In vivo calcium regulation in diabetic skeletal muscle

摘要: Abstract In skeletal muscle, dysfunctional contractile activity has been linked to impaired intracellular Ca 2+ concentration ([Ca ] i ) regulation. Muscle force production is and fatigability muscle fragility deteriorate with diabetes. Use of a novel in vivo model permits investigation [Ca homeostasis diabetic muscle. Within this environment we have shown that diabetes perturbs the regulatory system such resting following contractions compromised elevations are exacerbated. This review considers impact on capacity regulate , and, particular, relationship between fatigue elevated highly ecologically relevant circulation-intact environment. Importantly, role mitochondria calcium sequestration possibility impacts process explored. Given profound microcirculatory dysfunction preparation offers unique opportunity study interrelationships among microvascular function, blood-myocyte oxygen flux as they relate enhanced exercise intolerance.