Divergent cytokine response following maximum progressiveswimming in hot water.

Exercise promotes transitory alterations in cytokine secretion, and these changes are affected by exercise duration and intensity. Consideringthat exercise responses also are affected by environmental factors, the goal of the present study was to investigate the effect of watertemperature on the cytokine response to maximum swimming. Swiss mice performed a maximum progressive swimming exercise at 31 or38C, and plasma cytokine levels were evaluated immediately or 1, 6 or 24 h after exercise. The cytokine profile after swimming at 31Cwas characterized by increased interleukin (IL)-6 and monocyte chemotactic protein-1 (MCP-1) levels, which peaked 1 h after exercise, sug-gesting an adequate inflammatory milieu to induce muscle regeneration. Transitory reductions in IL-10 and IL-12 levels also were observedafter swimming at 31C. The cytokine response to swimming was modified when the water temperature was increased to 38C. Althoughexercise at 38C also led to IL-6 secretion, the peak in IL-6 production occurred 6 h after exercise, and IL-6 levels were significantly lowerthan those observed after maximum swimming at 31C(p =0030). Furthermore, MCP-1 levels were lower and tumour necrosis factor-alevels were higher immediately after swimming at 38C, suggesting a dysregulated pro-inflammatory milieu. These alterations in the cyto-kine profile can be attributed in part to reduced exercise total work because exhaustion occurred sooner in mice swimming at 38C than inthose swimming at 31oC

Plasma cytokine response, lipid peroxidation and NF-κB activation in skeletal muscle following maximum progressive swimming.

Our objective was to determine lipid peroxidation and nuclear factor-κB (NF-κB) activation in skeletal muscle and the plasma cytokine profile following maximum progressive swimming. Adult male Swiss mice (N = 15) adapted to the aquatic environment were randomly divided into three groups: immediately after exercise (EX1), 3 h after exercise (EX2) and control. Animals from the exercising groups swam until exhaustion, with an initial workload of 2% of body mass attached to the tail. Control mice did not perform any exercise but were kept immersed in water for 20 min. Maximum swimming led to reactive oxygen species (ROS) generation in skeletal muscle, as indicated by increased thiobarbituric acid reactive species (TBARS) levels (4062.67 ± 1487.10 vs 19,072.48 ± 8738.16 nmol malondialdehyde (MDA)/mg protein, control vs EX1). Exercise also promoted NF-κB activation in soleus muscle. Cytokine secretion following exercise was marked by increased plasma interleukin-6 (IL-6) levels 3 h post-exercise (P < 0.05). Interleukin-10 (IL-10) levels were reduced following exercise and remained reduced 3 h post-exercise (P < 0.05). Plasma levels of other cytokines investigated, monocyte chemotactic protein-1 (MCP-1), tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-γ) and interleukin-12 (IL-12), were not altered by exercise. The present findings showed that maximum swimming, as well as other exercise models, led to lipid peroxidation and NF-κB activation in skeletal muscle and increased plasma IL-6 levels. The plasma cytokine response was also marked by reduced IL-10 levels. These results were attributed to exercise type and intensity

Swim training does not protect mice from skeletal muscle oxidative damage following a maximum exercise test.

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 31C (?1C). 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