Acute Elevated Glucose Promotes Abnormal Action Potential-Induced Ca2+ Transients in Cultured Skeletal Muscle Fibers

A common comorbidity of diabetes is skeletal muscle dysfunction,which leads to compromised physical function. previous studies of diabetes in skeletal muscle have shown alterations in excitation-contraction coupling (ecc) - the sequential link between action potentials (ap),intracellular ca2+ release,and the contractile machinery. yet,little is known about the impact of acute elevated glucose on the temporal properties of ap-induced ca2+ transients and ionic underlying mechanisms that lead to muscle dysfunction. here,we used high-speed confocal ca2+ imaging to investigate the temporal properties of ap-induced ca2+ transients,an intermediate step of ecc,using an acute in cellulo model of uncontrolled hyperglycemia (25 mm,48 h.). control and elevated glucose-exposed muscle fibers cultured for five days displayed four distinct patterns of ap-induced ca2+ transients (phasic,biphasic,phasic-delayed,and phasic-slow decay); most control muscle fibers show phasic ap-induced ca2+ transients,while most fibers exposed to elevated d-glucose displayed biphasic ca2+ transients upon single field stimulation. we hypothesize that these changes in the temporal profile of the ap-induced ca2+ transients are due to changes in the intrinsic excitable properties of the muscle fibers. we propose that these changes accompany early stages of diabetic myopathy. © 2017 erick o. hernández-ochoa et al.