Weak electromagnetic fields alter Ca2+ handling and protect against hypoxia-mediated damage in primary newborn rat myotube cultures

Weak electromagnetic fields (WEF) enhance Ca2+ entry into cells via voltage-gated Ca2+ channels and affect various aspects of metabolism, structure, and function. However, little information is available on the effect of WEF on skeletal muscle, which depends primarily on intracellular Ca2+ stores for function and metabolism. Here, we examine the effects of 30 min exposure of rat primary myotube cultures to WEF (1.75 mu T, 16 Hz) on Ca2+ handling and creatine kinase (CK) release. Free myoplasmic Ca2+ concentration ([Ca2+ (i)]) was measured with the ratiometric dye indo-1. WEF did not affect basal [Ca2+](i) but decreased the twitch [Ca2+](i) transient in a time-dependent manner, and the twitch amplitude was decreased to similar to 30 0 min. WEF completely abolished the increase in [Ca2+](i) induced by potassium chloride (similar to 60 mM) but had no effect on the increase induced by caffeine (similar to 6 mM). Hypoxia (2 h exposure to 100 resulted in a marked loss of CK into the medium (400 , as well as a rapid (within 20 min) and sustained increase in basal [Ca2+](i) (similar to 20 . However, during exposure to WEF, basal [Ca2+](i) remained constant during the initial 60 min of hypoxia and, thereafter, increased to levels similar to those observed in the absence of WEF. Finally, WEF blocked about 80 mediated CK release (P < 0.05). These data demonstrate that WEF inhibits increases in [Ca2+](i) by interfering with muscle excitation and protects against muscle damage induced by hypoxia. Thus, WEF may have therapeutic/protective effects on skeletal muscle.