Cellular function is modulated by the electric membrane potential controlling intracellular physiology and signal propagation from a motor neuron to a muscle fiber resulting in muscle contraction. Unlike electric fields, magnetic fields are not attenuated by biological materials and penetrate deep into the tissue. We used complex spatiotemporal magnetic fields (17–70 mT) to control intracellular signaling in skeletal muscle cells. By changing different parameters of the alternating magnetic field (amplitude, inversion time, rotation frequency), we induced transient depolarization of cellular membranes leading to i) Na⁺ influx through voltage-gated sodium channels (VGSC), ii) cytosolic calcium increase, and iii) VGSC- and ryanodine receptor-dependent increase of actin polymerization. The ion fluxes occurred only, when the field was applied and returned to baseline after the field was turned off. The 30-s-activation-cycle could be repeated without any loss of signal intensity. By contrast, static magnetic fields of the same strength exhibited no effect on myotube Ca²⁺ levels. Mathematical modeling suggested a role for the alternating magnetic field-induced eddy current, which mediates a local change in the membrane potential triggering the activation of VGSC. These findings might pave the way for the use of complex magnetic fields to improve function of skeletal muscles in myopathies.

细胞功能由控制细胞内生理的电膜电位和从运动神经元到肌肉纤维的信号传播导致肌肉收缩来调节。与电场不同，磁场不会被生物材料衰减，而会渗透到组织的深处。我们使用复杂的时空磁场（17–70 mT）控制骨骼肌细胞中的细胞内信号传导。通过改变交变磁场的不同参数（振幅，反转时间，旋转频率），我们诱导了细胞膜的瞬时去极化，从而导致i）Na ⁺通过电压门控钠通道（VGSC）流入，ii）胞质钙增加，iii）肌动蛋白聚合反应依赖VGSC和ryanodine受体的增加。离子通量仅在施加电场时发生，并且在关闭电场后返回基线。可以重复30 s的激活周期，而不会损失任何信号强度。相反，相同强度的静磁场对肌管Ca ²⁺水平没有影响。数学模型表明了交变磁场感应的涡流的作用，它介导了膜电位的局部变化，从而触发了VGSC的激活。这些发现可能为使用复杂磁场改善肌病中骨骼肌的功能铺平了道路。