Sports Science Update: How Lactic Acid Prevents Fatigue

Published October 22, 2010 08:00AM

Two new studies demonstrate that much-maligned lactate is benign at worst and beneficial at best.

It happens sooner or later every July. I’ll be watching television coverage of the Tour de France on Versus and either Paul Sherwin or Phil Liggett will make some reference to “massive lactic acid buildup” causing a particular cyclist to bonk. In these moments I doubt that the masses will ever get the memo that everything they were once taught about lactic acid is wrong.

The old line on lactic acid is that 1) it is a byproduct of anaerobic muscle metabolism at high exercise intensities, 2) it causes fatigue by making the muscles more acidic, 3) it cannot be used directly by the muscles as fuel, and 4) it causes post-workout muscle soreness. The new line on lactic acid is that 1) the muscles don’t produce it at all, but instead produce its close cousin, lactate, 2) lactate is not a byproduct of anaerobic metabolism but an intermediate product of aerobic metabolism, 3) about 75 percent of the lactate produced by the muscles is used aerobically within them as fuel, 4) lactate does not cause fatigue by making the muscles more acidic but actually prevents fatigue in a manner I’ll explain in the next few paragraphs, and 5) lactate has no relationship to muscle soreness whatsoever.

A new study out of Aarhus University in Denmark provides evidence for point #4. Before I discuss it, though, let me first say this: muscles work kind of like batteries. They run on electricity and, like batteries, they are most powerful when they are highly polarized. When you start exercise, there is a large disparity in the strength of the positive electrical charge between the interior of the muscle cell and the extracellular space outside it. This allows electrical signals sent to the muscle cell from the brain through nerves to pass through the cell membrane easily and induce strong contractions. But as high-intensity exercise continues, potassium ions steadily leak out of the muscle cell into the extracellular space, causing a depolarizing effect. As the charge difference between the inside and outside of the muscle cell decreases, electrical currents have a harder time getting in and muscle contractions become weaker.

Now, it so happens that the accumulation of potassium ions and the buildup of lactate during high-intensity exercise are highly synchronized. This suggests that the two processes are somehow linked. Researchers at Aarhus University wanted to figure out how these two processes interacted, so they designed the following experiment.

Leg muscles were removed from rats and place in fluid baths with electrical currents hooked up to them. By measuring the strength of these muscles’ contractions in response to a consistent amount of electrical stimulation, the researchers were able to determine the effects of different things they added to the fluid bath on the fatigue state of the muscles. The two things they added, both separately and together, were potassium ions and lactic acid.

What did they find? They found that extreme acidification alone caused the muscles to lose contractile power—that is, it caused them to fatigue. They found that adding a bunch of potassium ions to the fluid bath also caused fatigue. But when potassium ions and lactic acid were added together, the muscles function just as well as they did when neither substance was added.

What does this tell us? It tells us that, far from causing fatigue in the exercising muscle, lactate production actually prevents fatigue by counteracting the effects of depolarization. To draw an analogy, depolarization is like the drain on your cell phone’s battery that happens while you use it. Lactate production is like plugging your phone into a charger while you use it. It counteracts the drain.

While I have your attention, I’ll tell you briefly about another new study involving potassium ions and lactate. As you know from experience, the harder you run, the harder you breathe. The physiological mechanisms that cause you to breathe harder as you exercise harder are complex and not fully understood. Researchers at the University of North Carolina recently set up an experiment designed to determine if increased ventilation during exercise was related to the accumulation of either potassium ions or lactate in the blood.

The researchers had a group of triathletes hop on exercise bikes and ride at incrementally increasing intensity until they were exhausted. They did this on two occasions, once with normal muscle glycogen levels and once with low muscle glycogen levels. Since lactate comes from glycogen, the purpose of having the triathletes perform the test with low glycogen levels was to reduce lactate production at higher exercise intensities. Since potassium ion accumulation would be unaffected by reduced glycogen, this protocol allowed the researchers to separate the effects of potassium ions and lactate on breathing.

What did they find? The relationship between potassium ion accumulation and breathing intensity was consistent between the two trials, whereas the relationship between blood lactate levels and ventilation differed. This finding suggests that lactate accumulation is not a major trigger of increased breathing intensity during exercise.

Will this fact make Phil Liggett and Paul Sherwin stop blaming “lactic acid” for making cyclists bonk in next July’s Tour de France? Not a chance!