title: Eccentric exercise leads to performance decrease and insulin signaling impairment.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: 1School of Physical Education and Sport of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, BRAZIL; 2Sport Sciences Course, Faculty of Applied Sciences, State University of Campinas, Limeira, São Paulo, BRAZIL; and 3Exercise Biochemistry and Physiology Laboratory Postgraduate Program in Health Sciences, Health Sciences Unit, University of Southern Santa Catarina, Criciuma, Santa Catarina, BRAZIL.
authors.forename: Bruno C
authors.initials: BC
authors.lastname: Pereira
authors.forename: José R
authors.initials: JR
authors.lastname: Pauli
authors.forename: Claudio T
authors.initials: CT
authors.lastname: De Souza
authors.forename: Eduardo R
authors.initials: ER
authors.lastname: Ropelle
authors.forename: Dennys E
authors.initials: DE
authors.lastname: Cintra
authors.forename: Ellen C
authors.initials: EC
authors.lastname: Freitas
authors.forename: Adelino Sanchez Ramos
authors.initials: AS
authors.lastname: da Silva
mesh_terms: D000818:Animals; D016207:Cytokines / Q000378:metabolism; D005080:Exercise Test; D007249:Inflammation / Q000378:metabolism*; D007328:Insulin / Q000378:metabolism*; D055504:Insulin Receptor Substrate Proteins / Q000378:metabolism; D008297:Male; D051379:Mice; D009124:Muscle Proteins / Q000378:metabolism*; D018482:Muscle, Skeletal / Q000378:metabolism*; D010766:Phosphorylation; D010805:Physical Conditioning, Animal; D011494:Protein Kinases / Q000378:metabolism; D011972:Receptor, Insulin / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D016207:Cytokines; D007328:Insulin; D055504:Insulin Receptor Substrate Proteins; D009124:Muscle Proteins; D011494:Protein Kinases; D011972:Receptor, Insulin