Repeated static contractions increase mitochondrial vulnerability toward oxidative stress in human skeletal muscle.
Document identifier: oai:dalea.du.se:2310
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10.1152/japplphysiol.01007.2005Keyword: Medical and Health Sciences,
Basic Medicine,
Medicin och hälsovetenskap,
Medicinska och farmaceutiska grundvetenskaper,
Calcium homeostasis; exercise; mitochondria; oxidative phosphorylationPublication year: 2006Relevant Sustainable Development Goals (SDGs):
The SDG label(s) above have been assigned by OSDG.aiAbstract: Repeated static contractions (RSC) induce large fluctuations in tissue oxygen tension and increase the generation of reactive oxygen species (ROS). This study investigated the effect of RSC on muscle contractility, mitochondrial respiratory function, and in vitro sarcoplasmic reticulum (SR) Ca2+ kinetics in human muscle. Ten male subjects performed five bouts of static knee extension with 10-min rest in between. Each bout of RSC (target torque 66% of maximal voluntary contraction torque) was maintained to fatigue. Muscle biopsies were taken preexercise and 0.3 and 24 h postexercise from vastus lateralis. Mitochondria were isolated and respiratory function measured after incubation with H2O2 (HPX) or control medium (Con). Mitochondrial function was not affected by RSC during Con. However, RSC exacerbated mitochondrial dysfunction during HPX, resulting in decreased respiratory control index, decreased mitochondrial efficiency (phosphorylated ADP-to-oxygen consumed ratio), and increased noncoupled respiration (HPX/Con post- vs. preexercise). SR Ca2+ uptake rate was lower 0.3 vs. 24 h postexercise, whereas SR Ca2+ release rate was unchanged. RSC resulted in long-lasting changes in muscle contractility, including reduced maximal torque, low-frequency fatigue, and faster torque relaxation. It is concluded that RSC increases mitochondrial vulnerability toward ROS, reduces SR Ca2+ uptake rate, and causes low-frequency fatigue. Although conclusive evidence is lacking, we suggest that these changes are related to increased formation of ROS during RSC.
Authors
Kent Sahlin
Other publications
>>
J.S. Nielsen
Other publications
>>
M Mogensen
Other publications
>>
Michail Tonkonogi
Högskolan Dalarna; Medicinsk vetenskap
Other publications
>>
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header:
identifier: oai:dalea.du.se:2310
datestamp: 2021-04-15T13:27:02Z
setSpec: SwePub-du
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recordInfo:
recordContentSource: du
recordCreationDate: 2006-10-02
identifier:
http://urn.kb.se/resolve?urn=urn:nbn:se:du-2310
10.1152/japplphysiol.01007.2005
16728514
titleInfo:
@attributes:
lang: eng
title: Repeated static contractions increase mitochondrial vulnerability toward oxidative stress in human skeletal muscle.
abstract: Repeated static contractions (RSC) induce large fluctuations in tissue oxygen tension and increase the generation of reactive oxygen species (ROS). This study investigated the effect of RSC on muscle contractility mitochondrial respiratory function and in vitro sarcoplasmic reticulum (SR) Ca2+ kinetics in human muscle. Ten male subjects performed five bouts of static knee extension with 10-min rest in between. Each bout of RSC (target torque 66% of maximal voluntary contraction torque) was maintained to fatigue. Muscle biopsies were taken preexercise and 0.3 and 24 h postexercise from vastus lateralis. Mitochondria were isolated and respiratory function measured after incubation with H2O2 (HPX) or control medium (Con). Mitochondrial function was not affected by RSC during Con. However RSC exacerbated mitochondrial dysfunction during HPX resulting in decreased respiratory control index decreased mitochondrial efficiency (phosphorylated ADP-to-oxygen consumed ratio) and increased noncoupled respiration (HPX/Con post- vs. preexercise). SR Ca2+ uptake rate was lower 0.3 vs. 24 h postexercise whereas SR Ca2+ release rate was unchanged. RSC resulted in long-lasting changes in muscle contractility including reduced maximal torque low-frequency fatigue and faster torque relaxation. It is concluded that RSC increases mitochondrial vulnerability toward ROS reduces SR Ca2+ uptake rate and causes low-frequency fatigue. Although conclusive evidence is lacking we suggest that these changes are related to increased formation of ROS during RSC.
subject:
@attributes:
lang: eng
authority: uka.se
topic:
Medical and Health Sciences
Basic Medicine
@attributes:
lang: swe
authority: uka.se
topic:
Medicin och hälsovetenskap
Medicinska och farmaceutiska grundvetenskaper
@attributes:
lang: eng
topic: calcium homeostasis; exercise; mitochondria; oxidative phosphorylation
language:
languageTerm: eng
genre:
publication/journal-article
vet
note:
Published
4
name:
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type: personal
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Sahlin
Kent
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Nielsen
J.S.
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namePart:
Mogensen
M
role:
roleTerm: aut
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type: personal
authority: du
namePart:
Tonkonogi
Michail
role:
roleTerm: aut
affiliation:
Högskolan Dalarna
Medicinsk vetenskap
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mtn
0000-0003-1619-9758
originInfo:
dateIssued: 2006
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titleInfo:
title: Journal of applied physiology
identifier:
8750-7587
1522-1601
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type: volume
number: 101
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type: issue
number: 3
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