Abstract
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.
Highlights
Ca2+ regulatory excitation-contraction coupling properties are key topics of interest in the development of workrelated muscle myalgia and may constitute an underlying cause of muscle pain and loss of force generating capacity
While muscle fatigue relates to impaired sarcoplasmic reticulum (SR) Ca2+ release rate [11, 12], cell damage relates to a sustained increase in [Ca2+]i above normal for a prolonged time period [13]
Since animal models may be more apt than human studies for highly invasive procedures to analyze subcellular mechanisms, we utilized a well-established rat model of high repetition high force (HRHF) work compared with foodrestricted control (FRC) rats to investigate if declines in sensorimotor behaviors were related to potential changes in intracellular Ca2+ homeostasis and injury markers. e rat model has shown grip strength declines in parallel with painrelated symptoms in rats [23,24,25], similar to findings in humans [24]
Summary
Work-related muscle pain is considered a public health problem and increases the incidence of sick leave absences in otherwise healthy individuals [1]. 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 weakness and reduced capacity to rapidly produce force and muscle pain [19,20,21,22]. Since animal models may be more apt than human studies for highly invasive procedures to analyze subcellular mechanisms, we utilized a well-established rat model of high repetition high force (HRHF) work compared with foodrestricted control (FRC) rats to investigate if declines in sensorimotor behaviors were related to potential changes in intracellular Ca2+ homeostasis and injury markers. All original data from behavioral and tissue analyses used to support the findings of this study are available from the corresponding author upon request
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