It’s no surprise that most people don’t feel well in the gym when taking antibiotics. After all, if you’re taking it, it usually means you’re sick or just recovering from an illness. But lately there has been renewed scientific interest in the idea of a gut-muscle axis, which posits that the microbes in your gut are affected by physical activity and, in turn, affect your ability to perform physical activity. This raises an interesting question: Do antibiotics, which wipe out large swathes of your gut flora, have a direct effect on athletic performance?
There have been a bunch of studies supporting the idea of a bidirectional gut-muscle axis, mostly in mice. Transplanting fecal bacteria from exceptionally healthy aged humans into mice makes them stronger. Eliminate gut bacteria in mice with a broad-spectrum antibiotic reduces running endurance. More importantly, in 2019, a lactate-eating bacteria found in the poop of Boston marathon runners made mice faster. But beyond the headlines, the current research remains confusing and contradictory: Each study seems to find a different magic bug.
The good news, then: two new studies on the effects of antibiotics on exercise come to similar conclusions. There are still plenty of caveats – both studies are in mice, for one thing. But they suggest an interesting twist: The greatest athletic effect of antibiotics may be on the brain, not the muscles.
The first study, led by Monica McNamara and Theodore Garland of the University of California, Riverside and Posted in Behavioral processes, compared two different types of mice. One was the famous High Runner line. In 1993, researchers began selecting mice that exhibited abnormally high levels of voluntary running and breeding them with each other. The mice in the UC Riverside study belong to the 89th generation of this program, and they now choose to run about three times as much per day as the mice in the control group, which came from the same original group of mice but did not have not been selectively bred. to run.
After two weeks of the baseline run, the mice were put on broad-spectrum antibiotics (meaning they killed most gut bacteria rather than certain strains) for ten days. Here’s what their average “race log” looked like, measured in revolutions of the wheels in their cages:
Daily distance drops by 21% in High Runner mice and does not return to normal over the next 12 days. In control mice, on the other hand, nothing seems to change. Neither group showed any signs of illness: their weight and food consumption were unaffected. This suggests that some of everything raised in the High Runner mice is affected by the antibiotics.
One possibility is that it is a gut-muscle axis effect. High Runner mice have some sort of microbial advantage – something like the lactate-eating microbe of Boston marathon runners – that makes it easier for them to physically run, which is why they run so much. Take that advantage away, and running isn’t as fun, so they do less of it.
The other possibility is that it is the gut-brain axis in action. McNamara cites previous research showing that the gut microbiome can influence motivation and reward circuits in the brain: Antibiotics affect how certain amino acids are absorbed from the gut into the bloodstream, after which they travel to the brain where they are transformed into brain chemicals. like dopamine and serotonin. McNamara’s experiment cannot distinguish between these two possibilities, but either way, the motivation to exercise seems to wane.
The second study, led by Noah Hutchinson and Jeffrey Woods of the University of Illinois at Urbana-Champaign and published in Medicine and science in sport and exercise, has a similar configuration. They compared normal lab mice with and without broad-spectrum antibiotics, as well as a group of “germ-free” mice that were specially bred from birth to have no microbiome at all. In this case, the researchers looked at how antibiotics affected training adaptations: After six weeks of voluntary running, would the antibiotic-free, germ-free mice gain as much fitness as the control group? Their guess was no.
Again, voluntary wheel travel was reduced by 22% in the antibiotic group and 26% in the germ-free group. Here’s what their daily mileage looked like (the squares are the control group, the circles are on antibiotics, and the triangles are germ-free):
But their answer at this training tells a slightly different story. In a treadmill test to exhaustion, antibiotic mice improved similarly to non-antibiotic mice (their improvement was slightly weaker, but the difference was not statistically significant, and we found expected anyway since they chose to run less during the training period) . Additionally, gene expression and muscle property tests also revealed that the antibiotic group did just as well.
The germ-free mice, on the other hand, did not improve as much after the training period. Since the antibiotic group was unaffected by its lack of microbiome, this suggests that the germ-free mice had some kind of pre-existing developmental deficit through their growth without the microbiome that compromised their ability to respond to the coaching.
The practical conclusion, according to Hutchinson and his co-authors, is that if you have to take antibiotics before an important competition, it is unlikely to affect your training adaptations or your performance. I think that is a reasonable and reassuring position, given all the inherent uncertainties in applying mouse studies to human behavior.
But it’s the apparent change in motivation to exercise that really intrigues me. Is there anything that helps explain who among us ends up as High Runner? If so, can it be manipulated? It’s easy to see how you could get caught up in the excitement of potential new probiotic supplements that change not only your ability, but also your desire to exercise. Garland, in a UC Riverside press release, alludes to this possibility. But his advice, for now, is suitably grounded in current reality. If you want a healthy microbiome, he suggests, you should eat a balanced diet and exercise regularly.
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