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The liver is remarkably important during exercise outcomes due to its contribution to detoxification, synthesis, and release of biomolecules, and energy supply to the exercising muscles. Recently, liver has been also shown to play an important role in redox status and inflammatory modulation during exercise. However, while several studies have described the adaptations of skeletal muscles to acute and chronic exercise, hepatic changes are still scarcely investigated. Indeed, acute intense exercise challenges the liver with increased reactive oxygen species (ROS) and inflammation onset, whereas regular training induces hepatic antioxidant and anti-inflammatory improvements. Acute and regular exercise protocols in combination with antioxidant and anti-inflammatory supplementation have been also tested to verify hepatic adaptations to exercise. Although positive results have been reported in some acute models, several studies have shown an increased exercise-related stress upon liver. A similar trend has been observed during training: while synergistic effects of training and antioxidant/anti-inflammatory supplementations have been occasionally found, others reported a blunting of relevant adaptations to exercise, following the patterns described in skeletal muscles. This review discusses current data regarding liver responses and adaptation to acute and regular exercise protocols alone or combined with antioxidant and anti-inflammatory supplementation. The understanding of the mechanisms behind these modulations is of interest for both exercise-related health and performance outcomes.

Background and Objective: Although hard training is mandatory in elite level futsal training, few studies have proposed a biochemical follow up in futsal players during a whole season. Therefore, the aim of this study was to compare functional and biochemical markers in Brazilian elite level futsal players throughout a competition season., Materials and Methods: Eight players aged 25.5±5.4 years were evaluated at three time points: preseason (T1), immediately before the FIFA ® -Intercontinental-Futsal-Cup (T2), and at the end of the season (T3), with a tapering period of 1 week before T2. Functional parameters (weight, height, body fat, VO 2 max, heart rate, and distance ran) and blood sampling for cell count and lipid profile (cholesterol, HDL-C, LDL-C, triglycerides) were assessed at each time point. After, a Yo-Yo R2 test was carried out in each time point (T1, T2 and T3) and blood samples to assess skeletal muscle damage (creatine kinase [CK], lactate dehydrogenase [LDH]), inflammation (C-reactive protein [CRP]) and oxidative stress markers (ischemia modified albumin [IMA], and advanced oxidation protein products [AOPP]) were obtained before and after the tests., Results: Although functional parameters did not change throughout the season, greater total number of erythrocytes (P≤0.05), and hemoglobin (P≤0.05) were found at T2 compared to T1. Similarly, lower LDH (P≤0.05) and CK (P≤0.05) levels were found at T2 compared to T1. CPR levels were also decreased at T2 in comparison to T1 both before and after Yo-Yo R2 test (P≤0.05), while IMA and AOPP levels showed only a season effect (P≤0.05)., Conclusions: The tapering strategy was successful considering players presented lower levels of muscle damage, inflammation and oxidative stress makers before T2, which preceded the main championship of the year. These results are of great relevance, considering the team won the FIFA ® -Intercontinental-Futsal-Cup, which happened at T2. Thus, it seems that routine-based biochemical markers may be useful as training control means in this population., (Copyright © 2017 The Lithuanian University of Health Sciences. Production and hosting by Elsevier Sp. z o.o. All rights reserved.)

Oxidative stress is characterized by imbalanced reactive oxygen species (ROS) production and antioxidant defenses. Two main antioxidant systems exist. The nonenzymatic system relies on molecules to directly quench ROS and the enzymatic system is composed of specific enzymes that detoxify ROS. Among the latter, the superoxide dismutase (SOD) family is important in oxidative stress modulation. Of these, manganese-dependent SOD (MnSOD) plays a major role due to its mitochondrial location, i.e., the main site of superoxide (O(2)(·-)) production. As such, extensive research has focused on its capacity to modulate oxidative stress. Early data demonstrated the relevance of MnSOD as an O(2)(·-) scavenger. More recent research has, however, identified a prominent role for MnSOD in carcinogenesis. In addition, SOD downregulation appears associated with health risk in heart and brain. A single nucleotide polymorphism which alters the mitochondria signaling sequence for the cytosolic MnSOD form has been identified. Transport into the mitochondria was differentially affected by allelic presence and a new chapter in MnSOD research thus begun. As a result, an ever-increasing number of diseases appear associated with this allelic variation including metabolic and cardiovascular disease. Although diet and exercise upregulate MnSOD, the relationship between environmental and genetic factors remains unclear., (© 2015 Elsevier Inc. All rights reserved.)

Aims: Caffeine has been widely used in sports competitions due to its ergogenic effects. Most of the studies regarding caffeine and exercise have focused on muscle and plasma adaptations, while the impact on the liver is scarcely described. The aim is to analyze the effects of caffeine and exercise training on oxidative stress markers and injury-related parameters in the liver., Main Methods: Rats were divided into sedentary/saline, sedentary/caffeine, exercise/saline, and exercise/caffeine groups. Exercise groups underwent 4 weeks of swimming training, and caffeine (6 mg/kg, p.o.) was supplemented throughout the training protocol. Injury-related liver parameters were assessed in plasma, while redox status and oxidative stress markers were measured on liver homogenates., Key Findings: Exercise training increased muscle citrate synthase activity in the muscle, while in caffeine decreased its activity in both sedentary and trained rats. Aspartate transaminase levels were increased after training, and caffeine intake suppressed this elevation (p<0.05). Caffeine also diminished alanine transaminase levels in both sedentary and exercised rats (p<0.05). Exercise training induced a significant increase on the activity of the enzymes superoxide dismutase and glutathione peroxidase, as an increase on thiobarbituric acid-reactive substances levels was also reached (p<0.05); caffeine intake blunted these alterations. Caffeine intake also suppressed liver catalase activity in both sedentary and exercise groups (p<0.05)., Significance: Our data suggest that caffeine modified the hepatic responses associated to exercise-induced oxidative stress without affecting the performance, exerting different actions according to the tissue. However, further studies are needed to better understand caffeine's role on liver under exercise training., (Copyright © 2013 Elsevier Inc. All rights reserved.)

Objectives: In humans, the manganese-superoxide dismutase (MnSOD) gene contains a polymorphism (Ala16Val) that has been related to several metabolic dysfunctions and chronic diseases. However, the obtained results suggest that risks related to this polymorphism are directly influenced by environmental factors. Because few studies have analyzed this possible influence, we performed a controlled study to evaluate if the oxidative stress caused by exercise is differentially modulated by the Ala16Val MnSOD polymorphism., Design and Methods: Fifty-seven males were previously genotyped and 10 subjects per genotype were selected to perform a bout of controlled intense exercise. MnSOD mRNA expression, protein content, enzyme activity, and total glutathione and thiol content from peripheral blood mononuclear cells were evaluated before and 1h after a bout of intense exercise., Results: The AA genotype participants showed increased post-exercise MnSOD mRNA expression and enzyme activity compared to baseline values. Conversely, MnSOD mRNA expression did not change but protein thiol content decreased significantly after the bout of exercise in VV carriers. A comparison of the genotypes showed that the AA genotype presented a higher MnSOD protein content than VV volunteers after exercise; while a dose-effect for the A allele was found for enzyme activity., Conclusion: This study supports recent evidence that genotypes of key antioxidant enzymes may be associated with differential oxidative stress modulation and the hypothesis that the risk of disease associated with the MnSOD Ala16Val gene polymorphism may be controlled by environmental factors., (Copyright © 2012 The Canadian Society of Clinical Chemists. Published by Elsevier Inc. All rights reserved.)

Background and Aims: Although 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., Methods: Wistar 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., Results: Trained 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., Conclusions: Swimming 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.

Although the intake of nonsteroidal anti-inflammatory drugs ( NSAIDs) intake by athletes prevents soreness, little is known concerning their role in exercise performance. This study assessed the effects of ibuprofen intake on an exhaustive protocol test after 6 weeks of swimming training in rats. Animals were divided into sedentary and training groups. After training, animals were subdivided into two subsets: saline or ibuprofen. Afterwards, three repeated swimming bouts were performed by the groups. Ibuprofen (15 mg/kg) was administered once a day. Pain measurements were performed and inflammatory and oxidative stress parameters were assayed in cerebral cortex and gastrocnemius muscle. Training, ibuprofen administration, or both combined ( P < 0.05; 211 ± 18s, 200 ± 31s, and 279 ± 23s) increased exercise time to exhaustion. Training decreased the acetylcholinesterase ( AChE) activity ( P < 0.05; 149 ± 11) in cerebral cortex. Ibuprofen intake decreased the AChE activity after exhaustive protocol test in trained and sedentary rats ( P < 0.05; 270 ± 60; 171 ± 38; and 273 ± 29). It also prevented neuronal tumor necrosis factor-α ( TNF-α) and interleukin ( IL 1β) increase. Fatigue elicited by this exhaustive protocol may involve disturbances of the central nervous system. Additive anti-inflammatory effects of exercise and ibuprofen intake support the hypothesis that this combination may constitute a more effective approach. In addition, ergogenic aids may be a useful means to prevent exercise-induced fatigue. [ABSTRACT FROM AUTHOR]

The relevance of reactive oxygen species (ROS) production relies on the dual role shown by these molecules in aerobes. ROS are known to modulate several physiological phenomena, such as immune response and cell growth and differentiation; on the other hand, uncontrolled ROS production may cause important tissue and cell damage, such as deoxyribonucleic acid oxidation, lipid peroxidation, and protein carbonylation. The manganese superoxide dismutase (MnSOD) antioxidant enzyme affords the major defense against ROS within the mitochondria, which is considered the main ROS production locus in aerobes. Structural and/or functional single nucleotide polymorphisms (SNP) within the MnSOD encoding gene may be relevant for ROS detoxification. Specifically, the MnSOD Ala16Val SNP has been shown to alter the enzyme localization and mitochondrial transportation, affecting the redox status balance. Oxidative stress may contribute to the development of type 2 diabetes, cardiovascular diseases, various inflammatory conditions, or cancer. The Ala16Val MnSOD SNP has been associated with these and other chronic diseases; however, inconsistent findings between studies have made difficult drawing definitive conclusions. Environmental factors, such as dietary antioxidant intake and exercise have been shown to affect ROS metabolism through antioxidant enzyme regulation and may contribute to explain inconsistencies in the literature. Nevertheless, whether environmental factors may be associated to the Ala16Val genotypes in human diseases still needs to be clarified. [ABSTRACT FROM AUTHOR]