The old paradigm: lactic acid is a corrosive byproduct of hard exercise that makes your muscles burn and eventually brings you to a halt.
The new paradigm: lactic acid doesn’t even exist in your body. Instead, it’s lactate (a molecule that has one less hydrogen ion than lactic acid) that accumulates in your muscles and blood, and it helps fuel your muscles, carries signals that tell your body how to adapt to training—and, according to a new study, maybe even moderates your appetite.
I’ll admit, I’m a sucker for studies about lactate, because its reputation has undergone such a dramatic reversal in my lifetime. It’s true that lactate is produced as a byproduct of intense exercise, an observation first made in 1807 by Swedish chemist Jöns Jacob Berzelius, who (along with devising the forerunner of modern chemical notation, e.g. H2O and CO2 and so on) observed high lactate levels in stags that had been hunted to exhaustion. Races or other maximal efforts that last somewhere between one and 10 minutes tend to produce the highest levels of lactate, and anyone who has truly gone to the well in a race of that duration will attest to how brutally unpleasant it can feel.
But correlation isn’t causation, and the current view of lactate is that it doesn’t directly cause your muscles to fail, although there’s some evidence that, in combination with other metabolites, it triggers nerve fibers that your brain interprets as pain. Instead, it seems to serve a whole bunch of different signaling roles that are crucial to how your body responds to exercise, and scientists are continually learning more about its function.
The latest development comes in a Journal of Applied Physiology paper from researchers at Wilfrid Laurier University in Canada, led by Tom Hazell. They’ve been studying the links between exercise, appetite, and caloric balance, and had published earlier research that seemed to link lactate to appetite hormones. In a 2017 study, they found that more intense workouts suppressed levels of ghrelin, a hormone that makes you want to eat, and bumped up levels of two other hormones that suppress appetite. Intriguingly, the subjects did indeed eat less in the days following the most intense workout.
Still, that’s just a correlation. Hazell and his colleagues wanted to figure out whether lactate actually caused the change in appetite hormones, so they set up a neat double-blind, placebo-controlled crossover experiment. They had 11 volunteers do an interval workout of 10 times one minute hard with one minute recovery on an exercise bike. They repeated this protocol twice at the same intensity, on separate days at least a week apart, once following a dose of baking soda and the other time following a dose of salt as a placebo.
Baking soda, also known as sodium bicarbonate, is a base (i.e. the opposite of an acid) that partially counteracts rising acidity in your bloodstream during intense exercise. For that reason, it’s often used as a legal performance-enhancer by track cyclists and middle-distance runners—and it allows you to tolerate higher levels of lactate in your bloodstream for a given level of exercise. That’s exactly what you see when you compare lactate levels during and after the 10 x one minute workout with baking soda (bicarb) and salt (placebo):
So now you’re comparing the same people doing the same workout but with different lactate levels. And sure enough, that also changes the response of their appetite hormones. Here are the ghrelin levels, showing lower levels (i.e. less hunger) in the high-lactate bicarb condition:
There are similar results for the two appetite-suppressing hormones: higher lactate leads to higher hormone levels, meaning less hunger. And the subjective reports of hunger over the 90 minutes following the workout are indeed lower when lactate is higher.
There are some caveats. For example, baking soda is sometimes associated with gastrointestinal distress. There were no apparent differences between the baking soda and placebo groups in this case, but it’s possible some subtle stomach upset contributed to the hunger ratings (though it presumably wouldn’t have affected the appetite hormones).
The bigger question is whether subtle changes in appetite hormones really have any meaningful impact on long-term patterns of calorie intake and weight change. It’s probably fair to say that the current scientific consensus (insofar as one exists) is that exercise plays at most a very minor role in weight control. I’ve always been a little skeptical of whether that consensus really applies to people training at the level of a moderately serious endurance athlete, and this research offers further evidence that intense exercise probably affects appetite in ways that go beyond simple calorie-burning.
That definitely doesn’t mean that hard interval workouts designed to fill your veins with lactate—the minute-on, minute-off reps used in the study are a pretty good example—are some sort of new miracle weight-loss strategy. Do those workouts because they supercharge your VO2 max, and because they offer a possible path to self-transcendence. Just remember to eat afterwards.
For more Sweat Science, join me on Twitter and Facebook, sign up for the email newsletter, and check out my book Endure: Mind, Body, and the Curiously Elastic Limits of Human Performance.
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