Lactic Acid is not the bad guy…

Lactic Acid, Manual Therapy and DOMS: Why a Hundred Year Old Story Still Won’t Die

If you’ve spent any time in a sports massage clinic, a gym changing room or a clinical textbook from the 1990s, you’ll have heard some version of the same story. Hard training builds up lactic acid in the muscles. That lactic acid causes the burn during the session, the soreness the next day and the stiffness that follows. A good massage “flushes it out”. It’s one of the most persistent ideas in clinical and sports practice. It’s also wrong on almost every count.

This piece looks at where the story came from, what has actually happened in the laboratory since, and what we now understand about both delayed onset muscle soreness (DOMS) and the role of lactate in the working body.

Where the story started

The narrative that casts lactic acid as the villain is genuinely old. Fletcher and Hopkins (1907) first showed that lactic acid accumulated in contracting amphibian muscle when oxygen was absent and disappeared when oxygen returned. In the 1920s, Otto Meyerhof’s experiments on frog legs and Archibald Hill’s heat measurement work in humans combined into what became known as the Hill and Meyerhof theory of muscle energetics: a contracting muscle would run short of oxygen, glycogen would break down to lactic acid, and lactic acid would be implicated in fatigue (Hill and Meyerhof, 1923). The pair shared the 1922 Nobel Prize for Physiology or Medicine, which helped cement the idea in textbooks for decades.

It is worth pausing on what those experiments actually showed. Meyerhof’s frog legs were dissected, sealed in jars and electrically stimulated until they stopped twitching. The setup was deeply artificial and the conclusions translated poorly to intact, circulating mammals, but by the time anyone questioned this the lactic acid story had become orthodoxy. It had also been pulled into massage therapy, where it grew an extra layer: not only does lactic acid hurt you, the story went, but a therapist can manually flush it out of the tissues.

Then someone actually tested it

For most of the twentieth century the claim that manual therapy flushes out lactic acid was repeated without anyone checking it. When researchers finally did, the results were not what the profession expected.

Wiltshire and colleagues (2010) at Queen’s University in Ontario set out to test directly whether sports massage improved blood flow and lactate clearance after exercise. Twelve participants performed intense isometric handgrip exercise, then recovered under one of three conditions: passive rest, light active recovery, or effleurage and pétrissage massage. Forearm blood flow and venous lactate were measured every minute. The massage condition did not speed lactate clearance. It slowed it. The mechanical pressure of the hands impeded venous return, and active recovery cleared lactate the most effectively. The authors concluded that massage “impairs lactate and H+ removal from muscle after strenuous exercise by mechanically impeding blood flow” (Wiltshire et al., 2010, p. 1062).

Two years later, Crane and colleagues (2012), working with Tarnopolsky at McMaster, took muscle biopsies from the quadriceps of eleven young men after exhaustive cycling, comparing a massaged leg with an unmassaged one. Massage produced clear and impressive effects, but not on lactate. The authors explicitly reported that massage had “no effect on muscle metabolites (glycogen, lactate)”. What massage did do was dampen inflammatory cytokine signalling (TNF-α and IL-6) and promote markers of mitochondrial biogenesis. In other words, when massage helps, it does not help by flushing waste; it helps by modulating the inflammatory response and supporting tissue repair.

So what actually causes DOMS?

DOMS, that 24 to 72 hour ache after an unaccustomed session, was originally pinned on lactate by association rather than evidence. The trouble is that blood lactate returns to baseline within roughly an hour of exercise stopping, while DOMS often peaks two or three days later. The timing simply does not work (Cheung, Hume and Maxwell, 2003).

The dominant model now is mechanical and inflammatory. Eccentric (lengthening) contractions cause microtrauma to the sarcomeres, particularly disruption at the Z line, which triggers a localised inflammatory cascade. Neutrophils and macrophages arrive to clear damaged tissue, reactive oxygen species are released, and sensory nerve endings are sensitised by the resulting chemical environment of bradykinin, prostaglandins and nerve growth factor (Hotfiel et al., 2018; Hody et al., 2019). The pain you feel on day two is not waste product sitting in the tissue. It is the body actively repairing itself, with inflammation as the messenger.

This also explains why massage and other manual therapies still seem to help with DOMS even though they do nothing to lactate. They modulate inflammation, and inflammation is the actual driver (Crane et al., 2012).

Lactate is fuel, not waste

The bigger reframe is that lactate is not the bad guy at all. Robergs, Ghiasvand and Parker (2004) demonstrated that lactate production actually consumes protons and so retards rather than causes acidosis. The “burn” of high intensity work comes from elsewhere in the glycolytic pathway, principally ATP hydrolysis, and not from lactate itself.

George Brooks’s work on the lactate shuttle, developed over four decades, has gone further still and reframed lactate as one of the most important metabolic intermediates the body has (Brooks, 2018). Lactate produced in fast twitch fibres is taken up by neighbouring slow twitch fibres, by cardiac muscle, by the brain and by the liver. In working muscle, the heart and the brain it is oxidised back to pyruvate, fed into the TCA cycle and used to make ATP directly. In the liver it enters gluconeogenesis and is rebuilt into glucose through the Cori cycle (Cori and Cori, 1929), which is then released back into circulation to fuel further work. Far from a toxin to be flushed out, lactate is an energy currency that the body deliberately produces, traffics and reuses. During hard exercise, lactate flux can exceed glucose flux as a fuel source (Brooks, 2018).

Where this leaves clinical practice

None of this means manual therapy is useless. The evidence that hands on work eases pain, improves perceived recovery, reduces inflammatory signalling and simply feels good is solid. What is not defensible any more is the explanation we have been giving for it. Telling a client you are going to flush the lactic acid out of their legs misrepresents the physiology in two directions at once. It treats lactate as waste when it is actually fuel, and it credits massage with a mechanism that has been directly disproved in well designed studies.

The better story is honest and more interesting. Manual therapy appears to influence pain processing, support the resolution of inflammation and contribute to the neural and tissue environment of recovery. That is plenty to be getting on with. Lactate was never the enemy, and a hundred years of blaming it has obscured what is really going on.

References

Brooks, G.A. (2018) ‘The science and translation of lactate shuttle theory’, Cell Metabolism, 27(4), pp. 757–785.

Cheung, K., Hume, P.A. and Maxwell, L. (2003) ‘Delayed onset muscle soreness: treatment strategies and performance factors’, Sports Medicine, 33(2), pp. 145–164.

Cori, C.F. and Cori, G.T. (1929) ‘Glycogen formation in the liver from d- and l-lactic acid’, Journal of Biological Chemistry, 81(2), pp. 389–403.

Crane, J.D., Ogborn, D.I., Cupido, C., Melov, S., Hubbard, A., Bourgeois, J.M. and Tarnopolsky, M.A. (2012) ‘Massage therapy attenuates inflammatory signaling after exercise induced muscle damage’, Science Translational Medicine, 4(119), 119ra13.

Fletcher, W.M. and Hopkins, F.G. (1907) ‘Lactic acid in amphibian muscle’, Journal of Physiology, 35(4), pp. 247–309.

Hill, A.V. and Meyerhof, O. (1923) ‘Über die Vorgänge bei der Muskelkontraktion’, Ergebnisse der Physiologie, 22, pp. 299–344.

Hody, S., Croisier, J.L., Bury, T., Rogister, B. and Leprince, P. (2019) ‘Eccentric muscle contractions: risks and benefits’, Frontiers in Physiology, 10, 536.

Hotfiel, T., Freiwald, J., Hoppe, M.W., Lutter, C., Forst, R., Grim, C., Bloch, W., Hüttel, M. and Heiss, R. (2018) ‘Advances in delayed onset muscle soreness (DOMS): Part I, pathogenesis and diagnostics’, Sportverletzung Sportschaden, 32(4), pp. 243–250.

Robergs, R.A., Ghiasvand, F. and Parker, D. (2004) ‘Biochemistry of exercise induced metabolic acidosis’, American Journal of Physiology, Regulatory, Integrative and Comparative Physiology, 287(3), pp. R502–R516.

Wiltshire, E.V., Poitras, V., Pak, M., Hong, T., Rayner, J. and Tschakovsky, M.E. (2010) ‘Massage impairs postexercise muscle blood flow and “lactic acid” removal’, Medicine and Science in Sports and Exercise, 42(6), pp. 1062–1071.