Four days of bed rest increases intrinsic mitochondrial respiratory capacity in young healthy males

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Four days of bed rest increases intrinsic mitochondrial respiratory capacity in young healthy males. / Larsen, Steen; Lundby, Anne-Kristine M; Dandanell, Sune; Oberholzer, Laura; Keiser, Stefanie; Andersen, Andreas Breenfeldt; Haider, Thomas; Lundby, Carsten.

I: Physiological Reports, Bind 6, Nr. 18, e13793, 2018.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Larsen, S, Lundby, A-KM, Dandanell, S, Oberholzer, L, Keiser, S, Andersen, AB, Haider, T & Lundby, C 2018, 'Four days of bed rest increases intrinsic mitochondrial respiratory capacity in young healthy males', Physiological Reports, bind 6, nr. 18, e13793. https://doi.org/10.14814/phy2.13793

APA

Larsen, S., Lundby, A-K. M., Dandanell, S., Oberholzer, L., Keiser, S., Andersen, A. B., ... Lundby, C. (2018). Four days of bed rest increases intrinsic mitochondrial respiratory capacity in young healthy males. Physiological Reports, 6(18), [e13793]. https://doi.org/10.14814/phy2.13793

Vancouver

Larsen S, Lundby A-KM, Dandanell S, Oberholzer L, Keiser S, Andersen AB o.a. Four days of bed rest increases intrinsic mitochondrial respiratory capacity in young healthy males. Physiological Reports. 2018;6(18). e13793. https://doi.org/10.14814/phy2.13793

Author

Larsen, Steen ; Lundby, Anne-Kristine M ; Dandanell, Sune ; Oberholzer, Laura ; Keiser, Stefanie ; Andersen, Andreas Breenfeldt ; Haider, Thomas ; Lundby, Carsten. / Four days of bed rest increases intrinsic mitochondrial respiratory capacity in young healthy males. I: Physiological Reports. 2018 ; Bind 6, Nr. 18.

Bibtex

@article{a7a86d0a09ce4578a98510ec93938bad,
title = "Four days of bed rest increases intrinsic mitochondrial respiratory capacity in young healthy males",
abstract = "Bed rest leads to impaired glucose tolerance. Whether this is linked to maladaptation's in skeletal muscle mitochondrial function and in particular to the level of reactive oxygen species (ROS) is at present unknown. The aim of this longitudinal study was to quantify skeletal muscle mitochondrial function (respiratory capacity and ROS production) together with glucose tolerance after 4 days of strict bed rest in healthy young male subjects (n = 14). Mitochondrial function was determined in permeabilized muscle fibers using high-resolution respirometry and fluorometry, mitochondrial content (citrate synthase [CS] activity) and antioxidant protein expression levels were assessed in parallel to this. Glucose tolerance was determined by means of oral glucose tolerance tests. Intrinsic mitochondrial respiratory capacity was augmented after the bed rest period (CI + IIP : 0.43 ± 0.12 vs. 0.55 ± 0.14 [pmol/sec/mg]/CS activity), due to a decreased CS activity (158 ± 39 vs. 129 ± 25 mU/mg dw.). No differences were observed in ROS production (per mg of tissue or when normalized to CS activity). Furthermore, the protein content for catalase was increased while superoxide dismutase and glutathione peroxidase remained unaffected. These findings were accompanied by an impaired glucose tolerance after the bed rest period (Matsuda index: 12 ± 6 vs. 9 ± 5). The change in intrinsic mitochondrial respiratory capacity could be an early indication in the development of impaired glucose tolerance. The increased catalase protein content might explain that no change was seen in ROS production after 4 days of bed rest. Whether these findings can be extrapolated to lifestyle-dependent decrements in physical activity and the development of type-2-diabetes remains unknown.",
keywords = "Bed rest, glucose tolerance, mitochondria, reactive oxygen species production",
author = "Steen Larsen and Lundby, {Anne-Kristine M} and Sune Dandanell and Laura Oberholzer and Stefanie Keiser and Andersen, {Andreas Breenfeldt} and Thomas Haider and Carsten Lundby",
note = "(ekstern)",
year = "2018",
doi = "10.14814/phy2.13793",
language = "English",
volume = "6",
journal = "Physiological Reports",
issn = "2051-817X",
publisher = "Wiley Periodicals, Inc.",
number = "18",

}

RIS

TY - JOUR

T1 - Four days of bed rest increases intrinsic mitochondrial respiratory capacity in young healthy males

AU - Larsen, Steen

AU - Lundby, Anne-Kristine M

AU - Dandanell, Sune

AU - Oberholzer, Laura

AU - Keiser, Stefanie

AU - Andersen, Andreas Breenfeldt

AU - Haider, Thomas

AU - Lundby, Carsten

N1 - (ekstern)

PY - 2018

Y1 - 2018

N2 - Bed rest leads to impaired glucose tolerance. Whether this is linked to maladaptation's in skeletal muscle mitochondrial function and in particular to the level of reactive oxygen species (ROS) is at present unknown. The aim of this longitudinal study was to quantify skeletal muscle mitochondrial function (respiratory capacity and ROS production) together with glucose tolerance after 4 days of strict bed rest in healthy young male subjects (n = 14). Mitochondrial function was determined in permeabilized muscle fibers using high-resolution respirometry and fluorometry, mitochondrial content (citrate synthase [CS] activity) and antioxidant protein expression levels were assessed in parallel to this. Glucose tolerance was determined by means of oral glucose tolerance tests. Intrinsic mitochondrial respiratory capacity was augmented after the bed rest period (CI + IIP : 0.43 ± 0.12 vs. 0.55 ± 0.14 [pmol/sec/mg]/CS activity), due to a decreased CS activity (158 ± 39 vs. 129 ± 25 mU/mg dw.). No differences were observed in ROS production (per mg of tissue or when normalized to CS activity). Furthermore, the protein content for catalase was increased while superoxide dismutase and glutathione peroxidase remained unaffected. These findings were accompanied by an impaired glucose tolerance after the bed rest period (Matsuda index: 12 ± 6 vs. 9 ± 5). The change in intrinsic mitochondrial respiratory capacity could be an early indication in the development of impaired glucose tolerance. The increased catalase protein content might explain that no change was seen in ROS production after 4 days of bed rest. Whether these findings can be extrapolated to lifestyle-dependent decrements in physical activity and the development of type-2-diabetes remains unknown.

AB - Bed rest leads to impaired glucose tolerance. Whether this is linked to maladaptation's in skeletal muscle mitochondrial function and in particular to the level of reactive oxygen species (ROS) is at present unknown. The aim of this longitudinal study was to quantify skeletal muscle mitochondrial function (respiratory capacity and ROS production) together with glucose tolerance after 4 days of strict bed rest in healthy young male subjects (n = 14). Mitochondrial function was determined in permeabilized muscle fibers using high-resolution respirometry and fluorometry, mitochondrial content (citrate synthase [CS] activity) and antioxidant protein expression levels were assessed in parallel to this. Glucose tolerance was determined by means of oral glucose tolerance tests. Intrinsic mitochondrial respiratory capacity was augmented after the bed rest period (CI + IIP : 0.43 ± 0.12 vs. 0.55 ± 0.14 [pmol/sec/mg]/CS activity), due to a decreased CS activity (158 ± 39 vs. 129 ± 25 mU/mg dw.). No differences were observed in ROS production (per mg of tissue or when normalized to CS activity). Furthermore, the protein content for catalase was increased while superoxide dismutase and glutathione peroxidase remained unaffected. These findings were accompanied by an impaired glucose tolerance after the bed rest period (Matsuda index: 12 ± 6 vs. 9 ± 5). The change in intrinsic mitochondrial respiratory capacity could be an early indication in the development of impaired glucose tolerance. The increased catalase protein content might explain that no change was seen in ROS production after 4 days of bed rest. Whether these findings can be extrapolated to lifestyle-dependent decrements in physical activity and the development of type-2-diabetes remains unknown.

KW - Bed rest

KW - glucose tolerance

KW - mitochondria

KW - reactive oxygen species production

U2 - 10.14814/phy2.13793

DO - 10.14814/phy2.13793

M3 - Journal article

VL - 6

JO - Physiological Reports

JF - Physiological Reports

SN - 2051-817X

IS - 18

M1 - e13793

ER -

ID: 203897339