Comparison of HIIT and MICT and further detraining on metabolic syndrome and asprosin signaling pathway in metabolic syndrome model of rats

Abstract

Abstract Physical activity promotes various metabolic benefits by balancing pro and anti-inflammatory adipokines. Recent studies suggest that asprosin might be involved in progression of metabolic syndrome (MetS), however, the underlying mechanisms have not been understood yet. This study aimed to evaluate the effects of High-intensity interval training (HIIT), moderate-intensity continuous training (MICT) and further detraining on MetS indices, insulin resistance, serum and the liver levels of asprosin, and AMP-activated protein kinase (AMPK) pathway in menopause–induced MetS model of rats. A total of 64 Wistar rats were used in this study and divided into 8 groups: Sham1, OVX1(ovariectomized), Sham2, OVX2, OVX + HIIT, OVX + MICT, OVX + HIIT + Det (detraining) and OVX + MICT + Det. Animals performed the protocols, and then serum concentrations of asprosin, TNF-α, insulin, fasting glucose, and lipids profile (TC, LDL, TG, and HDL) were assessed. Additionally, the liver expression of asprosin, AMPK, P-AMPK were measured by western blotting. Both HIIT and MICT caused a significant decrease in weight, waist circumference, BMI, and serum levels of glucose, insulin, asprosin, triglyceride, total cholesterol, low-density lipoprotein (LDL), and TNF-α, but an increase in AMPK, P-AMPK, and P-AMPK/AMPK in the liver (P = 0.001), compared with OVX2 nonexercised group(P = 0.001). MICT was superior to HIIT in reducing serum asprosin, TNF-a, TG, LDL, insulin, fasting glucose, HOMA-IR, QUEKI index, AMPK and p-AMPK. Although after two month of de-training almost all indices returned to the pre exercise values (p < 0.05). Our findings suggest that MICT effectively alleviates MetS–induced by menopause at least partly via activating liver signaling of P-AMPK and reducing asprosin and TNF-α.