Swimming Training Induces Liver Mitochondrial Adaptations to Oxidative Stress in Rats Submitted to Repeated Exhaustive Swimming Bouts

Frederico D Lima,João B Rocha,Javier González-Gallego,Félix A Soares,Guilherme Bresciani,Daniel N Stamm,Nélson R De Carvalho,Luiz Fernando F Royes,Iuri D Della-Pace,Fernando Dobrachinski,Juan Sastre

doi:10.1371/journal.pone.0055668

Abstract

Background and AimsAlthough acute exhaustive exercise is known to increase liver reactive oxygen species (ROS) production and aerobic training has shown to improve the antioxidant status in the liver, little is known about mitochondria adaptations to aerobic training. The main objective of this study was to investigate the effects of the aerobic training on oxidative stress markers and antioxidant defense in liver mitochondria both after training and in response to three repeated exhaustive swimming bouts.MethodsWistar rats were divided into training (n = 14) and control (n = 14) groups. Training group performed a 6-week swimming training protocol. Subsets of training (n = 7) and control (n = 7) rats performed 3 repeated exhaustive swimming bouts with 72 h rest in between. Oxidative stress biomarkers, antioxidant activity, and mitochondria functionality were assessed.ResultsTrained group showed increased reduced glutathione (GSH) content and reduced/oxidized (GSH/GSSG) ratio, higher superoxide dismutase (MnSOD) activity, and decreased lipid peroxidation in liver mitochondria. Aerobic training protected against exhaustive swimming ROS production herein characterized by decreased oxidative stress markers, higher antioxidant defenses, and increases in methyl-tetrazolium reduction and membrane potential. Trained group also presented higher time to exhaustion compared to control group.ConclusionsSwimming training induced positive adaptations in liver mitochondria of rats. Increased antioxidant defense after training coped well with exercise-produced ROS and liver mitochondria were less affected by exhaustive exercise. Therefore, liver mitochondria also adapt to exercise-induced ROS and may play an important role in exercise performance.

Highlights

Exercise represents a physical stress that transiently disrupts homeostasis [1], and the working skeletal muscle is clearly the organ most directly affected during physical activity [2]
Statistical analysis revealed that blood lactate concentration increased progressively for both trained and control rats, though the trained group presented lower lactate concentrations comparing to the control group [F(1,12) = 23.41; p,0.05; Fig. 2A]
The exhaustive exercise protocol test resulted in increased GSH levels and GSH/GSSG ratio in the trained group, while GSSG levels were significantly higher in the control group [F(1,20) = 9.39; p,0.05; Figure 3B]

Summary

Introduction

Exercise represents a physical stress that transiently disrupts homeostasis [1], and the working skeletal muscle is clearly the organ most directly affected during physical activity [2]. The metabolic adaptations to exercise are not restricted to the working muscle; exercise is a major challenge to other organs such as cardiac muscle, stomach or brain [10,11] This is relevant to the liver due to its central role in the maintenance of energy supply to the exercising muscle [12]. Studies aiming to evaluate the effects of the acute exercise on oxidative stress in the liver have shown increased lipid peroxidation [13,14,15], and protein carbonylation [16,17], and decreased antioxidant defenses [18,19]. Acute exhaustive exercise is known to increase liver reactive oxygen species (ROS) production and aerobic training has shown to improve the antioxidant status in the liver, little is known about mitochondria adaptations to aerobic training. The main objective of this study was to investigate the effects of the aerobic training on oxidative stress markers and antioxidant defense in liver mitochondria both after training and in response to three repeated exhaustive swimming bouts

Objectives

Methods

Results

Conclusion