Nonfunctional overreaching in an animal model and endoplasmic reticulum stress in liver and heart

Author(s)

Ana Paula Pinto

• Document type: Master's Dissertation
• Press: Ribeirão Preto.
• Institution: Universidade de São Paulo (USP). Faculdade de Medicina de Ribeirão Preto (PCARP/BC)
• Defense date: 2017-03-03

Examining board members

Adelino Sanchez Ramos da Silva; Hugo Celso Dutra de Souza; Angelina Zanesco

• Advisor: Adelino Sanchez Ramos da Silva

Abstract

Newly, we verified that different running overtraining (OT) protocols with same external load but performed in downhill (OTR/down), uphill (OTR/up) and without inclination (OTR), directed to hepatic fat accumulation. Knowing the disruption of endoplasmic reticulum (ER) homeostasis is linked to animal models of fatty liver, we explored the effects of these OT models on the proteins related to ER stress (i.e., BiP, IRE1, PERK, eIF2alpha, ATF6beta, and GRP94), apoptosis (CHOP, Caspase-3, 4 and 12, Bax and TRAF2) and inflammation (SAPKJNK and IKK) in livers of C57BL/6 mice. Because aerobic training can diminish cardiac ER stress and increase exercise capacity, we also verified whether the performance decrease induced by our OT protocols is linked to ER stress and apoptosis in mouse hearts. Rodents were divided into naive (N. sedentary mice), control (CT, sedentary mice submitted to the performance evaluations), trained (TR), OTR/down, OTR/up and OTR groups. Rotarod, incremental load, exhaustive and grip force tests were used to estimate performance. Thirteen six hours after the grip force test, the livers and cardiac muscles (i.e., left ventricle) were removed and used for immunoblotting. All OT protocols led to similar responses of the performance parameters and showed significantly lower values of hepatic ATF6beta compared to the N group. The OTR/down group exhibited inferior values of liver cleaved caspase-3 compared to the CT group. The cardiac proteins related to ER stress and apoptosis were not modulated in the experimental groups. (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 Opportunities: Scholarships in Brazil - Master