Excessive treadmill training enhances the insulin signaling pathway and glycogen deposition in mice hearts

Author(s):Show less -

Oliveira, Luciana da C. ^[1] ; de Morais, Gustavo P. ^[2] ; da Rocha, Alisson L. ^[1] ; Teixeira, Giovana R. ^[3] ; Pinto, Ana P. ^[1] ; de Vicente, Larissa G. ^[1] ; Pauli, Jose R. ^[4] ; de Moura, Leandro P. ^[4] ; Mekary, Rania A. ^{[5, 6]} ; Ropelle, Eduardo R. ^[4] ; Cintra, Dennys E. ^[4] ; da Silva, Adelino S. R. ^{[1, 2]}

Affiliation

^[1] Univ Sao Paulo, Ribeirao Preto Med Sch, Postgrad Program Rehabil & Funct Performance, Ave Bandeirantes 3900, BR-14040907 Ribeirao Preto, SP - Brazil

^[2] Univ Sao Paulo, Sch Phys Educ & Sport Ribeirao Preto, Postgrad Program Phys Educ & Sport, Ribeirao Preto, SP - Brazil

^[3] State Univ Sao Paulo UNESP, Dept Phys Educ, Presidente Prudente, SP - Brazil

^[4] Univ Campinas UNICAMP, Sch Appl Sci, Lab Mol Biol Exercise LaBMEx, Campinas, SP - Brazil

^[5] MCPHS Univ, Dept Pharmaceut Business & Adm Sci, Boston, MA - USA

^[6] Harvard Med Sch, Brigham & Womens Hosp, Dept Surg, Boston, MA - USA

• Document type: Journal article
• Source: Journal of Cellular Biochemistry; v. 120, n. 2, p. 1304-1317, FEB 2019.
• Web of Science Citations: 1

Abstract

Exhaustive and chronic physical exercise leads to peripheral inflammation, which is one of the molecular mechanisms responsible for the impairment of the insulin signaling pathway in the heart. Recently, 3 different running overtraining models performed downhill (OTR/down), uphill (OTR/up), and without inclination (OTR) increased the serum levels of proinflammatory cytokines. This proinflammatory status induced insulin signaling impairment in the skeletal muscle; however, the response of this signaling pathway in the cardiac muscle of overtrained mice was still unknown. Thus, we investigated the effects of OTR/down, OTR/up, and OTR protocols on the protein levels of phosphorylation of insulin receptor (pIR) (Tyr), phosphorylation of protein kinase B (pAkt) (Ser473), plasma membrane glucose transporter-1 (GLUT1) and GLUT4, phosphorylation of insulin receptor substrate-1 (pIRS-1) (Ser307), phosphorylation of IB kinase /) (pIKK/ (Ser180/181), phosphorylation of p38 mitogen-activated protein kinase (p-p38MAPK) (Thr180/Tyr182), phosphorylation of stress-activated protein kinases-Jun amino-terminal kinases (pSAPK-JNK) (Thr183/Tyr185), and glycogen content in mice hearts. The rodents were divided into naive (N, sedentary mice), control (CT, sedentary mice submitted to performance evaluations), trained (TR, performed the training protocol), OTR/down, OTR/up, and OTR groups. After the grip force test, the cardiac muscles (ie, left ventricle) were removed and used for immunoblotting and histology. Although the OTR/up and OTR groups exhibited higher cardiac levels of pIR (Tyr), only the OTR group exhibited higher cardiac levels of pAkt (Ser473) and plasma membrane GLUT4. On the contrary, the OTR/down group exhibited higher cardiac levels of pIRS-1 (Ser307). The OTR model enhanced the cardiac insulin signaling pathway. All overtraining models increased the left ventricle glycogen content, with this probably acting as a compensatory organ in response to skeletal muscle insulin signaling impairment. (AU)

• 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