A mitochondrial‐targeted antioxidant improves myofilament Ca2+ sensitivity during prolonged low frequency force depression at low PO2

A mitochondrial‐targeted antioxidant improves myofilament Ca2+ sensitivity during prolonged low... IntroductionFollowing a period of fatigue inducing contractions, skeletal muscle can demonstrate a long lasting impairment in submaximal force development that has been named “prolonged low frequency force depression” (PLFFD) (Edwards et al. ; Bruton et al. ; Balog, ; Cheng et al. ). PLFFD can last for up to 24 h or more in humans (Edwards et al. ; Place et al. ). Therefore, understanding the alterations that occur in skeletal muscle following fatigue may be of great relevance for the development of strategies to avoid a reduction in muscle function during and after strenuous physical activity. This is particularly important under conditions in which fatigue resistance is impaired by tissue hypoxia, such as during exercise at high altitude or for different chronic diseases states as in chronic obstructive pulmonary disease (COPD) (Gea et al. ) and chronic heart failure (CHF) (Rehn et al. ).The mechanisms causing PLFFD remain unclear (Bruton et al. ; Balog, ; Place et al. ; Watanabe et al. ). One of the proposed mechanisms is that an increased generation of reactive oxygen species (ROS) resulting from a fatiguing contractile bout leads to oxidative modifications of proteins that will decrease the sarcoplasmic reticulum (SR) Ca2+ release and myofibrillar Ca2+ sensitivity during PLFFD (Bruton et al. ; Cheng http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Physiology Wiley

A mitochondrial‐targeted antioxidant improves myofilament Ca2+ sensitivity during prolonged low frequency force depression at low PO2

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Publisher
Wiley Subscription Services, Inc., A Wiley Company
Copyright
Journal compilation © 2018 The Physiological Society
ISSN
0022-3751
eISSN
1469-7793
D.O.I.
10.1113/JP275470
Publisher site
See Article on Publisher Site

Abstract

IntroductionFollowing a period of fatigue inducing contractions, skeletal muscle can demonstrate a long lasting impairment in submaximal force development that has been named “prolonged low frequency force depression” (PLFFD) (Edwards et al. ; Bruton et al. ; Balog, ; Cheng et al. ). PLFFD can last for up to 24 h or more in humans (Edwards et al. ; Place et al. ). Therefore, understanding the alterations that occur in skeletal muscle following fatigue may be of great relevance for the development of strategies to avoid a reduction in muscle function during and after strenuous physical activity. This is particularly important under conditions in which fatigue resistance is impaired by tissue hypoxia, such as during exercise at high altitude or for different chronic diseases states as in chronic obstructive pulmonary disease (COPD) (Gea et al. ) and chronic heart failure (CHF) (Rehn et al. ).The mechanisms causing PLFFD remain unclear (Bruton et al. ; Balog, ; Place et al. ; Watanabe et al. ). One of the proposed mechanisms is that an increased generation of reactive oxygen species (ROS) resulting from a fatiguing contractile bout leads to oxidative modifications of proteins that will decrease the sarcoplasmic reticulum (SR) Ca2+ release and myofibrillar Ca2+ sensitivity during PLFFD (Bruton et al. ; Cheng

Journal

The Journal of PhysiologyWiley

Published: Jan 15, 2018

Keywords: ; ;

References

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