dr. sc. KRALJEVIĆ JASENKA dr.med.
„EFFECT OF AEROBIC INTERVAL TRAINING ON PATHOLOGICAL REMODELLING AND MITOCHONDRIAL DYSFUNCTION IN POST-INFARCTION HEART FAILURE IN RAT“
Doctoral dissertation full text
prof. dr. sc. LJUBKOVIĆ MARINOVIĆ JASNA
Qualifying research publications:
Kraljevic J, Marinovic J, Pravdic D, Zubin P, Dujic Z, Wisloff U, Ljubkovic M.Aerobic interval training attenuates remodelling and mitochondrial dysfunction in the post-infarction failing rat heart. Cardiovasc Res. 2013;99(1):55-64.
IF (JCR 2013) 5.808
Effect of aerobic interval training on pathological remodelling and mitochondrial dysfunction in the post-infarction failing rat heart
Aims: Following a large myocardial infarction (MI), remaining viable muscle often undergoes pathological remodelling and progresses towards chronic heart failure (CHF). Mitochondria may also be affected by this process and, due to their functional importance, likely contribute to the progression of the disease. Aerobic interval training (AIT) has been shown effective in diminishing pathological myocardial transformation, but the effects of AIT on mitochondrial function in hearts undergoing remodelling are not known.
Methods and Results: Adult female Sprague-Dawley rats were randomized to either 8 weeks of aerobic interval treadmill running (5 days/week), which started 4 weeks after left coronary artery ligation (MI-Trained), or a sedentary group (MI-Sedentary). Echocardiography was performed before and after the 8-week period, at which point the left ventricles (LV) were also harvested. Twelve weeks after surgery, MI-Sedentary rats had significantly lower LV fractional shortening compared to MI-Trained. Complex I – dependent respiration assessed in isolated LV mitochondria was decreased by ~37% in MI-Sedentary and 17% in MI-Trained (group differences p<0.05), compared to sham-operated animals. This was paralleled with diminished ATP-production and increased degree of protein oxidation in MI-Sedentary rats. The enzymatic activity of complex I was also decreased to the greater extent in MI-Sedentary than in MI-Trained animals, with no evidence of its reduced expression. When complex II substrate was used, no differences among the three groups were observed.
Conclusions: Exercise reduces the left ventricle contractile deterioration in post-infarction heart failure and alleviates the extent of mitochondrial dysfunction, which is paralleled with preserved complex I activity.
Keywords: myocardial infarction; heart failure; aerobic interval training; animal model; mitochondria
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