Effects of high-intensity interval versus moderate continuous exercise on plasma concentration of nitric oxide and level of blood pressure in inactive obese men

Document Type : Research Paper I Open Access I Released under (CC BY-NC 4.0) license

Authors

1 MSc of Exercise Physiology, Faculty of Sport Sciences, University of Guilan, Rasht, Iran

2 Assistant Professor of Exercise Physiology, Faculty of Sport Sciences, University of Guilan, Rasht, Iran

3 Professor of sport exercise physiology, Faculty of physical education and sports sciences. university of guilan. Rasht, Iran

Abstract

Aim:  Physical activity is one of the most effective ways to improve cardiovascular function. The present study was performed to evaluate cardiovascular responses following high-intensity interval exercise (HIIE) and moderate-intensity continuous exercise (MICE) in inactive obese men. Methods:  In the present semi-experimental study, eight inactive obese men (age: 22.5 2 2.5 years, body mass index: 31.5 ± 1.5 kg / m2) using a randomized crossover design, participated in three HIIE, MICE and control interventions.  Blood samples were taken before, immediately and one hour after exercise to measure nitric oxide (NO) concentration. Also, heart rate and blood pressure were measured before, immediately and every 15 minutes for one hour after exercises.  Results:  No significant changes in hemodynamic factors and NO were observed in the control group. However, after HIIE and MICE protocols, a significant decrease (p <0.05) in systolic blood pressure (SBP) was observed compared to baseline conditions, which this phenomenon has persisted for a long time following HIIE. Heart rate and NO increased significantly after both protocols (p <0.05), with the increase in NO following HIIE persisting for longer. Conclusion: It seems that training intensity can be an influential factor in the development of PEH. Also, due to the longer increase in NO caused by HIIE compared to MICE, it can be considered that longer PEH after HIIE is probably related to the mechanism of NO-induced vasodilation.

Keywords


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