is an erroneous explanation of what takes place. The muscles, to begin with, do not become anaerobic for any more than a few seconds (otherwise, you would die). The accumulation of lactate is a result of factors such as glycolytic rate and other metabolic ‘coping’ responses – rather than as a result of anaerobic conditions. Also, the use of the word threshold is inappropriate. The process is gradual; it doesn’t suddenly spike as suggested. In training, anaerobic threshold training is conducted so that a swimmer will be able to maintain, for longer, the period in which the body can balance lactate production with its removal. I have already covered why there is no justification for this type of training. Furthermore, even if the emphasis was moved to using anaerobic threshold training to directly improve fitness (VO2 max) as it tends to be faster than normal aerobic paces, we know that intensities above “anaerobic threshold” are only effective in improving VO2 max. The latter has been shown to have very little to do with race performances. In short, anaerobic threshold training is a waste of time!

In closing, huge amounts of dogma exist in the world of lactate, and it’s testing. The best an analysis of a swimmer’s anaerobic threshold (or lactate threshold) can achieve is, to inform the athlete, or whoever is concerned, that their physiology has ‘changed’. This is perhaps useful when observing someone who wishes to move from an untrained state to one which is trained. Thereafter, a change (caused by training) may be evident, but what has that got to do with swimming performances? Nothing. Certainly not for those swimming in-pool competitive events. Hopefully, this article will prevent a couple of coaches from straying toward an erroneous belief-based practice and can now better spend their time on evidence-based training. At the very least I hope this will stop just one coach/swimmer/parent from explaining a ‘bad’ performance was on account of lactate, or worse – lactic acid!

Yours in Swimming,

SwimCoachStu

References:

Brooks, G. A., Wolfel, E. E., Groves, B. M., Bender, P. R., Butterfield, G. E., Cymerman, A., Mazzeo, R. S., Sutton, J. R., Wolfe, R. R., & Reeves, J. T. (1992). Muscle accounts for glucose disposal but not blood lactate appearance during exercise after acclimatization to 4,300 m. Journal of Applied Physiology, 72, 2435-2445.

Miller, B. F., J. A. Fattor, K. A. Jacobs, M. A. Horning, F. Navazio, M. I. Lindinger, and G. A. Brooks. (2002) Lactate and glucose interactions during rest and exercise in men: effect of exogenous lactate infusion. J Physiol. 544, 963-975.

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