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Post-myocardial infarction exercise training improved calcium sensitivity and cardiac function

After myocardial infarction (MI), the wounded heart undergoes detrimental remodeling, which induces ventricular dilation, fibrosis, and deteriorated cardiac function. Previous studies reported Post-MI exercise training attenuated remodeling-induced adverse effect. The purpose of this study was to investigate whether post-MI endurance training (ET) improves cardiomyocytes Ca²⁺ sensitivity. MI was surgically induced in 7-wk-old rats. The survivors were assigned to 3 groups: Sham (no MI, no exercise; n=7), MI-Sed (MI, no exercise; n=7), and MI-ET (MI, plus endurance training). Exercise training began 1-week after surgery for MI-ET. MI-ET exercise entailed 10-16m/min running on a rodent treadmill inclined to 5° for 50 minutes per day, 5 days per week for a total of 10 weeks. Animals were treated in accordance with NIH Gide for the Care and Use of laboratory Animals. During the experiment, rats were anesthetized with 2% isoflurane mixed with oxygen. Buprenex (pain killer, 0.05mg/kg body weight) was administered subcutaneously for two days after surgery. Our results showed that both MI-Sed and ET had comparable left ventricular end-diastolic dimension (LVEDd, 11.81±0.10 vs 11.84±0.15mm, p>0.05). MI-ET had shorter (P<0.05) LV end systolic-dimension (LVESd) than their sedentary counterparts (9.71±0.26 vs 10.46±0.14mm). As such, the fractional shortening (FS%) was higher (P<0.05) in MI-ET (17.99±1.54%) than that of MI-Sed (11.43± 1.12%). The pCa50, a measure of Ca²⁺ sensitivity of tension, was higher in MI-ET than that of MI-Sed (5.9±0.06 vs 5.75±0.06). These results suggest that post-MI endurance training improved cardiac function. The increased cardiac contractility may be, in part, due to the enhanced Ca²⁺ sensitivity of the cardiomyocytes.