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1.
Eur J Appl Physiol ; 112(7): 2523-30, 2012 Jul.
Article in English | MEDLINE | ID: mdl-22075638

ABSTRACT

We investigated whether swim training protects skeletal muscle from oxidative damage in response to a maximum progressive exercise. First, we investigated the effect of swim training on the activities of the antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx), in the gastrocnemius muscle of C57Bl/6 mice, 48 h after the last training session. Mice swam for 90 min, twice a day, for 5 weeks at 31°C (± 1°C). The activities of SOD and CAT were increased in trained mice (P < 0.05) compared to untrained group. However, no effect of training was observed in the activity of GPx. In a second experiment, trained and untrained mice were submitted to a maximum progressive swim test. Compared to control mice (untrained, not acutely exercised), malondialdehyde (MDA) levels were increased in the skeletal muscle of both trained and untrained mice after maximum swim. The activity of GPx was increased in the skeletal muscle of both trained and untrained mice, while SOD activity was increased only in trained mice after maximum swimming. CAT activity was increased only in the untrained compared to the control group. Although the trained mice showed increased activity of citrate synthase in skeletal muscle, swim performance was not different compared to untrained mice. Our results show an imbalance in the activities of SOD, CAT and GPx in response to swim training, which could account for the oxidative damage observed in the skeletal muscle of trained mice in response to maximum swim, resulting in the absence of improved exercise performance.


Subject(s)
Muscle, Skeletal/physiology , Oxidoreductases/metabolism , Physical Conditioning, Animal/methods , Physical Endurance/physiology , Reactive Oxygen Species/metabolism , Swimming/physiology , Task Performance and Analysis , Animals , Male , Mice , Mice, Inbred C57BL , Muscle, Skeletal/injuries , Oxidation-Reduction
2.
Cell Biochem Funct ; 29(7): 610-6, 2011 Oct.
Article in English | MEDLINE | ID: mdl-21887695

ABSTRACT

Exercise promotes transitory alterations in cytokine secretion, and these changes are affected by exercise duration and intensity. Considering that exercise responses also are affected by environmental factors, the goal of the present study was to investigate the effect of water temperature on the cytokine response to maximum swimming. Swiss mice performed a maximum progressive swimming exercise at 31 or 38°C, and plasma cytokine levels were evaluated immediately or 1, 6 or 24 h after exercise. The cytokine profile after swimming at 31°C was characterized by increased interleukin (IL)-6 and monocyte chemotactic protein-1 (MCP-1) levels, which peaked 1 h after exercise, suggesting an adequate inflammatory milieu to induce muscle regeneration. Transitory reductions in IL-10 and IL-12 levels also were observed after swimming at 31°C. The cytokine response to swimming was modified when the water temperature was increased to 38°C. Although exercise at 38°C also led to IL-6 secretion, the peak in IL-6 production occurred 6 h after exercise, and IL-6 levels were significantly lower than those observed after maximum swimming at 31°C (p = 0·030). Furthermore, MCP-1 levels were lower and tumour necrosis factor-α levels were higher immediately after swimming at 38°C, suggesting a dysregulated pro-inflammatory milieu. These alterations in the cytokine profile can be attributed in part to reduced exercise total work because exhaustion occurred sooner in mice swimming at 38°C than in those swimming at 31°C.


Subject(s)
Hot Temperature , Interleukin-6/metabolism , Physical Conditioning, Animal/physiology , Swimming/physiology , Animals , Chemokine CCL2/blood , Chemokine CCL2/metabolism , Exercise Test/methods , Heat Exhaustion , Inflammation/immunology , Interleukin-10/blood , Interleukin-10/metabolism , Interleukin-12/blood , Interleukin-12/metabolism , Interleukin-6/blood , Male , Mice , Tumor Necrosis Factor-alpha/blood , Tumor Necrosis Factor-alpha/metabolism
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