Study of the relation ship between oxidative damage, antioxidant defense system and mitochondrial activity in rats induced to a treadmill overtraining protocol

Author(s)

Rodrigo Luiz Perroni Ferraresso

• Document type: Master's Dissertation
• Press: Campinas, SP.
• Institution: Universidade Estadual de Campinas (UNICAMP). Instituto de Biologia
• Defense date: 2010-10-12

Examining board members

Denise Vaz de Macedo; Eduardo Rochete Ropelle; Claudio Alexandre Gobatto

• Advisor: Rodrigo Hohl; Denise Vaz de Macedo

Abstract

Overtraining is a continuous process with possible outcomes of functional-overreaching (FOR) and nonfunctional-overreaching (NFOR). FOR is characterized by a short-term decline in performance that leads eventually to an improvement in performance after a short recovery (daysweeks). NFOR is a decline in performance that can be reversed by a longer regenerative period (weeks-months). We developed an animal model of training-overtraining that led Wistar rats to FOR and NFOR states after a training adaptation period where they achieved increased performance (Tr group). The animal performance was evaluated through six tests during the protocol. These tests have served to separate our experimental groups. Our objective was to investigate the oxidative stress-related changes in mitochondrial activity hypothesis as a possible cause of the performance drop during the overtraining installation. We analyzed the antioxidant enzymes catalase (CAT), superoxide dismutase (SOD) and glutathione reductase (GR) activity, ROS generator xanthine oxidase (XO) activity and oxidative damage indicator through the analysis of substances which react to thiubarbituric acid (TBARS) production. In addiction we analyzed citrate syntase (CS) enzyme activity and mitochondrial complexes of the electron transport chain (complex I and IV) activity. We also analyzed, for potencial biomarkers, the antioxidant capacity of blood through the FRAP (ferric reducing ability of plasma), albumin and uric acid analysis. Lipid peroxidation in plasma was obtained by malondialdehyde (MDA) and the muscle damage marker used was blood creatine kinase (CK). The results are presented by boxplots with their respective confidence intervals (95%) giving a significance or not of differences between analysis. The results pointed to significant decreases in complex IV and CS activity plus an increased of antioxidant enzymes SOD and CAT activities in NFOR group when compared to Tr and FOR groups respectively. Furthermore, the lipid peroxidation TBARS and MDA markers were found significantly increased in NFOR group when compared to CO, Tr and FOR. These data suggest that the performance drop in the NFOR state may be related to decreased oxidative capacity due to a mitochondrial oxidative stress installation. However the mechanisms involved in this process yet to be clarified. (AU)