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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.

Non-alcoholic fatty liver disease (NAFLD) is the most common liver disease in adults and its prevalence is rising around the world. This pathology is characterized by accumulation of liver fat, which exceeds 5% of liver weight in absence of alcohol consumption, viral infection or other hepatic etiology. Since NAFLD has been associated with obesity, insulin resistance, diabetes or alteration of lipid profiles, it is considered as the liver manifestation of metabolic syndrome. Pathogenic mechanisms of NAFLD have not been clearly elucidated, but different events such as lipid accumulation, insulin resistance, oxidative and endoplasmic reticulum stress, mitochondrial dysfunction and inflammation are involved. Modifications in lifestyle constitute the first line for the management of NAFLD. Nutritional interventions include low fat and carbohydrate diet with higher polyunsaturated fatty acids ingestion. Moreover, supplementation with antioxidant and cytoprotective agents could be useful to decrease oxidative stress, inflammation and fibrosis. Physical activity enables to reduce the expression of lipogenic genes, fat accumulation, or insulin resistance and improves cardiorespiratory fitness. Benefits have been found following both aerobic exercise and resistance training, and remain even after exercise cessation. However, more studies are required to analyze the molecular and cellular mechanisms involved in nutritional and physical intervention, and to define the volume of activity required and its association with weight loss. In this paper, we offer an updated overview of the mechanisms implicated in the progression of NAFLD, and analyze the beneficial effects of nutritional interventions and physical exercise in the prevention and treatment of this condition.

The effects of aerobic and anaerobic physical conditioning on fibrinolysis were studied before and immediately after physical exercise. Moderately active controls (group A) were compared with aerobically- (group B) or anaerobically-conditioned (group C) subjects. Comparison of the resting parameters revealed that FgDP were significantly higher in group B as a compared to groups A and C. FbDP did not significantly differ between groups B and C and were significantly lower in group A. t-PA antigen and PAI antigen did not significantly differ between the three groups, but t-PA activity was elevated and PAI activity and t-PA/PAI complexes were reduced in group B. Following a maximal exercise test on the treadmill both FbDP and FgDP were significantly increased in all groups, although values for FbDP in group B and values for FgDP in group C reached a higher level than in group A. t-PA antigen and t-PA activity were also increased in the three groups. PAI activity was significantly reduced in groups A and C. t-PA/PAI complexes were significantly enhanced in all cases, but increased to a lower degree in group B. These results indicate that both aerobic and anaerobic physical conditioning induce activation of the fibrinolytic system.

In this study the influence of low-dose oral contraceptives (OC) on the different components of the fibrinolytic system before and immediately after maximal exercise was examined in a group of 18 moderately active women. Nine women using OC and nine control women performed a maximal effort treadmill protocol. Comparison of the resting parameters revealed higher plasma FbDP, plasminogen, alpha 2-antiplasmin and protein C concentrations, and lower PAI activity in the OC group. No differences were observed in plasma concentrations of t-PA antigen, t-PA activity, PAI antigen, antithrombin III, and protein S. Acute maximal exercise resulted in significant increases in t-PA antigen, t-PA activity, t-PA/PAI complexes, and FbDP in both groups of subjects, while PAI activity was reduced. No significant differences were found for the change in those parameters between control and OC users. Exercise induced no variation in any of the groups for PAI antigen, alpha 2-antiplasmin, plasminogen, protein C, or protein S. Our data suggest that changes in the fibrinolytic system induced by physical exercise are not affected by oral contraceptives.