Artículos de revistas
Excessive Training Impairs The Insulin Signal Transduction In Mice Skeletal Muscles
Registro en:
Journal Of Endocrinology. Bioscientifica Ltd, v. 230, p. 93 - 104, 2016.
0022-0795
1479-6805
WOS:000379880200013
10.1530/JOE-16-0063
Autor
Pereira
Bruno C.; da Rocha
Alisson L.; Pinto
Ana P.; Pauli
Jose R.; de Moura
Leandro P.; Mekary
Rania A.; de Freitas
Ellen C.; da Silva
Adelino S. R.
Institución
Resumen
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) 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. 230 1 93 104 Sao Paulo Research Foundation (FAPESP) [2013/19985-7, 2013/20591-3, 2014/25459-9, 2015/08013-0] Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)