Miller JZHere’s the first installment of Dr Miller’s Q&A column, Adaptions. If you have any physiology, performance, or nutrition related questions, email Ben at



Dr. Miller,

We often hear riders and coaches talk about Lactic Acid.  I’ve heard pro riders say they spin their legs out the day after a hard race or workout session to “clear the lactic acid” out of their legs.  I heard a coach say that post workout soreness is due to Lactic Acid buildup in the muscles.   I heard another coach say it isn’t actually “acid” at all and that it is a necessary energy source for anaerobic efforts.  I’ve done some reading and research about Lactic Acid and though much of it over my head, what I think I understand makes most of what I hear sound like nonsense but I’m not really sure what to believe or if it even really matters.

Would you please describe Lactic Acid, what it is, why it appears, and anything else you think relevant in this area?  Also, please address if we as racers should even really concern ourselves with it. 
Jeff Homan


It is always a challenge to make lactate metabolism simple and understandable.  It is not simple and requires a lot of knowledge of biochemistry.  However, some of it can be explained, I think, in a clear way.Rio haystack tt

History and background:

First, why does lactate historically have a bad name?  In the early 1900’s, experiments in an isolated frog muscle established that when you contract a muscle to fatigue, there is a large increase in lactic acid.  Subsequently, when oxygen was delivered, the lactic acid gradually declined and force was regained.  Therefore it was concluded that lactate accumulates as a result of oxygen deprivation and causes fatigue.  The scientists who performed these studies were preeminent scientists of the early 20th century and even received Nobel prizes (A.V. Hill), which is why the idea went unchallenged for so long.  These ideas also provided the foundations for the anaerobic threshold concept.  Despite the fact that the anaerobic threshold concept was thoroughly and completely discounted over 20 years ago (see (Brooks, 1985) for the destruction of the idea), it still appears in coaching vernacular as a “scientific” explanation.  Two important things to consider about the original experiments; 1) the experiments were performed on frog muscle which has a very different fiber type composition as humans, and 2) the experiments were performed in the absence of oxygen, a situation that does not occur in the human body.  

Something that often plagues reasoning is that if two things are occurring at the same time they are causally related.  As we exercise at a higher intensity, lactate concentration increases.  There is also a point in an incremental exercise test (the break point) were lactate concentration increases to a greater extent.  This point, the “lactate threshold” happens to coincide with a point were exercise gets increasingly difficult to sustain, which makes it easy to believe that it is that the lactate is causing the increased difficulty.  However, at this point the rate of breathing, heart rate, and sweat rate are all increasing too.  In controlled conditions, it would be just as easy to correlate sweat rate with the difficulty in sustaining exercise.  Does this mean increased sweating is CAUSING the inability to sustain exercise?  Of course it does not.  In the same vain, the increase in blood lactate is not necessarily causing the difficulty either.



“Lactic Acid” – What it is not:

The very thought of “lactic acid” makes most of us cringe.  The truth is, there is almost no lactic acid in the body at any point.  At the pH of the body, almost all of lactic acid is dissociated to H+ (what causes acidity) and the lactate anion (Lac-). Further, if you look at a textbook or biochemistry the H+ (again what is responsible for acidity) is liberated many reactions before the formation of lactate.  Therefore, lactic acid may never even be formed during normal metabolism. To be clear though, at any given time in your body, you have lactate NOT lactic acid.  Portable analyzers measure lactate.

Many point the finger at lactic acid in the fatigue process.  Indeed there is evidence that H+ accumulation (which I pointed out is likely not from “lactic acid”) can have a detrimental effect on exercise by inhibiting muscle contractions.  However, the view on this is even changing.  It now appears that rather than H+, the loss of potassium ion (K+) from inside the cell (intracellular) to outside the cell (extracellular), may be a main culprit in fatigue.  Excitable cells such as muscle have to maintain certain concentrations of ions inside and outside the cell to remain excitable.  When a muscle cell is activated it loses K+ to the outside and then pumps it back in to become excitable again.  Over time there is a progressive loss of the K+ and the cell becomes less excitable (i.e. fatigue).  One very important study has even described the PROTECTIVE effect of lactic acid against fatigue (Pedersen et al., 2003).  Another recent study compared trained versus untrained legs in the same person (by doing one-legged kicking training on an ergometer) and found that the prolonged time to fatigue in the trained leg was the result of a lower accumulation of K+ outside the muscle (Nielsen et al., 2004).  A second, player in fatigue may be phosphate.  The predominant source of phosphate is the creatine phosphate reaction, which is very active during high intensity exercise.  For a nice review of phosphate versus acidosis as the cause of fatigue see (Westerblad et al., 2002). What about lactate itself since it is increased at fatigue?  Recent studies in isolated muscles indicate that lactate has minimal to no effect on fatigue (Posterino & Fryer, 2000).

Finally, is lactic acid the cause of pain?   There is very little evidence that lactate stimulates pain receptors.  I will tell you a minor, but informative, measurement I made in an experiment.  We had cyclists work at a hard intensity and measured lactate levels.  On subsequent days we had the subjects exercise at an easier intensity, and then at the same easy intensity with lactate infused to the same concentration as during the hard exercise bout (Miller et al., 2002a;Miller et al., 2002b).  When we had the subject provide an objective measure of difficulty, the difficulty scaled to the exercise intensity and had nothing to do with how much lactate was in their blood.  Could you then conclude that lactate is causing the pain? Finally, the cause of muscle pain the day after a hard workout is certainly not due to lactate as it is cleared rapidly (certainly within 30 min) from the blood and muscles.  Something to think about the next time someone goes for a spin to “get the lactic acid out of the legs”.  The source of muscle pain with exertion is still relatively unknown.   

 Lactate – What it is:

First and foremost lactate is a carbohydrate meaning it is an energy source.  Lactate moves between cells quite easily (much more easily than glucose) and is at many times a preferred substrate for energy.  Lactate is used for energy in skeletal muscle, the heart, and the brain. For a full discussion see these important reviews (Brooks, 2002;Brooks, 2000;Brooks, 1991;Gladden, 2000).   Unfortunately in the coaching community lactate is so often made to be the bad guy that it is not recognized how valuable and necessary it is.   

In 1985 (getting close to 30 yrs ago) an idea called the lactate shuttle was proposed.  Basically, what it states is that even when we have a lot of oxygen, lactate is being produced and moved around the body to the areas it can be used for energy.  To understand the implications of this you must grasp that the main fate (75% or more) of lactate is oxidation for energy.  Therefore, local production of lactate is simply moved to other sites to be used as an energy source.  What is also true is that during exercise, lactate oxidation often EXCEEDS glucose oxidation (Bergman et al., 1999; Miller et al., 2002a).   These are not simply theories anymore; the lactate shuttle has been repeatedly supported in many experimental designs and is now universally accepted.  What is the main secondary site of lactate disposal besides oxidation?  It heads to the liver to make glucose.  In fact of all the 3 carbon gluconeogenic (the making of glucose) precursors, lactate is the preferred source (Miller et al., 2002a).   


There is a lot of misinformation in the coaching and athlete communities about lactate.  It is not the inducer of all things evil during exercise and quite to the contrary is probably necessary for sustained exercise. The question always comes up, if not lactate, what is causing fatigue, pain, etc?  At least for fatigue, it looks like potassium or inorganic phosphate could be the culprits.  To explain what is happening at the so-called lactate threshold, you have to remember that a correlation does not mean causality.  I believe that the measurement of lactate is just a surrogate measure for all the things that are occurring simultaneously as a function of workload.  Your muscles have a certain ability to maintain force production.  Training increases the amount of work that we can sustain (endurance training) or the peak force production we can achieve (resistance or power training).

Reference List

Bergman, B. C., Wolfel, E. E., Butterfield, G. E., Lopaschuk, G. D., Casazza, G. A., Horning, M. A., & Brooks, G. A. (1999). Active muscle and whole body lactate kinetics after endurance training in men. J.Appl.Physiol87, 1684-1696.

Brooks, G. A. (1985). Anaerobic threshold: review of the concept and directions for future research. Med.Sci.Sports Exerc.17, 22-34.

Brooks, G. A. (1991). Current concepts in lactate exchange. Med.Sci.Sports Exerc.23, 895-906.

Brooks, G. A. (2000). Intra- and extra-cellular lactate shuttles. Med.Sci.Sports Exerc.32, 790-799.

Brooks, G. A. (2001). Lactate doesn’t necessarily cause fatigue: why are we surprised? J.Physiol536, 1.

Brooks, G. A. (2002). Lactate shuttles in nature. Biochem.Soc.Trans.30, 258-264.

Dalsgaard, M. K., Quistorff, B., Danielsen, E. R., Selmer, C., Vogelsang, T., & Secher, N. H. (2004). A reduced cerebral metabolic ratio in exercise reflects metabolism and not accumulation of lactate within the human brain. J Physiol554, 571-578.

Gladden, L. B. (2000). Muscle as a consumer of lactate. Med Sci Sports Exerc.32, 764-771.

Miller, B. F., Fattor, J. A., Jacobs, K. A., Horning, M. A., Navazio, F., Lindinger, M. I., & Brooks, G. A. (2002a). Lactate and glucose interactions during rest and exercise in men: effect of exogenous lactate infusion. J.Physiol544, 963-975.

Miller, B. F., Fattor, J. A., Jacobs, K. A., Horning, M. A., Suh, S. H., Navazio, F., & Brooks, G. A. (2002b). Metabolic and cardiorespiratory responses to “the lactate clamp”. Am.J.Physiol Endocrinol.Metab283, E889-E898.

Miller, B. F., Fattor, J. A., Jacobs, K. A., LeBlanc, P. J., Heigenhauser, G. J., & Brooks, G. A. (2004). Haematological and acid-base changes in men during prolonged exercise with and without sodium-lactate infusion. J.PhysiolIn press.

Nielsen, J. J., Mohr, M., Klarskov, C., Kristensen, M., Krustrup, P., Juel, C., & Bangsbo, J. (2004). Effects of high-intensity intermittent training on potassium kinetics and performance in human skeletal muscle. The Journal of Physiology Online554, 857-870.

Pedersen, T. H., Clausen, T., & Nielsen, O. B. (2003). Loss of force induced by high extracellular [K+] in rat muscle: effect of temperature, lactic acid and beta2-agonist. The Journal of Physiology Online551, 277-286.

Pellerin, L. & Magistretti, P. J. (1994). Glutamate uptake into astrocytes stimulates aerobic glycolysis: a mechanism coupling neuronal activity to glucose utilization. Proc.Natl.Acad.Sci U.S.A91, 10625-10629.

Posterino, G. S. & Fryer, M. W. (2000). Effects of high myoplasmic L-lactate concentration on E-C coupling in mammalian skeletal muscle. Journal of Applied Physiology 89, 517-528.

Westerblad, H., Allen, D. G., & Lannergren, J. (2002). Muscle fatigue: lactic acid or inorganic phosphate the major cause? News Physiol Sci.17, 17-21.