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Calcium Fluxes in Work-Related Muscle Disorder: Implications from a Rat Model
Umeå University, Faculty of Medicine, Department of Public Health and Clinical Medicine, Occupational and Environmental Medicine.ORCID iD: 0000-0003-4864-7842
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2019 (English)In: BioMed Research International, ISSN 2314-6133, E-ISSN 2314-6141, Vol. 2019, article id 5040818Article in journal (Refereed) Published
Abstract [en]

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.

Place, publisher, year, edition, pages
2019. Vol. 2019, article id 5040818
National Category
Neurology
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URN: urn:nbn:se:umu:diva-165114DOI: 10.1155/2019/5040818ISI: 000491982600001PubMedID: 31662979OAI: oai:DiVA.org:umu-165114DiVA, id: diva2:1369364
Available from: 2019-11-11 Created: 2019-11-11 Last updated: 2019-11-11Bibliographically approved

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