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Effects of lactate administration on hypertrophy and mTOR signaling activation in mouse skeletal muscle
Lactate is a metabolic product of glycolysis and has recently been shown to act as a signaling molecule that induces adaptations in oxidative metabolism. In this study, we investigated whether lactate administration enhanced muscle hypertrophy and protein synthesis responses during resistance exerci...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9393907/ https://www.ncbi.nlm.nih.gov/pubmed/35993446 http://dx.doi.org/10.14814/phy2.15436 |
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author | Shirai, Takanaga Kitaoka, Yu Uemichi, Kazuki Tokinoya, Katsuyuki Takeda, Kohei Takemasa, Tohru |
author_facet | Shirai, Takanaga Kitaoka, Yu Uemichi, Kazuki Tokinoya, Katsuyuki Takeda, Kohei Takemasa, Tohru |
author_sort | Shirai, Takanaga |
collection | PubMed |
description | Lactate is a metabolic product of glycolysis and has recently been shown to act as a signaling molecule that induces adaptations in oxidative metabolism. In this study, we investigated whether lactate administration enhanced muscle hypertrophy and protein synthesis responses during resistance exercise in animal models. We used male ICR mice (7–8 weeks old) were used for chronic (mechanical overload induced by synergist ablation: [OL]) and acute (high‐intensity muscle contraction by electrical stimulation: [ES]) resistance exercise models. The animals were intraperitoneally administrated a single dose of sodium lactate (1 g/kg of body weight) in the ES study, and once a day for 14 consecutive days in the OL study. Two weeks of mechanical overload increased plantaris muscle wet weight (main effect of OL: p < 0.05) and fiber cross‐sectional area (main effect of OL: p < 0.05), but those were not affected by lactate administration. Following the acute resistance exercise by ES, protein synthesis and phosphorylation of p70 S6 kinase and ribosomal protein S6, which are downstream molecules in the anabolic signaling cascade, were increased (main effect of ES: p < 0.05), but lactate administration had no effect. This study demonstrated that exogenous lactate administration has little effect on the muscle hypertrophic response during resistance exercise using acute ES and chronic OL models. Our results do not support the hypothesis that elevated blood lactate concentration induces protein synthesis responses in skeletal muscle. |
format | Online Article Text |
id | pubmed-9393907 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-93939072022-08-24 Effects of lactate administration on hypertrophy and mTOR signaling activation in mouse skeletal muscle Shirai, Takanaga Kitaoka, Yu Uemichi, Kazuki Tokinoya, Katsuyuki Takeda, Kohei Takemasa, Tohru Physiol Rep Original Articles Lactate is a metabolic product of glycolysis and has recently been shown to act as a signaling molecule that induces adaptations in oxidative metabolism. In this study, we investigated whether lactate administration enhanced muscle hypertrophy and protein synthesis responses during resistance exercise in animal models. We used male ICR mice (7–8 weeks old) were used for chronic (mechanical overload induced by synergist ablation: [OL]) and acute (high‐intensity muscle contraction by electrical stimulation: [ES]) resistance exercise models. The animals were intraperitoneally administrated a single dose of sodium lactate (1 g/kg of body weight) in the ES study, and once a day for 14 consecutive days in the OL study. Two weeks of mechanical overload increased plantaris muscle wet weight (main effect of OL: p < 0.05) and fiber cross‐sectional area (main effect of OL: p < 0.05), but those were not affected by lactate administration. Following the acute resistance exercise by ES, protein synthesis and phosphorylation of p70 S6 kinase and ribosomal protein S6, which are downstream molecules in the anabolic signaling cascade, were increased (main effect of ES: p < 0.05), but lactate administration had no effect. This study demonstrated that exogenous lactate administration has little effect on the muscle hypertrophic response during resistance exercise using acute ES and chronic OL models. Our results do not support the hypothesis that elevated blood lactate concentration induces protein synthesis responses in skeletal muscle. John Wiley and Sons Inc. 2022-08-22 /pmc/articles/PMC9393907/ /pubmed/35993446 http://dx.doi.org/10.14814/phy2.15436 Text en © 2022 The Authors. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Articles Shirai, Takanaga Kitaoka, Yu Uemichi, Kazuki Tokinoya, Katsuyuki Takeda, Kohei Takemasa, Tohru Effects of lactate administration on hypertrophy and mTOR signaling activation in mouse skeletal muscle |
title | Effects of lactate administration on hypertrophy and mTOR signaling activation in mouse skeletal muscle |
title_full | Effects of lactate administration on hypertrophy and mTOR signaling activation in mouse skeletal muscle |
title_fullStr | Effects of lactate administration on hypertrophy and mTOR signaling activation in mouse skeletal muscle |
title_full_unstemmed | Effects of lactate administration on hypertrophy and mTOR signaling activation in mouse skeletal muscle |
title_short | Effects of lactate administration on hypertrophy and mTOR signaling activation in mouse skeletal muscle |
title_sort | effects of lactate administration on hypertrophy and mtor signaling activation in mouse skeletal muscle |
topic | Original Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9393907/ https://www.ncbi.nlm.nih.gov/pubmed/35993446 http://dx.doi.org/10.14814/phy2.15436 |
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