Exercise, mitochondrial biogenesis and disuse-induced atrophy
In addition to the physiological and cellular effects of exercise, many studies demonstrated that exercise could prevent skeletal muscle atrophy due to disuse. Mitochondria, which are powerhouses in cells, are at the top of the molecular mechanisms that control muscle function. Mitochondria play an...
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Format: | Article |
Language: | English |
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Turkish Sports Medicine Association
2021-06-01
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Series: | Spor Hekimligi Dergisi |
Subjects: | |
Online Access: |
https://journalofsportsmedicine.org/eng/full-text-pdf/568/eng
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author | Şenay Akın Gökhan Burçin Kubat1 2 Haydar A. Demirel1 3 |
author_facet | Şenay Akın Gökhan Burçin Kubat1 2 Haydar A. Demirel1 3 |
author_sort | Şenay Akın |
collection | DOAJ |
description | In addition to the physiological and cellular effects of exercise, many studies demonstrated that exercise could prevent skeletal muscle atrophy due to disuse. Mitochondria, which are powerhouses in cells, are at the top of the molecular mechanisms that control muscle function. Mitochondria play an essential role in regulating protein synthesis and degradation through various signaling pathways such as ubiquitin-proteolysis, mitochondrial biogenesis, fusion, and fission dynamics autophagy, and apoptosis. Regular exercise protects the skeletal muscle against different stresses by improving cellular oxidative capacity. Eventually, exercise controls the expression of proteins that have been shown to protect muscle from atrophy caused by disuse and activates many cellular signaling pathways. In this review, the role of mitochondria in muscle cells, the effect of disuse atrophy on mitochondria, and the effect of exercise on peroxisome proliferator-activated receptor-gamma coactivator (PGC-1α) that plays a crucial role in mitochondrial biogenesis are discussed. |
first_indexed | 2024-04-10T10:30:45Z |
format | Article |
id | doaj.art-3ccb3c15e5254415b6d7311b8ee778bb |
institution | Directory Open Access Journal |
issn | 1300-0551 2587-1498 |
language | English |
last_indexed | 2024-04-10T10:30:45Z |
publishDate | 2021-06-01 |
publisher | Turkish Sports Medicine Association |
record_format | Article |
series | Spor Hekimligi Dergisi |
spelling | doaj.art-3ccb3c15e5254415b6d7311b8ee778bb2023-02-15T16:21:07ZengTurkish Sports Medicine AssociationSpor Hekimligi Dergisi1300-05512587-14982021-06-01562919710.47447/tjsm.0491568Exercise, mitochondrial biogenesis and disuse-induced atrophyŞenay Akın0Gökhan Burçin Kubat1122Haydar A. Demirel1334 Exercise and Sport Physiology Department, Faculty of Sport Sciences, Hacettepe University, Ankara, Turkey Exercise and Sport Physiology Department, Faculty of Sport Sciences, Hacettepe University, Ankara, Turkey Exercise and Sport Physiology Department, Faculty of Sport Sciences, Hacettepe University, Ankara, Turkey Exercise and Sport Physiology Department, Faculty of Sport Sciences, Hacettepe University, Ankara, Turkey Exercise and Sport Physiology Department, Faculty of Sport Sciences, Hacettepe University, Ankara, Turkey In addition to the physiological and cellular effects of exercise, many studies demonstrated that exercise could prevent skeletal muscle atrophy due to disuse. Mitochondria, which are powerhouses in cells, are at the top of the molecular mechanisms that control muscle function. Mitochondria play an essential role in regulating protein synthesis and degradation through various signaling pathways such as ubiquitin-proteolysis, mitochondrial biogenesis, fusion, and fission dynamics autophagy, and apoptosis. Regular exercise protects the skeletal muscle against different stresses by improving cellular oxidative capacity. Eventually, exercise controls the expression of proteins that have been shown to protect muscle from atrophy caused by disuse and activates many cellular signaling pathways. In this review, the role of mitochondria in muscle cells, the effect of disuse atrophy on mitochondria, and the effect of exercise on peroxisome proliferator-activated receptor-gamma coactivator (PGC-1α) that plays a crucial role in mitochondrial biogenesis are discussed. https://journalofsportsmedicine.org/eng/full-text-pdf/568/eng muscle atrophyfusion and fission dynamicsca2+ homeostasismitochondrial disease |
spellingShingle | Şenay Akın Gökhan Burçin Kubat1 2 Haydar A. Demirel1 3 Exercise, mitochondrial biogenesis and disuse-induced atrophy Spor Hekimligi Dergisi muscle atrophy fusion and fission dynamics ca2+ homeostasis mitochondrial disease |
title | Exercise, mitochondrial biogenesis and disuse-induced atrophy |
title_full | Exercise, mitochondrial biogenesis and disuse-induced atrophy |
title_fullStr | Exercise, mitochondrial biogenesis and disuse-induced atrophy |
title_full_unstemmed | Exercise, mitochondrial biogenesis and disuse-induced atrophy |
title_short | Exercise, mitochondrial biogenesis and disuse-induced atrophy |
title_sort | exercise mitochondrial biogenesis and disuse induced atrophy |
topic | muscle atrophy fusion and fission dynamics ca2+ homeostasis mitochondrial disease |
url |
https://journalofsportsmedicine.org/eng/full-text-pdf/568/eng
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