Calcium Fluxes in Work-Related Muscle Disorder: Implications from a Rat Model

J. Hadrevi, M. F. Barbe, N. Ørtenblad, U. Frandsen, E. Boyle, S. Lazar, G. Sjøgaard, K. Søgaard*

*Corresponding author for this work

Research output: Contribution to journalJournal articleResearchpeer-review

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Abstract

Introduction. Ca2+ regulatory excitation-contraction coupling properties are key topics of interest in the development of work-related muscle myalgia and may constitute an underlying cause of muscle pain and loss of force generating capacity. Method. A well-established rat model of high repetition high force (HRHF) work was used to investigate if such exposure leads to an increase in cytosolic Ca2+ concentration ([Ca2+]i) and changes in sarcoplasmic reticulum (SR) vesicle Ca2+ uptake and release rates. Result. Six weeks exposure of rats to HRHF increased indicators of fatigue, pain behaviors, and [Ca2+]i, the latter implied by around 50-100% increases in pCam, as well as in the Ca2+ handling proteins RyR1 and Casq1 accompanied by an ∼10% increased SR Ca2+ uptake rate in extensor and flexor muscles compared to those of control rats. This demonstrated a work-related altered myocellular Ca2+ regulation, SR Ca2+ handling, and SR protein expression. Discussion. These disturbances may mirror intracellular changes in early stages of human work-related myalgic muscle. Increased uptake of Ca2+ into the SR may reflect an early adaptation to avoid a sustained detrimental increase in [Ca2+]i similar to the previous findings of deteriorated Ca2+ regulation and impaired function in fatigued human muscle.

Original languageEnglish
Article number5040818
JournalBioMed Research International
Volume2019
Number of pages14
ISSN2314-6133
DOIs
Publication statusPublished - 30. Sep 2019

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Sarcoplasmic Reticulum
Muscular Diseases
Muscle
Rats
Fluxes
Calcium
Muscles
Myalgia
Rat control
Ryanodine Receptor Calcium Release Channel
Mirrors
Proteins
Fatigue of materials

Cite this

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title = "Calcium Fluxes in Work-Related Muscle Disorder: Implications from a Rat Model",
abstract = "Introduction. Ca2+ regulatory excitation-contraction coupling properties are key topics of interest in the development of work-related muscle myalgia and may constitute an underlying cause of muscle pain and loss of force generating capacity. Method. A well-established rat model of high repetition high force (HRHF) work was used to investigate if such exposure leads to an increase in cytosolic Ca2+ concentration ([Ca2+]i) and changes in sarcoplasmic reticulum (SR) vesicle Ca2+ uptake and release rates. Result. Six weeks exposure of rats to HRHF increased indicators of fatigue, pain behaviors, and [Ca2+]i, the latter implied by around 50-100{\%} increases in pCam, as well as in the Ca2+ handling proteins RyR1 and Casq1 accompanied by an ∼10{\%} increased SR Ca2+ uptake rate in extensor and flexor muscles compared to those of control rats. This demonstrated a work-related altered myocellular Ca2+ regulation, SR Ca2+ handling, and SR protein expression. Discussion. These disturbances may mirror intracellular changes in early stages of human work-related myalgic muscle. Increased uptake of Ca2+ into the SR may reflect an early adaptation to avoid a sustained detrimental increase in [Ca2+]i similar to the previous findings of deteriorated Ca2+ regulation and impaired function in fatigued human muscle.",
author = "J. Hadrevi and Barbe, {M. F.} and N. {\O}rtenblad and U. Frandsen and E. Boyle and S. Lazar and G. Sj{\o}gaard and K. S{\o}gaard",
year = "2019",
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Calcium Fluxes in Work-Related Muscle Disorder : Implications from a Rat Model. / Hadrevi, J.; Barbe, M. F.; Ørtenblad, N.; Frandsen, U.; Boyle, E.; Lazar, S.; Sjøgaard, G.; Søgaard, K.

In: BioMed Research International, Vol. 2019, 5040818, 30.09.2019.

Research output: Contribution to journalJournal articleResearchpeer-review

TY - JOUR

T1 - Calcium Fluxes in Work-Related Muscle Disorder

T2 - Implications from a Rat Model

AU - Hadrevi, J.

AU - Barbe, M. F.

AU - Ørtenblad, N.

AU - Frandsen, U.

AU - Boyle, E.

AU - Lazar, S.

AU - Sjøgaard, G.

AU - Søgaard, K.

PY - 2019/9/30

Y1 - 2019/9/30

N2 - Introduction. Ca2+ regulatory excitation-contraction coupling properties are key topics of interest in the development of work-related muscle myalgia and may constitute an underlying cause of muscle pain and loss of force generating capacity. Method. A well-established rat model of high repetition high force (HRHF) work was used to investigate if such exposure leads to an increase in cytosolic Ca2+ concentration ([Ca2+]i) and changes in sarcoplasmic reticulum (SR) vesicle Ca2+ uptake and release rates. Result. Six weeks exposure of rats to HRHF increased indicators of fatigue, pain behaviors, and [Ca2+]i, the latter implied by around 50-100% increases in pCam, as well as in the Ca2+ handling proteins RyR1 and Casq1 accompanied by an ∼10% increased SR Ca2+ uptake rate in extensor and flexor muscles compared to those of control rats. This demonstrated a work-related altered myocellular Ca2+ regulation, SR Ca2+ handling, and SR protein expression. Discussion. These disturbances may mirror intracellular changes in early stages of human work-related myalgic muscle. Increased uptake of Ca2+ into the SR may reflect an early adaptation to avoid a sustained detrimental increase in [Ca2+]i similar to the previous findings of deteriorated Ca2+ regulation and impaired function in fatigued human muscle.

AB - Introduction. Ca2+ regulatory excitation-contraction coupling properties are key topics of interest in the development of work-related muscle myalgia and may constitute an underlying cause of muscle pain and loss of force generating capacity. Method. A well-established rat model of high repetition high force (HRHF) work was used to investigate if such exposure leads to an increase in cytosolic Ca2+ concentration ([Ca2+]i) and changes in sarcoplasmic reticulum (SR) vesicle Ca2+ uptake and release rates. Result. Six weeks exposure of rats to HRHF increased indicators of fatigue, pain behaviors, and [Ca2+]i, the latter implied by around 50-100% increases in pCam, as well as in the Ca2+ handling proteins RyR1 and Casq1 accompanied by an ∼10% increased SR Ca2+ uptake rate in extensor and flexor muscles compared to those of control rats. This demonstrated a work-related altered myocellular Ca2+ regulation, SR Ca2+ handling, and SR protein expression. Discussion. These disturbances may mirror intracellular changes in early stages of human work-related myalgic muscle. Increased uptake of Ca2+ into the SR may reflect an early adaptation to avoid a sustained detrimental increase in [Ca2+]i similar to the previous findings of deteriorated Ca2+ regulation and impaired function in fatigued human muscle.

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DO - 10.1155/2019/5040818

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