Acute immune response in respect to exercise-induced oxidative stress.

The relationship between exhaustive exercise, oxidative stress, the protective capacity of the antioxidant defense system and cellular immune response has been determined. Exhaustive exercise in well-trained young men (n=19)-induced leukocytosis, decreased proportion of activated-lymphocyte subsets (CD4+ and CD8+) expressing CD69, decreased lymphocyte mitogenic response to concanavalin A (ConA) and phytohemagglutinin (PHA), increased lipid peroxidation, increased total antioxidant status (TAS) and catalase activity, immediately after exercise. Suppressed blood concentration of T-lymphocyte subsets (CD3+, CD4+, CD8+, NK), increased TAS and blood total glutathione (TGSH) in early recovery period (30 min after exercise) were found. Strong positive correlation was observed between TGSH and lymphocyte mitogenic response to ConA and PHA (r=0.85 and 0.85, respectively) immediately after exercise. Moderate positive correlation was observed between TAS and lymphocyte mitogenic response to PHA (r=0.59) immediately after exercise as well as between TAS and lymphocyte mitogenic response to PHA and ConA (r=0.69 and 0.54, respectively). Moderate to weak correlation was observed between TAS and conjugated dienes with exercise (r=0.66) as well as in 30-min recovery (r=0.50). After a short-term bout of exhaustive exercise, immune system was characterized by acute phase response, which was accompanied with oxidative stress. Suppression of the cellular immunity 30 min after exercise shows that this period is not enough for recovery after exhaustive exercise. The results suggest the interactions between exercise-induced oxidative stress and immune response.

Physical exercise induces activation of NF-kappaB in human peripheral blood lymphocytes.

Current understanding of nuclear factor-kappaB (NF-kappaB) activation is derived mostly from in vitro studies, and in vivo human data are limited. This study provides first evidence showing that physical exercise (80% maximal O2 consumption, 1 h) may trigger NF-kappaB activation, as determined by electrophoretic mobility shift assay, in peripheral blood lymphocytes of physically fit young men. Supershift assay showed that the NF-kappaB protein complex contained the transcriptionally active p65 protein. Plasma levels of NF-kappaB-directed gene products such as tumor necrosis factor-alpha and interleukin-2 receptor confirmed that physical exercise caused NF-kappaB transactivation. Exercise-induced NF-kappaB activation in lymphocytes was associated with elevated levels of lipid peroxidation by-products in the plasma.