Document Type : Research Paper I Open Access I Released under CC BY-NC 4.0 license
Authors
1 Department of Exercise Physiology,, Faculty of Sport Sciences and Health,, University of Tehran,, Tehran,, Iran
2 Department of Exercise Physiology, Faculty of Sport Sciences and Health, University of Tehran, Tehran, Iran.
3 Department of Exercise Physiology, Alborz Campus, University of Tehran, Tehran, Iran.
Abstract
Introduction: Polycystic ovary syndrome (PCOS) is associated with insulin resistance and metabolic disorders. This study aimed to compare the effects of eight weeks of high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) on insulin sensitivity, TGF-β levels, cardiorespiratory fitness, and metabolic indices in obese women with PCOS.
Methods: In this randomized controlled trial, 45 obese women with PCOS were divided into three groups of 15: HIIT, MICT, and control. The exercise training groups performed their respective protocols for eight weeks. Body composition, insulin sensitivity, serum levels of TGF-β1 and TGF-β2, lipid profile, liver enzymes, glucose homeostasis, and peak oxygen consumption (VO₂peak) were assessed before and after the intervention. Data were analyzed using paired t-tests and one-way ANOVA.
Results: Changes in VO₂peak and insulin sensitivity were significantly different among the three groups (P ≤ 0.05). Both exercise groups showed significant improvement in VO₂peak. However, only the HIIT group demonstrated a significant improvement in insulin sensitivity (P=0.02). No significant differences were observed in body composition indices, lipid profile, liver enzymes, and serum levels of TGF-β1 and TGF-β2 (P > 0.05).
Conclusion: The findings indicate that HIIT is a superior and time-efficient exercise strategy compared to MICT for improving insulin sensitivity in obese women with PCOS. This metabolic improvement occurred independently of weight loss and changes in body composition. The unchanged serum TGF-β levels suggest that the mechanisms of action are likely independent of the TGF-β pathway.
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