Effects of Lactate Administration on Mitochondrial Respiratory Function in Mouse Skeletal Muscle
Recent evidence has shown that mitochondrial respiratory function contributes to exercise performance and metabolic health. Given that lactate is considered a potential signaling molecule that induces mitochondrial adaptations, we tested the hypothesis that lactate would change mitochondrial respira...
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Frontiers Media S.A.
2022-06-01
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Series: | Frontiers in Physiology |
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Online Access: | https://www.frontiersin.org/articles/10.3389/fphys.2022.920034/full |
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author | Kenya Takahashi Yuki Tamura Yuki Tamura Yu Kitaoka Yutaka Matsunaga Hideo Hatta |
author_facet | Kenya Takahashi Yuki Tamura Yuki Tamura Yu Kitaoka Yutaka Matsunaga Hideo Hatta |
author_sort | Kenya Takahashi |
collection | DOAJ |
description | Recent evidence has shown that mitochondrial respiratory function contributes to exercise performance and metabolic health. Given that lactate is considered a potential signaling molecule that induces mitochondrial adaptations, we tested the hypothesis that lactate would change mitochondrial respiratory function in skeletal muscle. Male ICR mice (8 weeks old) received intraperitoneal injection of PBS or sodium lactate (1 g/kg BW) 5 days a week for 4 weeks. Mitochondria were isolated from freshly excised gastrocnemius muscle using differential centrifugation and were used for all analyses. Lactate administration significantly enhanced pyruvate + malate- and glutamate + malate-induced (complex I-driven) state 3 (maximal/ATP synthesis-coupled) respiration, but not state 2 (basal/proton conductance) respiration. In contrast, lactate administration significantly decreased succinate + rotenone-induced (complex II-driven) state 3 and 2 respiration. No significant differences were observed in malate + octanoyl-l-carnitine-induced state 3 or 2 respiration. The enzymatic activity of complex I was tended to increase and those of complexes I + III and IV were significantly increased after lactate administration. No differences were observed in the activities of complexes II or II + III. Moreover, lactate administration increased the protein content of NDUFS4, a subunit of complex I, but not those of the other components. The present findings suggest that lactate alters mitochondrial respiratory function in skeletal muscle. |
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format | Article |
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institution | Directory Open Access Journal |
issn | 1664-042X |
language | English |
last_indexed | 2024-04-13T15:53:34Z |
publishDate | 2022-06-01 |
publisher | Frontiers Media S.A. |
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series | Frontiers in Physiology |
spelling | doaj.art-ea37efcf6b544aeba9a4f16173ec39a62022-12-22T02:40:46ZengFrontiers Media S.A.Frontiers in Physiology1664-042X2022-06-011310.3389/fphys.2022.920034920034Effects of Lactate Administration on Mitochondrial Respiratory Function in Mouse Skeletal MuscleKenya Takahashi0Yuki Tamura1Yuki Tamura2Yu Kitaoka3Yutaka Matsunaga4Hideo Hatta5Department of Sports Sciences, The University of Tokyo, Tokyo, JapanGraduate School of Health and Sport Science, Nippon Sport Science University, Tokyo, JapanResearch Institute for Sport Science, Nippon Sport Science University, Tokyo, JapanDepartment of Human Sciences, Kanagawa University, Yokohama, JapanDepartment of Sports Sciences, The University of Tokyo, Tokyo, JapanDepartment of Sports Sciences, The University of Tokyo, Tokyo, JapanRecent evidence has shown that mitochondrial respiratory function contributes to exercise performance and metabolic health. Given that lactate is considered a potential signaling molecule that induces mitochondrial adaptations, we tested the hypothesis that lactate would change mitochondrial respiratory function in skeletal muscle. Male ICR mice (8 weeks old) received intraperitoneal injection of PBS or sodium lactate (1 g/kg BW) 5 days a week for 4 weeks. Mitochondria were isolated from freshly excised gastrocnemius muscle using differential centrifugation and were used for all analyses. Lactate administration significantly enhanced pyruvate + malate- and glutamate + malate-induced (complex I-driven) state 3 (maximal/ATP synthesis-coupled) respiration, but not state 2 (basal/proton conductance) respiration. In contrast, lactate administration significantly decreased succinate + rotenone-induced (complex II-driven) state 3 and 2 respiration. No significant differences were observed in malate + octanoyl-l-carnitine-induced state 3 or 2 respiration. The enzymatic activity of complex I was tended to increase and those of complexes I + III and IV were significantly increased after lactate administration. No differences were observed in the activities of complexes II or II + III. Moreover, lactate administration increased the protein content of NDUFS4, a subunit of complex I, but not those of the other components. The present findings suggest that lactate alters mitochondrial respiratory function in skeletal muscle.https://www.frontiersin.org/articles/10.3389/fphys.2022.920034/fulllactatemitochondriaoxygen consumption ratesupercomplexskeletal muscle |
spellingShingle | Kenya Takahashi Yuki Tamura Yuki Tamura Yu Kitaoka Yutaka Matsunaga Hideo Hatta Effects of Lactate Administration on Mitochondrial Respiratory Function in Mouse Skeletal Muscle Frontiers in Physiology lactate mitochondria oxygen consumption rate supercomplex skeletal muscle |
title | Effects of Lactate Administration on Mitochondrial Respiratory Function in Mouse Skeletal Muscle |
title_full | Effects of Lactate Administration on Mitochondrial Respiratory Function in Mouse Skeletal Muscle |
title_fullStr | Effects of Lactate Administration on Mitochondrial Respiratory Function in Mouse Skeletal Muscle |
title_full_unstemmed | Effects of Lactate Administration on Mitochondrial Respiratory Function in Mouse Skeletal Muscle |
title_short | Effects of Lactate Administration on Mitochondrial Respiratory Function in Mouse Skeletal Muscle |
title_sort | effects of lactate administration on mitochondrial respiratory function in mouse skeletal muscle |
topic | lactate mitochondria oxygen consumption rate supercomplex skeletal muscle |
url | https://www.frontiersin.org/articles/10.3389/fphys.2022.920034/full |
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