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 % after 30 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 % argon) resulted in a marked loss of CK into the medium (400 % of normoxic value), as well as a rapid (within 20 min) and sustained increase in basal [Ca2+](i) (similar to 20 % above baseline). 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 % of hypoxia-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.