Eccentric Exercise Leads to Glial Activation but not Apoptosis in Mice Spinal Cords

Pereira, Bruno; Lucas, Guilherme; Rocha, Aristides Almeida; Pauli, José Rodrigo; Ropelle, Eduardo Rochete; Cintra, Dennys Esper; Souza, Cláudio Teodoro de; Bueno, Carlos; Silva, A. S. da

doi:10.1055/s-0034-1395589

Cited by 35 publications

(65 citation statements)

References 42 publications

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“…However, here, we verified that the OTR/up group presented a lower change in the exhaustion velocity as compared with the other OT protocols. In addition, differently from Rocha's investigation (da Rocha et al 2015b), we showed that the OTR protocol also reduced the rotarod performance as compared with the CT group. These findings indicate that the application of the same OT protocols in different batches of C57BL/6 mice may induce minimal differences of adaptation.…”

Section: Discussioncontrasting

confidence: 99%

“…Indeed, da Rocha and coworkers (2015b) showed that OTR/down and OTR/up models upregulated the phosphorylation and inhibition of glycogen synthase kinase 3 beta (GSK3β), increasing hepatic glycogen deposition. In accordance with other studies (Zisman et al 2000, Kotani et al 2004, the authors concluded that liver acted as a compensatory organ when skeletal muscle presents insulin signaling impairment (da Rocha et al 2015b).…”

Section: Discussionsupporting

confidence: 88%

“…The performance evaluations of the experimental groups were performed on week 0 and 48 h after the last sessions of the OT protocols at the end of weeks 4 and 8, and consisted of the rotarod test (Turgeman et al 2008, Pereira et al 2015a, da Rocha et al 2015b, the ILT (Pereira et al 2012, 2014a,b, 2015a,b, da Rocha et al 2015a, the exhaustive test (Pereira et al 2012, 2014a,b, 2015a,b, da Rocha et al 2015a, and the grip force test (Anderson et al 2004, da Rocha et al 2015a,b, Pereira et al 2015a). On week 0, the experimental groups performed the ILT without inclination.…”

Section: Performance Evaluationsmentioning

confidence: 99%

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Excessive training impairs the insulin signal transduction in mice skeletal muscles

Pereira¹,

Rocha²,

Pinto³

et al. 2016

Journal of Endocrinology

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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 (pIRβ; 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 pIRβ was lower after the OTR/up and OTR protocols, the pAkt was higher after the OTR/up in the EDL. The phosphorylation of IκB kinase alpha and beta (pIKKα/β; Ser180/181), stress-activated protein kinases/Jun amino-terminal kinases (pSAPK-JNK; Thr183/Tyr185), factor nuclear kappa B (pNFκB 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. Journal of Endocrinology

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Section: Discussioncontrasting

confidence: 99%

Section: Discussionsupporting

confidence: 88%

Section: Performance Evaluationsmentioning

confidence: 99%

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Excessive training impairs the insulin signal transduction in mice skeletal muscles

Pereira¹,

Rocha²,

Pinto³

et al. 2016

Journal of Endocrinology

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“…Although the other two OT protocols performed in uphill and without inclination led to similar decrements in the analyzed performance parameters 3,12,13 , they induced particular modulations of the hepatic insulin signaling pathway 3 . Thus, we also evaluated their effects on the hepatic protein levels of APPL1 and APPL2.…”

Section: Introductionmentioning

confidence: 82%

“…The eight-week OT protocols based on downhill running, uphill running and running without inclination were performed as previously described 13 , and each experimental week consisted of five days of training followed by two days of recovery. During the first four weeks of the OT protocols (i.e.…”

Section: Overtraining Protocols and Performance Evaluationsmentioning

confidence: 99%

Nonfunctional overreaching and hepatic adaptations of APPL1 and APPL2

Morais

Vicente

Oliveira

et al. 2017

Motriz: rev. educ. fis.

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-Aims: Previously, we verified that overtrained mice upregulated the TRB3 levels, its association with Akt, and the hepatic concentrations of glycogen. It is known that APPL1 can limit the interaction between TRB3 and Akt, playing an important role in the glucose homeostasis. Thus, we verified the effects of three overtraining protocols on the hepatic levels of APPL1 and APPL2. Methods: 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). The hepatic contents of APPL1 and APPl2 were measured by the immunoblotting technique. Results: Significant elevation of APPL1 observed in the OTR/down and OTR/up groups, as well as the tendency of increase (p=0.071) observed in the OTR group. Conclusion: These results indicate that this particular protein is likely to participate in the glucose homeostasis previously observed in response to these OT protocols.

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

Oliveira

Morais

Rocha

et al. 2018

J of Cellular Biochemistry

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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 β (pIRβ) (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 IκB kinase α/β) (pIKKα/β (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 naïve (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 pIRβ (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.

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Eccentric Exercise Leads to Glial Activation but not Apoptosis in Mice Spinal Cords

Cited by 35 publications

References 42 publications

Excessive training impairs the insulin signal transduction in mice skeletal muscles

Excessive training impairs the insulin signal transduction in mice skeletal muscles

Nonfunctional overreaching and hepatic adaptations of APPL1 and APPL2

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

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