Abstract
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.
Highlights
Exercise has been extended from competitive sports to disease prevention and health promotion
The present study evaluated reactive oxygen species (ROS) generation and nuclear factor-κB (NF-κB) activation in skeletal muscle, as well as the plasma cytokine response to a single bout of maximum swimming in mice
To investigate whether maximum swimming can induce oxidative stress in skeletal muscle, the levels of TBARs were measured in samples of soleus muscle from non-exercised mice and from exercised mice immediately after (EX1) and 3 h after (EX2) exercise
Summary
Exercise has been extended from competitive sports to disease prevention and health promotion. Regular and moderate exercise has various beneficial health effects. It offers protection against all-cause mortality, primarily by protection against atherosclerosis, type 2 diabetes, colon and breast cancers [1]. Physical training is effective in the treatment of patients with ischemic heart disease, heart failure, and type 2 diabetes [2,3]. All physiologic systems are altered and the systemic effects of exercise result from cellular alterations promoted by each bout of exercise. Treadmill exercise has been associated with the increased generation of reactive oxygen species (ROS) in skeletal muscle [4,5]. Many reports suggest that exercise-induced ROS production
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