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

INTRODUCTION: Ca(2+) 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 Ca(2+) concentration ([Ca(2+)](i)) and changes in sarcoplasmic reticulum (SR) vesicle Ca(2+) uptake and release rates. RESULT: Six weeks exposure of rats to HRHF increased indicators of fatigue, pain behaviors, and [Ca(2+)](i), the latter implied by around 50–100% increases in pCam, as well as in the Ca(2+) handling proteins RyR1 and Casq1 accompanied by an ∼10% increased SR Ca(2+) uptake rate in extensor and flexor muscles compared to those of control rats. This demonstrated a work-related altered myocellular Ca(2+) regulation, SR Ca(2+) handling, and SR protein expression. DISCUSSION: These disturbances may mirror intracellular changes in early stages of human work-related myalgic muscle. Increased uptake of Ca(2+) into the SR may reflect an early adaptation to avoid a sustained detrimental increase in [Ca(2+)](i) similar to the previous findings of deteriorated Ca(2+) regulation and impaired function in fatigued human muscle.