Excessive training impairs the insulin signal transduction in mice skeletal muscles

Author(s)

Pereira, Bruno C. ^[1] ; da Rocha, Alisson L. ^[1] ; Pinto, Ana P. ^[1] ; Pauli, Jose R. ^[2] ; de Moura, Leandro P. ^[2] ; Mekary, Rania A. ^{[3, 4]} ; de Freitas, Ellen C. ^[5] ; da Silva, Adelino S. R. ^{[5, 1]}

Affiliation

^[1] Univ Sao Paulo, Ribeirao Preto Med Sch, Postgrad Program Rehabil & Funct Performance, BR-09500900 Sao Paulo - Brazil

^[2] Univ Estadual Campinas, Fac Sci Appl, Sport Sci Course, Sao Paulo - Brazil

^[3] Harvard Sch Publ Hlth, Dept Nutr, Boston, MA - USA

^[4] MCPHS Univ, Dept Social & Adm Sci, Boston, MA - USA

^[5] Univ Sao Paulo, Sch Phys Educ & Sport Ribeirao Preto, Sao Paulo - Brazil

• Document type: Journal article
• Source: Journal of Endocrinology; v. 230, n. 1, p. 93-104, JUL 2016.
• Web of Science Citations: 8

Abstract

The main aim of this investigation was to verify the effects of overtraining (OT) on the insulin and inflammatory signaling pathways in mice skeletal muscles. Rodents were divided into control (CT), overtrained by downhill running (OTR/down), overtrained by uphill running (OTR/up), and overtrained by running without inclination (OTR) groups. Rotarod, incremental load, exhaustive, and grip force tests were used to evaluate performance. Thirty-six hours after the grip force test, the extensor digitorum longus (EDL) and soleus were extracted for subsequent protein analyses. The three OT protocols led to similar responses of all performance evaluation tests. The phosphorylation of insulin receptor beta (pIR beta; Tyr), protein kinase B (pAkt; Ser473), and the protein levels of plasma membrane glucose transporter-4 (GLUT4) were lower in the EDL and soleus after the OTR/down protocol and in the soleus after the OTR/up and OTR protocols. While the pIR beta was lower after the OTR/up and OTR protocols, the pAkt was higher after the OTR/up in the EDL. The phosphorylation of I kappa B kinase alpha and beta (pIKK alpha/beta; Ser180/181), stress-activated protein kinases/Jun amino-terminal kinases (pSAPK-JNK; Thr183/Tyr185), factor nuclear kappa B (pNF kappa B p65; Ser536), and insulin receptor substrate 1 (pIRS1; Ser307) were higher after the OTR/down protocol, but were not altered after the two other OT protocols. In summary, these data suggest that OT may lead to skeletal muscle insulin signaling pathway impairment, regardless of the predominance of eccentric contractions, although the insulin signal pathway impairment induced in OTR/up and OTR appeared to be muscle fiber-type specific. (AU)

• FAPESP's process: 15/08013-0 - Overreaching not functional in animal model and endoplasmic reticulum stress in muscle heart and liver
• Grantee: Ana Paula Pinto
• Support type: Scholarships in Brazil - Master
• FAPESP's process: 14/25459-9 - Nonfunctional overreaching in animal model: inflammatory and hypertrophic adaptions of the cardiac muscle
• Grantee: Alisson Luiz da Rocha
• Support type: Scholarships in Brazil - Master
• FAPESP's process: 13/19985-7 - Effects of overtraining induced by exercise in treadmill without inclination, uphill and downhill on the content and activation of proteins of insulin signaling pathway and inflamation in mice
• Grantee: Bruno Cesar Pereira
• Support type: Scholarships in Brazil - Master
• FAPESP's process: 13/20591-3 - Responses of proteins from the inflammatory, insulinic and hypertrophic molecular pathways to nonfunctional overreaching induced by treadmill running performed in downhill, without inclination and uphill in skeletal muscle of mice
• Grantee: Adelino Sanchez Ramos da Silva
• Support type: Regular Research Grants