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Objective To investigated the different effect of moderate-intensity continuous training (MCT) and high-intensity interval exercise training (HIT) on ventricular remodeling and mitochondrial homeostasis after acute myocardial infarction (AMI).Methods The AMI rat model was achieved by ligating coronary artery.The AMI and sham operation rats were randomly (random number) divided into four groups:sham operation group (Sham),AMI control group (AMI),AMI MCT group (AMI + M),and AMI HIT group (AMI + H).Animals in the AMI + M and AMI + H groups underwent 4 weeks MCT and HIT respectively.Five weeks after AMI,hemodynamic changes,mitochondrial bioenergetics,and PINK1,Beclinl,Mfn2,Drp1,Tfam,COXⅣ,PGC-1α were detected.Results Comparing with AMI group,in AMI + M and AMI + H groups,Beclin1,PINK1,Mfn2 and PGC-1α expression elevated significantly (P ＜0.05 or P ＜0.01),whereas ROS generation and Drp1 expression showed dramatic decrease (P ＜ 0.05 or P＜0.01).In addition,in AMI + H group,±dp/dt max,mitochondrial membrane potential,ATP synthesis activity,Tfam and COXⅣ expression improved significantly (P ＜ 0.05).Comparing with AMI + M group,in AMI + H group,± dp/dt max,PGC-1α,Tfam and COX Ⅳ expression improved significantly (P ＜ 0.05).Conclusions HIT is superior to MCT for ameliorating ventricular remodeling and mitochondrial homeostasis after AMI.
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BACKGROUND:It is unclear whether short-term high-intensity interval training (HIT) can be used to protect against myocardium injury after acute myocardial infarction, as wel as the underlying mechanism. OBJECTIVE:To observe the effects of short-term HIT on the ventricular remodeling and mitochondrial content after acute myocardial infarction, and the biological effect of mitochondrial biogenesis and autophagy in this process. METHODS:Male Sprague-Dawley rats were modeled into acute myocardial infarction by ligating coronary artery. One week later, HIT was performed:each interval consisted of 4-minute high-intensity running (80%of maximal oxygen consumption) and 3-minute active recovery (40%of maximal oxygen consumption), for 4 consecutive weeks of 5 days each week, repeated 7 cycles. RESULTS AND CONCLUSION:Four-week HIT after acute myocardial infarction could markedly enhance left ventricular pump function and mitochondrial content, improve mitochondrial membrane potential and ATP synthetic activity, inhibit mitochondrial reactive oxygen species generation, up-regulate PGC-1α/Tfam induced mitochondrial biogenesis and Bnip3/Beclin-1 induced autophagy. These results indicate that short-term HIT can improve normal mitochondrial content after acute myocardial infarction, which in turn ameliorates myocardial systolic property and energy metabolism. As a cardiac rehabilitation method, HIT exhibits fine timeliness.
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[ABSTRACT]AIM:Toinvestigatetheeffectofhypoxiacombinedwithexercisetrainingonmitochondrialcon-tent, and the role of mitochondrial biogenesis and mitophagy in this process .METHODS:Male Sprague-Dawley rats were randomly divided into 4 groups:normoxia control (NC) group, normoxia+training (NT) group, hypoxia+control (HC) group, and hypoxia+training (HT) group.The hypoxic animals were housed in normobaric hypoxic tent (11.3 % oxy-gen) for consecutive 4 weeks.The exercise training animals were exercised on a motor-driven rodent treadmill (5°) at a speed of 15 m/min, 60 min/d, 5 d/week for 4 weeks.Mitochondrial membrane potential was determined using JC-1 fluo-rescent probe .ATP synthesis capacity was determined using a bioluminescence technique .The protein expression of cyto-chrome C oxidase IV (COXIV), voltage-dependent anion channel-1 (VDAC-1), peroxisome proliferator-activated receptor gamma cofactor 1 alpha (PGC-1α), mitochondrial transcription factor A (Tfam),Bcl-2/adenovirus E1B 19 kD-interacting protein 3 (Bnip3) and beclin-1 in the muscles was detected by Western blotting .RESULTS:Compared with NC group, hypoxia attenuated mitochondrial membrane potential , ATP synthesis capacity , and the expression of COXIV , VDAC-1, PGC-1αand Tfam.Furthermore, hypoxia increased the expression of Bnip 3 and beclin-1.Compared with HC group , the exercise training elevated mitochondrial membrane potential , ATP synthesis capacity , and the expression of COXIV , VDAC-1, PGC-1α, Tfam, Bnip3 and beclin-1.CONCLUSION:A combination of reduced mitochondrial biogenesis and increased mitophagy seems to be responsible for the decrease in mitochondrial content after hypoxia .Exercise training with hypoxia elevates mitochondrial content and function in hypoxia , which may be mediated by appropriate increase and co-reg-ulation of mitochondrial biogenesis and mitophagy .
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OBJECTIVE To check the defects of nosocomial infections reports,recording of the patient′s history,and antibiotics usage,so as to improve hospital management and reduce nosocomial infection.METHODS Patient′s records from Jan 1,2008 to Dec 31,2008 were reviewed to find out the defects and feedback to the physicians.RESULTS Some problems of 5995 cases were checked out and corrected,some suggestions were made.CONCLUSIONS Checking the patient′s records may supplement the defects of prospective monitor,direct the antibiotics therapy,and monitor occurrence of drug resistance.