Intracellular　calcium　(Ca-i(2+))　overload　induced　by　chronic　hypoxia　alters　Ca-i(2+)　homeostasis,　whereas　ameliorating　calcium　homeostasis　is　believed　to　be　responsible　for　cardioprotection.　We　hypothesize　that　cardioprotection　by　electromagnetic　fields　(EMF)　exposure　may　restore　Ca-i(2+)　homeostasis　altered　by　hypoxia　insults.　Cardiomyocytes　isolated　from　neonatal　Sprague-Dawley　rats　were　exposed　to　chronic　hypoxia　(1%　O-2,　5%　CO2,　37　degrees　C).　We　observed　that　cardiomyocytes　injury　and　hypertrophy　were　alleviated　in　hypoxic　cardiomyocytes　exposed　with　EMF　preconditioning.　Compared　with　hypoxic　cardiomyocytes,　the　diastolic　[Ca2+](i)　was　decreased,　the　amplitude　of　Ca-i(2+)　oscillations　was　recovered　when　cardiomyocytes　exposed　with　EMF.　In　addition,　we　also　found　that　EMF　exposure　significantly　increased　heat　shock　protein　70　(HSP70)　mRNA　expression　in　hypoxic　cardiomyocytes.　However,　treatment　with　HSP70　blocker　KNK437,　almost　completely　inhibited　the　EMF　induced-cardioprotection　and　the　beneficial　effects　of　Ca2+　oscillation　in　hypoxic　cardiomyocytes.　These　results　suggest　that　EMF　preconditioning　ameliorates　Ca-i(2+)　homeostasis　through　activating　HSP70,　thereby　producing　the　cardioprotective　effect　and　reduction　in　hypoxic　cardiomyocytes　damage.　(C)　2016　Elsevier　Ireland　Ltd.　All　rights　reserved.