Effects of High Intensity Interval Training on the Activity of the Myocardial Mitochondrial Respiratory Chain Complex of Rats / 中国运动医学杂志

ABSTRACT

Objective To explore the heart function and activity of the mitochondrial respiratory chain complex of rats with myocardial hypertrophy induced by the long-term high-intensity interval training(HIIT).Methods Ninety Wistar rats were randomly divided into an HIIT group,a moderate intensity continuous training(MICT) group and a rest control(RC) group,with each group allocated three subgroups according to the observation time(2,6 and 10 weeks),9 groups altogether(n=10 in each group).Each group was given intervention as their names implied.Then,the heart function was measured using the ultrasoundcardiogram,and the body weight as well as the weight of the heart was weighted.The myocardium mitochondria were extracted using the differential centrifugation after homoge nation to detect the activity of the myocardial and mitochondrial citrate synthase (CS),the activities of the respiratory chain complex C Ⅰ ～CⅣ as well as myocardial protein expression of peroxisome proliferator-activated receptor gamma coactivator 1α (PGC-1 α),α-myosin heavy chain (α-MHC),β-MHC,atrial natriuretic factor(ANF) and brain natriuretic peptide(BNP).Results The myocardial hypertrophy was found in HIIT and MICT groups after 1-week and 9-week intervention respectively.At the 2nd and 10th week,no significant differences were found in the heart function,respiratory chain complex activity and protein expression of all three groups(P＞0.05).At the 6th week,the left ventricular ejection fraction,left ventricular fractional shortening,myocardial α-MHC protein expression,and the activities of respiratory chain complex C Ⅰ,C Ⅲ and C Ⅳ of HIIT group were significantly lower while the myocardial β-MHC and BNP protein expression were significantly higher than those of RC and MICT groups(P＜0.05).Conclusion Long-term HIIT but not MICT can induce temporarily pathological myocardial hypertrophy and reduced heart function in Wistar rats,and the mechanism might be related to the downregulation of the myocardial mitochondrial respiratory chain complex activity.