Eccentric Exercise Leads to Performance Decrease and Insulin Signaling Impairment

Abstract

This study aimed to evaluate the effects of an overtraining (OT) protocol based on eccentric exercise (EE) sessions on the insulin and inflammatory signaling pathways in the skeletal muscles of Swiss mice. Rodents were divided into control (C; sedentary mice), trained (TR; performed the aerobic training protocol), and overtrained (OTR; performed the OT protocol). The incremental load test and exhaustive test were used to measure performances before and after exercise protocols. Twenty-four hours after the exhaustive test performed at the end of week 8, the extensor digitorum longus (EDL) and soleus muscles were removed for subsequent protein analysis by immunoblotting. The phosphorylation of insulin receptor beta (pIRbeta; Tyr1146) diminished for EDL and soleus muscles in OTR compared with C. The phosphorylation of insulin receptor substrate 1 (pIRS-1; Ser307) increased for EDL and soleus muscles in OTR compared with C and TR. The phosphorylation of protein kinase B (pAkt; Ser473) diminished for EDL and soleus muscles in OTR compared with C and TR. The phosphorylation of IκB kinase alpha and beta (pIKKalpha/beta; Ser176/180), stress-activated protein kinases/Jun amino-terminal kinases (pSAPK/JNK; Thr183/Tyr185), and the protein levels of suppressor of cytokine signaling 3 (SOCS3) increased for EDL and soleus muscles in OTR compared with C and TR. In summary, the current used OT protocol based on eccentric exercise sessions impaired the insulin signaling pathway with concomitant increases of IKK, SAPK/JNK, and SOCS3 protein levels.