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Trimethylamine N-Oxide Improves Exercise Performance by Reducing Oxidative Stress Through Activation of the Nrf2 Signaling Pathway

Overview
Journal Molecules
Publisher MDPI
Specialty Biology
Date 2024 Feb 24
PMID 38398511
Authors
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Abstract

Trimethylamine N-oxide (TMAO) has attracted interest because of its association with cardiovascular disease and diabetes, and evidence for the beneficial effects of TMAO is accumulating. This study investigates the role of TMAO in improving exercise performance and elucidates the underlying molecular mechanisms. Using C2C12 cells, we established an oxidative stress model and administered TMAO treatment. Our results indicate that TMAO significantly protects myoblasts from oxidative stress-induced damage by increasing the expression of Nrf2, heme oxygenase-1 (HO-1), NAD(P)H dehydrogenase (NQO1), and catalase (CAT). In particular, suppression of Nrf2 resulted in a loss of the protective effects of TMAO and a significant decrease in the expression levels of Nrf2, HO-1, and NQO1. In addition, we evaluated the effects of TMAO in an exhaustive swimming test in mice. TMAO treatment significantly prolonged swimming endurance, increased glutathione and taurine levels, enhanced glutathione peroxidase activity, and increased the expression of Nrf2 and its downstream antioxidant genes, including HO-1, NQO1, and CAT, in skeletal muscle. These findings underscore the potential of TMAO to counteract exercise-induced oxidative stress. This research provides new insights into the ability of TMAO to alleviate exercise-induced oxidative stress via the Nrf2 signaling pathway, providing a valuable framework for the development of sports nutrition supplements aimed at mitigating oxidative stress.

Citing Articles

Serum trimethylamine N-oxide and its precursors are associated with the occurrence of mild cognition impairment as well as changes in neurocognitive status.

Bai H, Zhang Y, Tian P, Wu Y, Peng R, Liang B Front Nutr. 2024; 11:1461942.

PMID: 39668903 PMC: 11634597. DOI: 10.3389/fnut.2024.1461942.

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