Like all great villains, lactic acid has been misunderstood. We’ve been blaming it for the pain we suffer during intense exercise for more than two centuries. There’s nothing worse, we say, than the “lactic burn” that locks our failing muscles into immobility. More recent tellings of the story have tried to rehabilitate lactic acid’s reputation, insisting that it’s actually trying to fuel our muscles rather than shut them down. But that version doesn’t capture the full complexity, either.
Into this confusion steps a new review in the European Journal of Applied Physiology, from veteran physiologists Simeon Cairns and Michael Lindinger. It’s a dense 35-page doorstop titled “Lactic Acidosis: Implications for Human Exercise Performance,” and the clearest conclusion we can draw from it is that the precise causes of muscle fatigue during intense exercise are still a topic of active research and vigorous debate among scientists. But the sudden popularity of baking soda as an acid-buffering performance aid has renewed conversations about how, exactly, lactic acid works in the body—and how we might counteract it. Here are some highlights from the latest research.
The Lactic Backstory
The first scientist to draw the connection between exercise and lactic acid was Jöns Jacob Berzelius, the Swedish chemist who devised the modern system of chemical notation (H2O and so on). Sometime around 1807, he noticed that the chopped-up muscles of dead deer contained lactic acid, a substance that had only recently been discovered in soured milk. Crucially, the muscles of stags that had been hunted to death contained higher levels of lactic acid, while deer from a slaughterhouse who had their limbs immobilized in a splint before their death had lower levels, suggesting that the acid was generated by physical exertion.
A century later, physiologists at the University of Cambridge used electric stimulation to make frogs’ legs twitch until they reached exhaustion, and observed high lactic acid levels. The levels were even higher if they performed the experiment in a chamber without oxygen, and lower if they provided extra oxygen. That finding helped establish the prevailing twentieth-century view: your muscles need oxygen to generate energy aerobically; if they can’t get enough oxygen, they switch to generating energy anaerobically, which produces lactic acid as a toxic byproduct that eventually shuts your muscles down.
There are two small problems—and one big one—with this picture. The first detail is that, while lactic acid can be measured in the muscles of dead deer and frogs, it doesn’t actually exist in living humans. In the chemical milieu of the body, what would be lactic acid is split into two components: lactate and hydrogen ions. That’s not just being persnickety about terminology: lactate and hydrogen ions behave differently than lactic acid would. In fact, they can have separate and sometimes even opposing effects.
The second detail is that lactate (and hydrogen ions) aren’t really produced because your muscles are “running out of oxygen.” The chemical reactions that use oxygen to turn food into muscle fuel are efficient but slow, great for powering relatively easy and sustained exercise. But they can’t provide energy fast enough to supply an all-out sprint. For that, you’ll eventually need to rely on lactate-producing anaerobic reactions, even if you’re huffing pure oxygen from a can.
The big problem with the old view of lactic acid is the idea that it’s a metabolic villain. It turns out that, far from being an inert byproduct, lactate can be recycled into fuel for your muscles. In fact, one of the key superpowers that well-trained athletes develop is the ability to reuse lactate more quickly. This rehabilitation of lactate’s reputation has been going on for a couple of decades now (though it still has a long way to go), but athletes are still left with an unanswered question: if lactate isn’t what causes muscle fatigue, what is?
What the New Review Reveals
The first thing that Cairns and Lindinger establish is that, yes, levels of lactate and hydrogen ions increase during intense exercise. This is most obvious during intense exercise lasting between about one and twenty minutes. Longer bouts of exercise are less intense, so they can be mostly fueled by non-lactate-producing aerobic energy, and bouts of exertion shorter than one minute simply don’t have time to produce much lactate.
The evidence is now clear that lactate itself doesn’t interfere in any significant way with muscle function. But lactate and hydrogen ions are produced simultaneously in exactly the same quantities during anaerobic exercise, which complicates the “lactic acid is a good guy after all” narrative. Lactate may be great, but it comes with an equivalent helping of hydrogen ions—and that may be a problem.
When you increase the concentration of hydrogen ions in a solution, you’re increasing its acidity. That’s how the pH scale is defined: it’s a measure of hydrogen ion concentration. During intense exercise, the pH in your fast-twitch muscle fibers (which seem to be particularly susceptible to hydrogen ion buildup) can drop from around 7.0 to 6.0. That change represents a ten-fold increase in the concentration of hydrogen ions—a situation that can wreak havoc on muscle contraction.
The idea that hydrogen ions are what cause muscle fatigue isn’t entirely straightforward either, though. When you start hard exercise, the concentration of hydrogen ions actually decreases for about 15 seconds while you use up another source of fast-acting muscle energy called phosphocreatine. And yet your muscles are already getting fatigued during this initial burst, losing some of their maximal force, while hydrogen ion levels are still lower than normal.
There’s also a disconnect when you stop exercising, or take a break between hard intervals. Hydrogen ion (and lactate) levels keep climbing for a few minutes, which is why the highest lactate levels are generally recorded several minutes after hard exercise. But you don’t get weaker after you stop exercising; you get stronger as you recover, despite the rising concentration of hydrogen ions. So hydrogen ions may play a role in muscle fatigue, but they can’t be the whole story.
Another possibility is that hydrogen ions may interact with other molecules to disrupt muscle contraction. The most prominent candidates are potassium and phosphate, both of which increase during exercise and are associated in some studies with muscle fatigue. What these and other candidates have in common is that there are a ton of conflicting results: they have different effects on muscle fibers depending on the level of acidity, the muscle temperature, and the test protocol. This suggests—not surprisingly—that there isn’t a single molecule that causes your muscles to lose their power. Instead, it’s the whole cocktail of things going on inside your muscles during hard exercise that matters.
What About the Burn?
Most of the research that Cairns and Lindinger describe deals with muscle properties: how quickly are your fibers losing their twitch force, and why? It’s true that, as a middle-distance runner, I’ve sometimes staggered down the finishing straight of a race with the sense that my legs were literally ceasing to function. It’s an awful feeling to experience, but satisfying to look back on: you know you left nothing out there.
Far more common, though, is a softer limit. You feel a red-hot burn and spreading numbness in your legs, and you choose to back off a bit. This feeling that we used to describe as “going lactic” is significant in its own right. In interviews with athletes who’ve begun using baking soda, a common theme is that they’re able to push harder for longer before feeling that burn in their legs, which in turn enables them to race faster.
One theory about the feeling of going lactic is that you’re literally starving your brain of oxygen. If you push hard enough, it’s not just your muscles that go more acidic; your whole bloodstream follows. Thanks to a phenomenon called the Bohr effect, rising acidity reduces the ability of your red blood cells to ferry oxygen from your lungs to the rest of your body, including your brain. In one study, all-out rowing caused oxygen saturation to drop from 97.5 to 89.0 percent, which is a big drop—big enough, perhaps, to slow you down and contribute to the out-of-body feeling at the end of hard races.
We also have nerve sensors that keep the brain informed about the metabolic status of the muscles. These group III/IV afferents, as they’re known, keep tabs on the real-time levels of molecules like lactate and hydrogen ions. If you block these nerves with spinal injections of fentanyl, exercise feels great—too great, in fact, because you’ll lose all sense of pacing, go out too hard, then hit the wall.
The most telling finding about the lactic burn, in my view, was a 2013 study where they injected various molecules into the thumbs of volunteers in an attempt to reproduce that familiar feeling. Injecting lactate didn’t do it. Neither did injecting hydrogen ions, or ATP, a fuel molecule whose levels are also elevated during hard exercise. Injecting them in pairs didn’t do it either. But injecting all three at the levels you’d experience during moderate exercise produced a sensation of fatigue in their thumbs, even though they weren’t moving them. And injecting higher levels turned fatigue into pain.
That’s a distinction I try to keep in mind in the late stages of hard workouts, and at the crux of races. That burning feeling is real, and it’s associated with lactate and acidity and muscular fuel levels. But it’s just a feeling. The lactate and ATP are actually helping me. The hydrogen ions, in combination with various other metabolites accumulating in my muscles, not so much. They’ll eventually stop me. But until they do, I can keep pushing.
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