Lactate Myths

Some things you should know.

Introduction

While idly surfing YouTube the other day I stumbled across this on the Specialized channel.

The video looks at the pre-season training and testing of sponsored professional cycling teams Astana and OPQS. Envy aside, the video offers an interesting insight into the preparations of these elite cycling teams, including some discussion of lactate testing around 3:10. Ordinarily I would wince at the mention of ‘lactate’ in any mainstream media, fearing the perpetuation of yet more misinformation. However, given the extensive sport science support behind these teams, I thought this might be a rare exception. All seems well at first, there are some glancing references to lactate and ‘base values’/‘zones’, but then at 3:46 the narrator states:

“The human body can only withstand a high intensity workload for a limited amount of time before the body’s lactate levels rise to a point that will cause it to shut down.”

Suffice to say, I can only hope the sport scientists had no input in the video production!

Lactate is perhaps the biggest headache for exercise scientists. I can’t think of any parallels in terms of sheer prevalence of misuse. Ignorance surrounding this basic metabolite is deeply entrenched in sport; watch any athletic event on TV and the commentators will no doubt reference the sinister opponent that is lactic acid. What’s more, this misunderstanding is not confined to the general public; it also pervades academia and the scientific literature1. This idea of lactate as the main suspect in muscular fatigue was popularised in the 1960s and ‘70s. Indeed, it is an attractive concept that an end product of metabolism would directly cause fatigue, as such ’negative feedback’ mechanisms are commonplace in enzyme biochemistry. However, these original ideas were founded on correlational data1. More recent, and more authentic evidence now suggests that this archaic approach to fatigue is incorrect. So here it is, my contribution to the cause of lactate education. In the interest of wider accessibility, I’ll keep details brief; those looking for greater detail should consult the cited references (I would strongly recommend the reviews under references 1, 3 and 4).

Lactic acid does not exist in the body2

At our bodily pH (the measure of acidity/alkalinity) virtually all (>99%) lactic acid exists as lactate.

Lactate does not cause fatigue3,14

Under bodily conditions, lactate that accumulates in the muscle during intense exercise does not affect force production.

Lactate production is beneficial

The formation of lactate allows you to maintain high-intensity exercise. Circulating lactate is also used as a fuel by numerous tissues in the body (namely the liver, kidneys, heart, lungs, brain, slow-twitch muscle fibres, inactive muscle fibres11). Furthermore, lactate acts as a pseudohormone11, stimulating endurance adaptations12.

Lactate may not cause acidosis4

Some readers will be aware of the idea that lactate is formed through the dissociation of an H+ ion from lactic acid (NB: an increase in H+ ion concentration == increase in acidity). During high-intensity exercise there is a drop in muscle pH (increase in acidity), but whether or not this is attributable to lactate production is debatable. It has been suggested H+ ions are the product of ATP breakdown (to liberate energy for muscle contraction), and glucose/glycogen metabolism outside of the mitochondria4. Furthermore, the formation and removal of lactate should actually counteract increases in acidity4,5. However, this view is not unanimously accepted14.

Blood lactate values return to baseline after ~30 minutes10

How often do people claim that they’re going on a recovery run/ride to ‘flush the lactate out’? Even though the levels of blood/muscle lactate have no direct significance where fatigue is concerned, I thought it best just to clarify that lactate is mostly cleared ~30 minutes after you stop exercising.

Acidosis is not a major factor in muscle fatigue1,3,6

Muscular fatigue is a complex and multifaceted phenomenon. There are many chemical factors implicated in fatigue, but the contribution of acidosis (under physiological conditions) is negligible, if not totally absent3. An increase in blood acidity, however, may increase the sensation of fatigue (RPE) via effects on the nervous system1.

Acidosis may actually be beneficial3

An increase in muscle acidity (drop in pH), at bodily temperatures, is protective against fatigue, and can actually increase force production6,7. Also note that most activities do not elicit a significant change in muscle pH—with maximal exercise of 1–10 minutes causing the greatest fall in pH1.

NB: This is a contentious issue. See here for a debate on the topic.

Some likely objections…

What about buffers?

Some will be familiar with the use of sodium bicarbonate (baking soda) to alkalinize the blood in order to resist acidification8—not to mention recreating the classic volcano science experiment with vomiting athletes. While these buffers do seem to enhance performance in events 1–10 min in duration, this is more likely due to reduced RPE as a result of attenuated blood acidosis, or increased blood oxygen saturation1. Similarly, some will be familiar with the ergogenic effects of beta-alanine, which effectively increases the buffering capacity of muscle (rather than the blood). The performance enhancing effects of beta-alanine are also likely attributable to other cellular mechanisms3,15.

Why do we train with lactate thresholds?

“A marker, not a maker”—Hakan Westerblad

Classically, there are thought to be three physiological determinants of performance: VO2max, lactate threshold(s), and movement economy9. Indeed, lactate threshold(s) are a better predictor of performance than VO2max in a group of similar athletes13. When we plot blood lactate against exercise intensity we get something of an exponential curve. As exercise intensity increases, there is an increasing contribution from anaerobic (i.e. non-oxygen dependant) metabolism. Eventually there comes a point at which the body cannot maintain a steady state, and exercise becomes unsustainable (technically termed the ‘Maximal Lactate Steady State’ or MLSS13). When we assess an individual’s lactate profile, we are using it as a proxy for anaerobic metabolism. In other words, blood lactate represents fatiguing processes; it does not cause them.

Take home message

The concept of lactic acid fatigue is outdated. Bear the above points in mind, and you too will realise how prolific this misunderstanding is. So next time you’re pushing out a hard interval, or you wake up after a hard session, and you need to describe your fatigue, just use the word ‘fatigue’. I can assure you that a more correct description would be far more long-winded.

References

  1. Cairns, S.P. Lactic acid and exercise performance. Sports Med. 36(4): 279–291, 2006.
  2. Halestrap, A. and Price, N. The proton-linked monocarboxylate transporter (MCT) family: structure, function and regulation. Biochem J. 343: 281–299, 1999.
  3. Allen, D.G., Lamb, G.D. and Westerblad, H. Skeletal muscle fatigue: cellular mechanisms. Physiological Reviews 88(1): 287–332, 2008.
  4. Robergs, R.A., Ghiasvand, F. and Parker, D. Biochemistry of exercise-induced metabolic acidosis. American Journal of Physiology.Regulatory, Integrative and Comparative Physiology 287(3): R502–16, 2004.
  5. Smith, G.L., Donoso, P., Bauer, C.J. and Eisner, D.A. Relationship between intracellular pH and metabolite concentrations during metabolic inhibition in isolated ferret heart. The Journal of Physiology 472: 11–22, 1993.
  6. Westerblad, H., Allen, D.G. and Lannergren, J. Muscle fatigue: lactic acid or inorganic phosphate the major cause? News in Physiological Sciences 17: 17–21, 2002.
  7. Nielsen, O.B., Paoli, F. and Overgaard, K. Protective effects of lactic acid on force production in rat skeletal muscle. The Journal of Physiology 536(1): 161–166, 2001.
  8. Mcnaughton, L.R., Siegler, J. and Midgley, A. Ergogenic effects of sodium bicarbonate. Current Sports Medicine Reports 7(4): 230–236, 2008.
  9. Coyle, E.F. Integration of the physiological factors determining endurance performance ability. Exercise and Sport Sciences Reviews 23: 25–63, 1995.
  10. Menzies, P., Menzies, C., Mcintyre, L., Paterson, P., Wilson, J. and Kemi, O.J. Blood lactate clearance during active recovery after an intense running bout depends on the intensity of the active recovery. Journal of Sports Sciences 28(9): 975–982, 2010.
  11. Brooks, G.A. Lactate shuttles in nature. Biochemical Society Transactions 30(2): 258–264, 2002.
  12. Messonnier, L.A., Emhoff, C.A., Fattor, J.A., Horning, M.A., Carlson, T.J. and Brooks, G.A. Lactate kinetics at the lactate threshold in trained and untrained men. J Appl Physiol. 114(11): 1593–1602, 2013.
  13. Faude, O., Kindermann, W. and Meyer, T. Lactate threshold concepts. Sports Med. 39(6): 469–490, 2009.
  14. Philp, A., Macdonald, A.L. and Watt, P.W. Lactate–a signal coordinating cell and systemic function. The Journal of Experimental Biology 208(24): 4561–4575, 2005.
  15. Danaher, J., Gerber, T., Wellard, R.M. and Stathis, C.G. The effect of β-alanine and NaHCO3 co-ingestion on buffering capacity and exercise performance with high-intensity exercise in healthy males. European Journal of Applied Physiology 114(8): 1715–24, 2014.