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Involvement of ammonia metabolism in the improvement of endurance performance by tea catechins in mice

Blood ammonia increases during exercise, and it has been suggested that this increase is both a central and peripheral fatigue factor. Although green tea catechins (GTCs) are known to improve exercise endurance by enhancing lipid metabolism in skeletal muscle, little is known about the relationship...

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Autores principales: Chen, Shu, Minegishi, Yoshihiko, Hasumura, Takahiro, Shimotoyodome, Akira, Ota, Noriyasu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7142105/
https://www.ncbi.nlm.nih.gov/pubmed/32269254
http://dx.doi.org/10.1038/s41598-020-63139-9
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author Chen, Shu
Minegishi, Yoshihiko
Hasumura, Takahiro
Shimotoyodome, Akira
Ota, Noriyasu
author_facet Chen, Shu
Minegishi, Yoshihiko
Hasumura, Takahiro
Shimotoyodome, Akira
Ota, Noriyasu
author_sort Chen, Shu
collection PubMed
description Blood ammonia increases during exercise, and it has been suggested that this increase is both a central and peripheral fatigue factor. Although green tea catechins (GTCs) are known to improve exercise endurance by enhancing lipid metabolism in skeletal muscle, little is known about the relationship between ammonia metabolism and the endurance-improving effect of GTCs. Here, we examined how ammonia affects endurance capacity and how GTCs affect ammonia metabolism in vivo in mice and how GTCs affect mouse skeletal muscle and liver in vitro. In mice, blood ammonia concentration was significantly negatively correlated with exercise endurance capacity, and hyperammonaemia was found to decrease whole-body fat expenditure and fatty acid oxidation–related gene expression in skeletal muscle. Repeated ingestion of GTCs combined with regular exercise training improved endurance capacity and the expression of urea cycle–related genes in liver. In C2C12 myotubes, hyperammonaemia suppressed mitochondrial respiration; however, pre-incubation with GTCs rescued this suppression. Together, our results demonstrate that hyperammonaemia decreases both mitochondrial respiration in myotubes and whole-body aerobic metabolism. Thus, GTC-mediated increases in ammonia metabolism in liver and resistance to ammonia-induced suppression of mitochondrial respiration in skeletal muscle may underlie the endurance-improving effect of GTCs.
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spelling pubmed-71421052020-04-11 Involvement of ammonia metabolism in the improvement of endurance performance by tea catechins in mice Chen, Shu Minegishi, Yoshihiko Hasumura, Takahiro Shimotoyodome, Akira Ota, Noriyasu Sci Rep Article Blood ammonia increases during exercise, and it has been suggested that this increase is both a central and peripheral fatigue factor. Although green tea catechins (GTCs) are known to improve exercise endurance by enhancing lipid metabolism in skeletal muscle, little is known about the relationship between ammonia metabolism and the endurance-improving effect of GTCs. Here, we examined how ammonia affects endurance capacity and how GTCs affect ammonia metabolism in vivo in mice and how GTCs affect mouse skeletal muscle and liver in vitro. In mice, blood ammonia concentration was significantly negatively correlated with exercise endurance capacity, and hyperammonaemia was found to decrease whole-body fat expenditure and fatty acid oxidation–related gene expression in skeletal muscle. Repeated ingestion of GTCs combined with regular exercise training improved endurance capacity and the expression of urea cycle–related genes in liver. In C2C12 myotubes, hyperammonaemia suppressed mitochondrial respiration; however, pre-incubation with GTCs rescued this suppression. Together, our results demonstrate that hyperammonaemia decreases both mitochondrial respiration in myotubes and whole-body aerobic metabolism. Thus, GTC-mediated increases in ammonia metabolism in liver and resistance to ammonia-induced suppression of mitochondrial respiration in skeletal muscle may underlie the endurance-improving effect of GTCs. Nature Publishing Group UK 2020-04-08 /pmc/articles/PMC7142105/ /pubmed/32269254 http://dx.doi.org/10.1038/s41598-020-63139-9 Text en © The Author(s) 2020 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Chen, Shu
Minegishi, Yoshihiko
Hasumura, Takahiro
Shimotoyodome, Akira
Ota, Noriyasu
Involvement of ammonia metabolism in the improvement of endurance performance by tea catechins in mice
title Involvement of ammonia metabolism in the improvement of endurance performance by tea catechins in mice
title_full Involvement of ammonia metabolism in the improvement of endurance performance by tea catechins in mice
title_fullStr Involvement of ammonia metabolism in the improvement of endurance performance by tea catechins in mice
title_full_unstemmed Involvement of ammonia metabolism in the improvement of endurance performance by tea catechins in mice
title_short Involvement of ammonia metabolism in the improvement of endurance performance by tea catechins in mice
title_sort involvement of ammonia metabolism in the improvement of endurance performance by tea catechins in mice
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7142105/
https://www.ncbi.nlm.nih.gov/pubmed/32269254
http://dx.doi.org/10.1038/s41598-020-63139-9
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