Lactate is no longer the villain: from enemy to fuel

El lactato ya no es el malo: de enemigo a combustible
Fred Laguía
Reviewed by Fred Laguía
Creator of «La Obsesión Ciclista de Fred», the most-listened Spanish-language cycling podcast (6M+ plays). 20+ years building technology, much of it for sport.
Prepared by the FredCoach science team, AI-assisted, from the cited sources · Performance scientist

In short. No. Lactate is not a waste product and it does not cause muscle soreness: your muscles make it all the time, even with plenty of oxygen, your heart and working muscles burn it as fuel, and your liver turns it into new glucose. What slows you down in a very hard effort is a mix of changes inside the muscle, and blood lactate remains a good marker of how hard you are going, not the culprit.

A century of bad press

In 1907, Walter Fletcher and Frederick Hopkins saw in frog muscle that lactic acid built up when the muscle contracted without oxygen and disappeared when oxygen returned. Some fifteen years later Archibald Hill, who shared the 1922 Nobel Prize in Physiology or Medicine with Otto Meyerhof, built with Hugh Lupton the explanation that lasted almost a century: when oxygen runs short, muscle takes a shortcut that leaves lactic acid behind as waste, and fatigue is that waste piling up.

That is where the lines everyone has heard on a group ride come from: "lactic acid burns your legs", "you'll be sore tomorrow from the lactate", "cool down to flush it out". But it rested on isolated muscle in the lab and on tools that could not follow lactate inside a living body.

Brooks and the lactate shuttle

In the 1980s George Brooks, a physiologist at the University of California, Berkeley, began labelling lactate with tracers to see where it came from and where it went. What he found rewrote the story: muscle makes lactate with plenty of oxygen available, at rest and during exercise, and that lactate is not left as rubbish. It travels from the fibres that make it to the fibres that burn it, to the heart, and to the liver, which uses it to build new glucose. Brooks called it the lactate shuttle.

It was a contested hypothesis at first. Today it is backed by decades of tracer studies in people, and Brooks himself has summarised it in recent reviews: lactate is at once a fuel, a raw material for making glucose and a signal that tells the body how energy use is going. A 2017 study in mice went further: lactate was what circulated most in their blood, more than glucose, and when fasting, most of the glucose their tissues burned (except the brain) had first passed through lactate. That was shown in mice; in people, what is established is that lactate is used as fuel during exercise, and a lot of it.

So what actually slows you down?

When you push very hard, the muscle becomes more acidic and loses force. For decades lactate took the blame. We now know that acidity and lactate travel together but are not the same thing: reviews over the last twenty years agree that lactate is not the main cause of fatigue and that other changes inside the fibre weigh more, such as the build-up of phosphate left over from spending energy. Exactly how much of the blame belongs to acidity is still debated.

Some studies on isolated rat muscle even found that acidity helped restore force when potassium outside the fibre was high, as happens in an intense effort. These are lab experiments and cannot be transferred as they are to your legs, but they point the same way: lactate is not the villain we were told about.

Muscle soreness is not lactate either. Lactate returns to normal shortly after the effort ends; soreness shows up one or two days later and is linked to small muscle damage and the inflammation that repairs it, especially after efforts where the muscle brakes while it lengthens, such as running downhill.

What it means for your training

Training makes you better at using lactate, not at avoiding it. With endurance training your muscle gains more mitochondria and more transporters that move lactate from one cell to another, and your body clears it from the blood faster. That is why, at the same watts, a trained cyclist has less lactate in the blood, mainly because they make less; and when they push harder, they clear and burn it faster.

The threshold is still useful. Lactate not being the enemy does not make measuring it pointless: the point where it starts to build up in the blood marks a real change in how your body handles the effort. Below it you can hold the pace for a long time; above it, every minute costs more. That point is different for everyone, which is why it makes sense for your zones to come from you and not from a textbook percentage of maximum heart rate.

You need both. Easy hours build the base that lets you use lactate and fat better; work above threshold is needed to raise your aerobic ceiling, including after 40. In amateurs, no way of distributing intensity has clearly beaten the others: keeping training going over time matters more than the exact recipe.

"Zone 2" is not magic. Part of the fame of zone 2 rides comes from studies by Brooks and Iñigo San-Millán in which professional cyclists had less lactate and burned more fat during a graded test than moderately active people or people with metabolic syndrome. That is a snapshot comparing groups, not a trial showing that training exactly in that zone is what improves you most.

Cool down for other reasons. Spinning easy after a hard effort does lower blood lactate sooner, but by the next morning it would be gone anyway. If you like it, do it, but not to "flush out lactic acid": it barely changes how you perform the next day and does not prevent soreness.

What is still open

  • How much acidity exactly contributes to fatigue in a real bike effort.
  • Lactate's role as a signal (what it switches on in muscle and other organs): well studied in the lab and in animals, less so in athletes.
  • How to find the threshold in amateurs without a blood test: power tests are a good approximation in trained cyclists and somewhat less precise in beginners.
FredCoachBETA

In FredCoach

FredCoach does not measure your lactate: it reads the power and heart rate of every ride. From them it estimates your threshold from your own efforts and revisits it as you change, so your zones are yours and not a textbook percentage. Each session you complete moves you towards the next step, and each ride is compared with your previous ones of the same kind to see how you handled it. Your week mixes easy riding and work above threshold according to your goal and where you are right now. Request access at coach.freds.cc (we are in beta).

Request access at coach.freds.cc
FredCoach Today screen: readiness rings and the coach message
FredCoach Sessions screen: the week and the next recommended session

FAQ

Does lactic acid cause muscle soreness?

No. Lactate returns to normal shortly after the effort ends, while soreness appears one or two days later. It is linked to small muscle damage and the inflammation that repairs it, especially after efforts where the muscle brakes while it lengthens.

Do I need a cool-down to flush out lactate?

Not because of lactate: your body clears it on its own and uses it as fuel. Easy spinning at the end does lower it sooner in the blood, but it does not prevent soreness and barely changes how you perform the next day.

What is the lactate threshold and why does it matter?

It is the intensity above which blood lactate no longer holds steady and keeps rising minute by minute, because more is produced than cleared (labs define it in several ways). It marks a real change in what you can sustain: below it you can last a long time, above it every minute costs more. It differs from person to person.

Do I need to test my lactate to train well?

No. In trained cyclists, a good power test (FTP) comes reasonably close to the maximal lactate steady state; in beginners it is less precise and tends to sit somewhat below it. With a power meter and heart rate you can set your zones without pricking your finger.

Sources

  1. Fletcher WM, Hopkins FG (1907). Lactic acid in amphibian muscle. The Journal of Physiology 35:247–309 · doi
  2. Hill AV, Lupton H (1923). Muscular exercise, lactic acid, and the supply and utilization of oxygen. QJM os-16:135–171 · doi
  3. Brooks GA (1986). Lactate production under fully aerobic conditions: the lactate shuttle during rest and exercise. Federation Proceedings 45(13):2924–2929 · enlace
  4. Bergman BC, Wolfel EE, Butterfield GE, Lopaschuk GD, Casazza GA, Horning MA, Brooks GA (1999). Active muscle and whole body lactate kinetics after endurance training in men. Journal of Applied Physiology 87(5):1684–1696 · doi
  5. Dubouchaud H, Butterfield GE, Wolfel EE, Bergman BC, Brooks GA (2000). Endurance training, expression, and physiology of LDH, MCT1, and MCT4 in human skeletal muscle. American Journal of Physiology-Endocrinology and Metabolism 278(4):E571–E579 · doi
  6. Nielsen OB, de Paoli F, Overgaard K (2001). Protective effects of lactic acid on force production in rat skeletal muscle. The Journal of Physiology 536:161–166 · doi
  7. Westerblad H, Allen DG, Lännergren J (2002). Muscle fatigue: lactic acid or inorganic phosphate the major cause?. News in Physiological Sciences 17:17–21 · doi
  8. Cheung K, Hume P, Maxwell L (2003). Delayed onset muscle soreness: treatment strategies and performance factors. Sports Medicine 33(2):145–164 · doi
  9. Robergs RA, Ghiasvand F, Parker D (2004). Biochemistry of exercise-induced metabolic acidosis. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 287:R502–R516 · doi
  10. Cairns SP (2006). Lactic acid and exercise performance: culprit or friend?. Sports Medicine 36(4):279–291 · doi
  11. Hui S, Ghergurovich JM, Morscher RJ, Jang C, Teng X, Lu W, et al. (2017). Glucose feeds the TCA cycle via circulating lactate. Nature 551:115–118 · doi
  12. San-Millán I, Brooks GA (2018). Assessment of metabolic flexibility by means of measuring blood lactate, fat, and carbohydrate oxidation responses to exercise in professional endurance athletes and less-fit individuals. Sports Medicine 48:467–479 · doi
  13. Brooks GA (2018). The science and translation of lactate shuttle theory. Cell Metabolism 27(4):757–785 · doi
  14. Brooks GA, Arevalo JA, Osmond AD, Leija RG, Curl CC, Tovar AP (2022). Lactate in contemporary biology: a phoenix risen. The Journal of Physiology 600(5):1229–1251 · doi
  15. Borszcz FK, Tramontin AF, Costa VP (2019). Is the functional threshold power interchangeable with the maximal lactate steady state in trained cyclists?. International Journal of Sports Physiology and Performance 14:1029–1035 · doi
  16. Valenzuela PL, Morales JS, Foster C, Lucia A, de la Villa P (2018). Is the functional threshold power a valid surrogate of the lactate threshold?. International Journal of Sports Physiology and Performance 13:1293–1298 · doi
  17. Schwane JA, Watrous BG, Johnson SR, Armstrong RB (1983). Is lactic acid related to delayed-onset muscle soreness?. The Physician and Sportsmedicine 11(3):124–131 · doi
  18. Böning D, Strobel G, Beneke R, Maassen N (2005). Lactic acid still remains the real cause of exercise-induced metabolic acidosis. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 289:R902–R903 · doi
  19. Van Hooren B, Peake JM (2018). Do we need a cool-down after exercise? A narrative review of the psychophysiological effects and the effects on performance, injuries and the long-term adaptive response. Sports Medicine 48(7):1575–1595 · doi