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

INTRODUCTION

Ca 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 concentration ([Ca]) and changes in sarcoplasmic reticulum (SR) vesicle Ca uptake and release rates.

RESULT

Six weeks exposure of rats to HRHF increased indicators of fatigue, pain behaviors, and [Ca], the latter implied by around 50-100% increases in pCam, as well as in the Ca handling proteins RyR1 and Casq1 accompanied by an ∼10% increased SR Ca uptake rate in extensor and flexor muscles compared to those of control rats. This demonstrated a work-related altered myocellular Ca regulation, SR Ca 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 into the SR may reflect an early adaptation to avoid a sustained detrimental increase in [Ca] similar to the previous findings of deteriorated Ca regulation and impaired function in fatigued human muscle.