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

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.

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.

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.

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.