Abstract
The objective of the present study was to investigate the effects of eccentric training on the activity of mitochondrial respiratory chain enzymes, oxidative stress, muscle damage, and inflammation of skeletal muscle. Eighteen male mice (CF1) weighing 30-35 g were randomly divided into 3 groups (N = 6): untrained, trained eccentric running (16°; TER), and trained running (0°) (TR), and were submitted to an 8-week training program. TER increased muscle oxidative capacity (succinate dehydrogenase and complexes I and II) in a manner similar to TR, and TER did not decrease oxidative damage (xylenol and creatine phosphate) but increased antioxidant enzyme activity (superoxide dismutase and catalase) similar to TR. Muscle damage (creatine kinase) and inflammation (myeloperoxidase) were not reduced by TER. In conclusion, we suggest that TER improves mitochondrial function but does not reduce oxidative stress, muscle damage, or inflammation induced by eccentric contractions.
Highlights
The production of reactive oxygen species (ROS) during physical training depends on the type, intensity, and duration of exercise [1]
A significant increase in succinate dehydrogenase (SDH) activity was observed in the trained eccentric running (TER) (8.4 ± 0.4 nmol?min-1?mg protein-1) and trained running (TR) (8.3 ± 0.3 nmol?min-1?mg protein-1) groups compared to the UT group (4.1 ± 0.5 nmol?min-1?mg protein-1) (Figure 1A)
This study presented data demonstrating that TER is not harmful to mitochondrial function, improving the oxidative capacity of muscle (SDH, complexes I and II) similar to TR
Summary
The production of reactive oxygen species (ROS) during physical training depends on the type, intensity, and duration of exercise [1]. Regular exercise training is associated with numerous health benefits, it can be viewed as an intense physical stressor leading to increased oxidative cellular damage, likely due to the enhanced production of ROS [2]. It appears that ROSmediated oxidation of proteins, lipids, and nucleic acids is not solely dependent on oxygen flux through the mitochondria, since oxygen uptake has been shown to differ drastically between exercise modes. Multiple factors, including xanthine oxidase, disruption of ironcontaining proteins, calcium imbalance secondary to muscle injury, and inflammatory-mediated production of ROS and subsequent oxidation of macromolecules after aerobic, concentric, and eccentric training, may be involved [3,4,5,6]. In eccentric exercise, the generation of ROS has been attributed to xanthine and NADPH oxidase production, ischemia/reperfusion, prostanoid metabolism, phagocyte respiratory burst, disruption of iron-containing proteins, and excessive calcium accumulation resulting from high-force eccentric exercise, which usually produces muscle injury [8,9,10]
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