Study
Urolithin A improves muscle strength, exercise performance, and biomarkers of mitochondrial health in a randomized trial in middle-aged adults
A randomised placebo-controlled trial (NCT03464500) found urolithin A improved muscle strength by about 12 percent and lowered inflammation markers in middle-aged adults over four months, though the primary endpoint of peak power output was not significantly met.
Summary Can urolithin A improve muscle strength and exercise performance? Show / hide ↓
Researchers gave 88 middle-aged adults either urolithin A or a placebo, a dummy pill, for four months. The study assigned treatments by chance, so the groups could be compared fairly. People taking urolithin A improved muscle strength by about 12 percent, and some measures of endurance and walking also improved. However, the main test, peak power output, meaning the highest power people could produce during exercise, did not improve significantly. Blood tests showed lower inflammation and signs that muscle cells were better at removing worn-out mitochondria, the parts of cells that make energy, but the trial was funded by the company that makes the product.
What this means for you: This is promising but not enough to show that urolithin A reliably improves fitness or strength for most people. There is no strong reason to buy it based on this one small trial, especially because its main outcome was negative.
early evidenceThis is the trial that established urolithin A's human evidence base. Run by Amazentis (the company behind Mitopure) with academic co-authors including Johan Auwerx at EPFL, it registered as NCT03464500. Middle-aged adults received urolithin A (postbiotic Mitopure) at two doses for four months in a randomised, placebo-controlled design. Results: muscle strength improved roughly 12 percent with urolithin A, a clinically meaningful effect size for this population. Aerobic endurance (peak VO2) and physical performance (6-minute walk test) also improved meaningfully. However, peak power output, the trial's stated primary endpoint, did not show significant improvement, which the paper reports plainly rather than reframing around the secondary endpoints that did succeed. Plasma acylcarnitines and C-reactive protein, markers linked to mitochondrial efficiency and inflammation, were significantly lower with urolithin A. Skeletal muscle biopsies showed increased expression of proteins linked to mitophagy and mitochondrial metabolism, giving a plausible mechanism (activation of mitophagy, the recycling of damaged mitochondria) behind the functional results. This remains the single strongest RCT in the commercial longevity-supplement category, and ATLAS 2 (NCT07231783 / ISRCTN47159002) is the ongoing attempt to confirm it in a larger, longer trial.
This study highlights the benefit of Urolithin A to improve muscle performance in middle-aged adults through activation of mitophagy and related biomarkers of mitochondrial health.
The trial's own stated primary endpoint, peak power output, was not significantly improved; the muscle-strength and endurance results that generated most marketing claims were secondary endpoints. Funded and co-authored by Amazentis, the company selling Mitopure, a standard but relevant conflict of interest to note.
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