Severe Exercise and Exercise Training Exert Opposite Effects on Human Neutrophil Apoptosis via Altering the Redox Status 英文参考文献.docVIP

SevereExerciseandExerciseTrainingExertOpposite EffectsonHumanNeutrophilApoptosisviaAlteringthe RedoxStatus Guan-DaSyu1,Hsiun-ingChen1,2,ChauyingJ.Jen1,2 * 1Institute of Basic Medical Sciences, National Cheng Kung University Medical College, Tainan, Taiwan, 2Department of Physiology, National Cheng Kung University MedicalCollege,Tainan,Taiwan Abstract Neutrophilspontaneousapoptosis,aprocesscrucialforimmuneregulation,ismainlycontrolledbyalterationsinreactive oxygen species (ROS) and mitochondria integrity. Exercise has been proposed to be a physiological way to modulate immunity;whileacutesevereexercise(ASE)usuallyimpedesimmunity,chronicmoderateexercise(CME)improvesit.This study aimed to investigate whether and how ASE and CME oppositely regulate human neutrophil apoptosis. Thirteen sedentary young males underwent an initial ASE and were subsequently divided into exercise and control groups. The exercisegroup(n=8)underwent2monthsofCMEfollowedby2monthsofdetraining.AdditionalASEparadigmswere performedattheendofeachmonth.Neutrophilswereisolatedfrombloodspecimensdrawnatrestandimmediatelyafter eachASEforassayingneutrophilspontaneousapoptosis(annexin-Vbindingontheoutersurface)alongwithredox-related parameters and mitochondria-related parameters. Our results showed that i) the initial ASE immediately increased the oxidative stress (cytosolic ROS and glutathione oxidation), and sequentially accelerated the reduction of mitochondrial membrane potential, the surface binding of annexin-V, and the generation of mitochondrial ROS; ii) CME upregulated glutathionelevel,retardedspontaneousapoptosisanddelayedmitochondriadeterioration;iii)mosteffectsofCMEwere unchanged after detraining; and iv) CME blocked ASE effects and this capability remained intact even after detraining. Furthermore,theASEeffectsonneutrophilspontaneousapoptosisweremimickedbyaddingexogenousH2O2,butnotby suppressing mitochondrial membrane potential. In conclusion, while ASE induced an oxidative state and resulted