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

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.

Pretreatment Hepatoprotective Effect of Regular Aerobic Training Against Hepatic Toxicity Induced by Doxorubicin In Rats

“…Therefore, in the present study, the hepatoprotection of the regular aerobic training against DOX-induced hepatotoxicity in rats could be attributed to its ability to restore the antioxidant enzymes SOD and GPx of liver cytosol or to the free radical scavenging activity of the pretratment. Liver plays an important role during exercise through glucose release to the bloodstream and gluconeogenesis, and mitochondria are clearly important in exercise performance due to aerobic energy production (Lima et al, 2013). While, current data demonstrate that exercise training protects the liver against Dox-induced oxidative stress, the mechanism(s) by which exercise training protects oxidative stress remain unclear.…”

“…In contrast, exercise seems to increase the oxygen consumption rate by 10-20 fold as reported earlier and might have released the above factors and thereby induced oxidant activity (Husain, 2002). Indeed, exercise training has been reported to produce adaptive responses to oxidative stress, as studied primarily on skeletal muscles, but also in the liver (Lima et al, 2013).…”

“…The metabolic adaptations to exercise are not restricted to the working muscle; exercise is also a major challenge to other organs such as cardiac muscle, stomach or brain (Lima et al, 2013). This is particularly relevant to the liver due to its central role in the maintenance of energy supply to the exercising muscle (Hoene et al, 2010).…”

“…This is particularly relevant to the liver due to its central role in the maintenance of energy supply to the exercising muscle (Hoene et al, 2010). Studies aiming to evaluate the effects of the acute exercise on oxidative stress in the liver have shown increased lipid peroxidation (Korivi et al, 2012), and decreased antioxidant defenses (Lima et al, 2013). Additionally, it is known that strenuous exercise causes a number of marked metabolic changes that may impair mitochondrial function in several ways, one major factor being mitochondrial ROS formation (Radak et al, 2004).…”

“…Additionally, it is known that strenuous exercise causes a number of marked metabolic changes that may impair mitochondrial function in several ways, one major factor being mitochondrial ROS formation (Radak et al, 2004). Interestingly, mitochondrial dysfunction appears to be a key issue during exhaustive exercise, and may cause oxidative damage and tissue injury to liver, among others organ (Lima et al, 2013).…”