Skeletal muscle mitochondrial H2O2 emission increases with immobilization and decreases after aerobic training in young and older men

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Skeletal muscle mitochondrial H2O2 emission increases with immobilization and decreases after aerobic training in young and older men. / Gram, Martin; Vigelsø, Andreas; Yokota, Takashi; Helge, Jørn Wulff; Dela, Flemming; Hey-Mogensen, Martin.

I: The Journal of Physiology, Bind 593, Nr. 17, 01.09.2015, s. 4011-4027.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Gram, M, Vigelsø, A, Yokota, T, Helge, JW, Dela, F & Hey-Mogensen, M 2015, 'Skeletal muscle mitochondrial H2O2 emission increases with immobilization and decreases after aerobic training in young and older men', The Journal of Physiology, bind 593, nr. 17, s. 4011-4027. https://doi.org/10.1113/JP270211

APA

Gram, M., Vigelsø, A., Yokota, T., Helge, J. W., Dela, F., & Hey-Mogensen, M. (2015). Skeletal muscle mitochondrial H2O2 emission increases with immobilization and decreases after aerobic training in young and older men. The Journal of Physiology, 593(17), 4011-4027. https://doi.org/10.1113/JP270211

Vancouver

Gram M, Vigelsø A, Yokota T, Helge JW, Dela F, Hey-Mogensen M. Skeletal muscle mitochondrial H2O2 emission increases with immobilization and decreases after aerobic training in young and older men. The Journal of Physiology. 2015 sep 1;593(17):4011-4027. https://doi.org/10.1113/JP270211

Author

Gram, Martin ; Vigelsø, Andreas ; Yokota, Takashi ; Helge, Jørn Wulff ; Dela, Flemming ; Hey-Mogensen, Martin. / Skeletal muscle mitochondrial H2O2 emission increases with immobilization and decreases after aerobic training in young and older men. I: The Journal of Physiology. 2015 ; Bind 593, Nr. 17. s. 4011-4027.

Bibtex

@article{29f0bf81c98643699e0703df73bbccb0,
title = "Skeletal muscle mitochondrial H2O2 emission increases with immobilization and decreases after aerobic training in young and older men",
abstract = "Mitochondrial dysfunction, defined as increased oxidative stress and lower capacity for energy production, may be seen with aging and may cause frailty, or it could be that it is secondary to physical inactivity. We studied the effect of two weeks of one-leg immobilization followed by six weeks of supervised cycle training on mitochondrial function in 17 young (23 ± 1 years, mean ± SEM) and 15 older (68 ± 1 years) healthy men. Submaximal hydrogen peroxide H2O2 emission and respiration were measured simultaneously at a predefined membrane potential in isolated mitochondria from skeletal muscle using two protocols pyruvate+malate (PM) and succinate+rotenone (SR). This allowed measurement of leak and ATP generating respiration from which the coupling efficiency can be calculated. Protein content of the antioxidants manganese superoxide dismuthase (MnSOD), CuZn-superoxide dismuthase (CuZnSOD), catalase and gluthathione peroxidase 1 (GPX1) were measured by Western Blotting. Immobilization decreased ATP generating respiration using PM and increased H2O2 emission using both PM and SR similarly in young and older men. Both were restored to baseline after the training period. Furthermore, MnSOD and catalase content increased with endurance training. The young men had a higher leak respiration at inclusion using PM and a higher membrane potential in state 3 using both substrate combinations. Collectively, this study supports the notion that increased mitochondrial ROS mediates the detrimental effects seen after physical inactivity. Age on the other hand was not associated with impairments in antioxidant protein levels, mitochondrial respiration or H2O2 emission using either protocol. This article is protected by copyright. All rights reserved.",
author = "Martin Gram and Andreas Vigels{\o} and Takashi Yokota and Helge, {J{\o}rn Wulff} and Flemming Dela and Martin Hey-Mogensen",
note = "This article is protected by copyright. All rights reserved.",
year = "2015",
month = "9",
day = "1",
doi = "10.1113/JP270211",
language = "English",
volume = "593",
pages = "4011--4027",
journal = "The Journal of Physiology",
issn = "0022-3751",
publisher = "Wiley-Blackwell",
number = "17",

}

RIS

TY - JOUR

T1 - Skeletal muscle mitochondrial H2O2 emission increases with immobilization and decreases after aerobic training in young and older men

AU - Gram, Martin

AU - Vigelsø, Andreas

AU - Yokota, Takashi

AU - Helge, Jørn Wulff

AU - Dela, Flemming

AU - Hey-Mogensen, Martin

N1 - This article is protected by copyright. All rights reserved.

PY - 2015/9/1

Y1 - 2015/9/1

N2 - Mitochondrial dysfunction, defined as increased oxidative stress and lower capacity for energy production, may be seen with aging and may cause frailty, or it could be that it is secondary to physical inactivity. We studied the effect of two weeks of one-leg immobilization followed by six weeks of supervised cycle training on mitochondrial function in 17 young (23 ± 1 years, mean ± SEM) and 15 older (68 ± 1 years) healthy men. Submaximal hydrogen peroxide H2O2 emission and respiration were measured simultaneously at a predefined membrane potential in isolated mitochondria from skeletal muscle using two protocols pyruvate+malate (PM) and succinate+rotenone (SR). This allowed measurement of leak and ATP generating respiration from which the coupling efficiency can be calculated. Protein content of the antioxidants manganese superoxide dismuthase (MnSOD), CuZn-superoxide dismuthase (CuZnSOD), catalase and gluthathione peroxidase 1 (GPX1) were measured by Western Blotting. Immobilization decreased ATP generating respiration using PM and increased H2O2 emission using both PM and SR similarly in young and older men. Both were restored to baseline after the training period. Furthermore, MnSOD and catalase content increased with endurance training. The young men had a higher leak respiration at inclusion using PM and a higher membrane potential in state 3 using both substrate combinations. Collectively, this study supports the notion that increased mitochondrial ROS mediates the detrimental effects seen after physical inactivity. Age on the other hand was not associated with impairments in antioxidant protein levels, mitochondrial respiration or H2O2 emission using either protocol. This article is protected by copyright. All rights reserved.

AB - Mitochondrial dysfunction, defined as increased oxidative stress and lower capacity for energy production, may be seen with aging and may cause frailty, or it could be that it is secondary to physical inactivity. We studied the effect of two weeks of one-leg immobilization followed by six weeks of supervised cycle training on mitochondrial function in 17 young (23 ± 1 years, mean ± SEM) and 15 older (68 ± 1 years) healthy men. Submaximal hydrogen peroxide H2O2 emission and respiration were measured simultaneously at a predefined membrane potential in isolated mitochondria from skeletal muscle using two protocols pyruvate+malate (PM) and succinate+rotenone (SR). This allowed measurement of leak and ATP generating respiration from which the coupling efficiency can be calculated. Protein content of the antioxidants manganese superoxide dismuthase (MnSOD), CuZn-superoxide dismuthase (CuZnSOD), catalase and gluthathione peroxidase 1 (GPX1) were measured by Western Blotting. Immobilization decreased ATP generating respiration using PM and increased H2O2 emission using both PM and SR similarly in young and older men. Both were restored to baseline after the training period. Furthermore, MnSOD and catalase content increased with endurance training. The young men had a higher leak respiration at inclusion using PM and a higher membrane potential in state 3 using both substrate combinations. Collectively, this study supports the notion that increased mitochondrial ROS mediates the detrimental effects seen after physical inactivity. Age on the other hand was not associated with impairments in antioxidant protein levels, mitochondrial respiration or H2O2 emission using either protocol. This article is protected by copyright. All rights reserved.

U2 - 10.1113/JP270211

DO - 10.1113/JP270211

M3 - Journal article

C2 - 26096818

VL - 593

SP - 4011

EP - 4027

JO - The Journal of Physiology

JF - The Journal of Physiology

SN - 0022-3751

IS - 17

ER -

ID: 140535091