DYANA SARVASTI (2019) MEKANISME PROTEKSI KARDIOVASKULAR LATIHAN FISIK INTERVAL INTENSITAS TINGGI PADA PASIEN PENYAKIT JANTUNG KORONER STABIL PASCAIMPLANTASI STENT KORONER (Evaluasi flow-mediated dilatation melalui jalur adrenalin, noradrenalin, eNOS, dan aktivitas SOD ekstraselular). Disertasi thesis, UNIVERSITAS AIRLANGGA.

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Abstract

Background: High-intensity interval training (HIIT) has been shown to improve aerobic capacity compared with moderate-intensity continuous training (MICT). Unfortunately, little data on the mechanism of HIIT is available. Objective: This study aimed to compare and determine the mechanism of cardiovascular protection variables in MICT and HIIT in stable coronary heart disease (CHD) patients after coronary stenting. Methods: This experimental study used the same subject and cross-over design. Eleven stable CHD patients after coronary stenting were randomly divided into two groups, MICT (29 min at 50-60% heart rate reserve) and HIIT (4x4 min intervals at 60-80% heart rate reserve, each followed by 3 min of active recovery at 40-50% heart rate reserve), three times a week for two weeks. The patients performed adrenaline, noradrenaline, endothelial nitric oxide synthase (eNOS) concentration, extracellular superoxide dismutase (EC-SOD) activity assayed, and flow-mediated dilatation (FMD) examination, before and after treatment was completed. Results: HIIT significantly increased noradrenaline and eNOS compared to MICT (p<0.05). HIIT was better to preserve EC-SOD activity and FMD compared to MICT (p<0.05). HIIT through the noradrenalin pathway had a direct and significant effect on eNOS (p<0.05). MICT through the noradrenaline pathways had a direct and significant effect on eNOS (p<0.05), and through the EC-SOD activity pathways had a direct and significant effect on FMD (p<0.05). MICT reduced EC-SOD activity, which results in a decrease in FMD value. Conclusion: HIIT is superior to MICT in increasing cardiovascular protection through the increment of noradrenalin and eNOS concentration, preserves EC-SOD activity and FMD in stable CHD patients after coronary stenting.

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