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

J Hadrevi¹, M F Barbe², N Ørtenblad³

¹Department of Public Health and Clinical Medicines, Occupational and Environmental Medicine, Umeå University, 901 87 Umeå, Sweden.

Biomed Research International

|October 31, 2019

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This summary is machine-generated.

Work-related muscle strain in rats altered cellular calcium regulation, increasing cytosolic calcium and sarcoplasmic reticulum (SR) Ca2+ uptake. These changes may reflect early stages of muscle myalgia in humans.

Area of Science:

Muscle physiology
Cellular biology
Occupational health

Background:

Excitation-contraction coupling (ECC) is crucial for muscle function.
Dysregulation of intracellular calcium (Ca2+) is implicated in muscle myalgia and force loss.
Understanding Ca2+ handling is vital for addressing work-related muscle disorders.

Purpose of the Study:

To investigate the impact of high repetition, high force (HRHF) work on myocellular Ca2+ regulation in a rat model.
To determine if HRHF exposure alters cytosolic Ca2+ concentration ([Ca2+]i) and sarcoplasmic reticulum (SR) Ca2+ handling.
To examine changes in SR Ca2+ uptake and release rates following HRHF exposure.

Main Methods:

Utilized a well-established rat model of HRHF work exposure.

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Measured indicators of fatigue and pain behaviors.

Assessed cytosolic Ca2+ concentration ([Ca2+]i) and SR Ca2+ handling protein expression (RyR1, Casq1).

Quantified SR Ca2+ uptake rates in extensor and flexor muscles.

Main Results:

HRHF exposure for six weeks increased fatigue indicators, pain behaviors, and [Ca2+]i.
Significant increases (50-100%) in pCam and Ca2+ handling proteins (RyR1, Casq1) were observed.
SR Ca2+ uptake rate increased by approximately 10% in muscles of exposed rats.
Demonstrated work-related alterations in myocellular Ca2+ regulation, SR Ca2+ handling, and SR protein expression.

Conclusions:

The observed disturbances in Ca2+ regulation may mirror early intracellular changes in human work-related myalgia.
Increased SR Ca2+ uptake could be an adaptive mechanism to prevent sustained detrimental increases in [Ca2+]i.
Findings align with previous research on deteriorated Ca2+ regulation and impaired function in fatigued human muscle.