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.
- Calcium-Binding Proteins/metabolism
- Disease Models, Animal
- Excitation Contraction Coupling/physiology
- Mitochondrial Proteins/metabolism
- Muscle Contraction/physiology
- Muscle, Skeletal/metabolism
- Muscular Diseases/metabolism
- Rats, Sprague-Dawley
- Ryanodine Receptor Calcium Release Channel/metabolism
- Sarcoplasmic Reticulum/metabolism
- Sarcoplasmic Reticulum Calcium-Transporting ATPases/metabolism