01.24.22
Supplementing with urolithin A, a byproduct of the gut microbiome which is found most strongly in people with high-polyphenol diets, was shown in a recent double-blind, randomized, placebo-controlled study to positively influence muscle performance and improve markers of mitochondrial health in people over the age of 65. The research, appearing in JAMA, was supported by Amazentis, a Swiss manufacturer of the urolithin A supplement used in the trial.
“This is relevant both to people with chronic diseases and people who want to be more active later in life,” lead author David Marcinek, a professor of radiology at the University of Washington School of Medicine, said. “Mitochondria are like batteries that power the cells in your body. But over time, they break down. The process of mitophagy recognizes this failure and proactively tears down the mitochondria, reducing it to elemental components that a cell can reuse. But with aging, mitophagy becomes less efficient and your body accumulates this pool of failing mitochondria. It’s one way that muscles become less functional as we age.”
Supplementation with urolithin A has been shown in animal tests and molecular studies of humans to stimulate mitophagy, however, little data exists on performance-based outcomes in people.
The present study relied on a small cohort of 66 people over the age of 65 who were randomized to receive a placebo or a daily supplement of 1,000 mg of urolithin A for four months. Each of the 66 subjects was confirmed at the outset to have average or subpar capacity to produce adenosine triphosphate (ATP), which mitochondria produce to help cells perform myriad functions. The hypothesis was that if urolithin A can boost mitophagy, these results should translate to better muscle function and greater ATP output.
Across both cohorts, two comparisons of muscle function were found to support the thesis, but two others didn’t display a significant difference.
Endurance was measured with exercises involving the hand and leg, and it was shown that significantly greater improvements were achieved in muscle contraction performance among the supplementation groups compared to placebo. However, distance covered during a six-minute walk and measures of maximal ATP production weren’t significantly different between the two groups.
“Even though we did not observe an effect of the supplement in whole body function (via six-minute measure and ATP production), these results are still exciting because they demonstrate that just taking a supplement for a short duration actually improved muscle endurance. Fatigue resistance got better in the absence of exercise,” Marcinek said.
Furthermore, supplementing with urolithin A was associated with a significant reduction in several acyl-carnitines and ceramides which are implicated for their roles in metabolic disorders involving mitochondria, the authors of the study reported.
“I think these changes suggest that the treatment affects the metabolic condition of people. Even though it didn't affect the maximum ATP production, it improved test subjects’ general metabolism,” Marcinek said.
“This is relevant both to people with chronic diseases and people who want to be more active later in life,” lead author David Marcinek, a professor of radiology at the University of Washington School of Medicine, said. “Mitochondria are like batteries that power the cells in your body. But over time, they break down. The process of mitophagy recognizes this failure and proactively tears down the mitochondria, reducing it to elemental components that a cell can reuse. But with aging, mitophagy becomes less efficient and your body accumulates this pool of failing mitochondria. It’s one way that muscles become less functional as we age.”
Supplementation with urolithin A has been shown in animal tests and molecular studies of humans to stimulate mitophagy, however, little data exists on performance-based outcomes in people.
The present study relied on a small cohort of 66 people over the age of 65 who were randomized to receive a placebo or a daily supplement of 1,000 mg of urolithin A for four months. Each of the 66 subjects was confirmed at the outset to have average or subpar capacity to produce adenosine triphosphate (ATP), which mitochondria produce to help cells perform myriad functions. The hypothesis was that if urolithin A can boost mitophagy, these results should translate to better muscle function and greater ATP output.
Across both cohorts, two comparisons of muscle function were found to support the thesis, but two others didn’t display a significant difference.
Endurance was measured with exercises involving the hand and leg, and it was shown that significantly greater improvements were achieved in muscle contraction performance among the supplementation groups compared to placebo. However, distance covered during a six-minute walk and measures of maximal ATP production weren’t significantly different between the two groups.
“Even though we did not observe an effect of the supplement in whole body function (via six-minute measure and ATP production), these results are still exciting because they demonstrate that just taking a supplement for a short duration actually improved muscle endurance. Fatigue resistance got better in the absence of exercise,” Marcinek said.
Furthermore, supplementing with urolithin A was associated with a significant reduction in several acyl-carnitines and ceramides which are implicated for their roles in metabolic disorders involving mitochondria, the authors of the study reported.
“I think these changes suggest that the treatment affects the metabolic condition of people. Even though it didn't affect the maximum ATP production, it improved test subjects’ general metabolism,” Marcinek said.
