Exercise-induced elevation in plasma oxidative generating capability augments the temporal inflammatory response stimulated by lipopolysaccharide
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Prolonged oxidative stress is detrimental to health; however, transient oxidative stress may improve immune capability. We examined whether exercise-induced increases in the plasma oxidative generating capability enhance immune responsiveness to potential pathogens. Twelve individuals underwent a 30-min row and pre and post-exercise bloods were collected for oxidative stress and immune assessment. We found that exercise induced a transient increase in plasma carbonyls (3.2–5.3 nmol/mg protein) and creatine kinase activity (0.5–1.2 absorbance/min/mg protein) and that lipopolysaccharide (LPS) stimulation (0.5–24 h) of pre- and post-exercise blood augmented temporal tumour necrosis factor-α (TNFα) secretion. Further characterisation of plasma using a modified dihydro-2′,7′-dichlorohydrofluorescein (DCF) assay revealed that addition of a sub-threshold of hydrogen peroxide to post-exercise (and not pre-exercise) plasma caused a sixfold increase in the radical oxygen species (ROS) generating capability after 15 min (555 ± 131 to 3607 ± 488 change in fluorescent intensity [ΔFI]), which was inhibited using 60 mM N-acetyl-l-cysteine (920 ± 154 ΔFI). Furthermore, cell experiments revealed that LPS stimulation of either THP-1 cells pre-incubated with post-exercise plasma or peripheral blood mononuclear cells pre-treated with pro-oxidants, modulated the temporal secretion of key cytokines that regulate the initiation, progression and resolution of an inflammatory response. These results indicate that exercise-induced changes in plasma parameters (e.g. oxidative generating capability—dependent or independent of inflammatory mediators) augment the temporal LPS response and support the notion that repeated transient oxidative stress (such as that induced by regular exercise) is important for a “healthy” immune system.
KeywordsExercise Reactive oxygen species Lipopolysaccharide Acute inflammation
We thank the individuals who agreed to participate in this study. Thanks also to Robyn Wells, Steve Payne and Kim Lo for their technical support, plus Drs Margot Skinner and Jeff Greenwood for their constructive advice in the writing of this manuscript. This work was funded by The New Zealand Institute of Plant and Food Research Ltd. The authors declare that the human and cell experiments comply with the current laws of New Zealand and was approved by The Northern Ethical Regional Committee (Region Y), Hamilton, Waikato, New Zealand (NTY/07/10/106). Furthermore, the human exercise trial was registered with the Australian New Zealand Clinical Trials Registry (# ACTRN12608000317392).
Conflict of interest statement
The authors declare that they have no conflict of interest.
- Childs A, Jacobs C, Kaminski T, Halliwell B, Leeuwenburgh C (2001) Supplementation with vitamin C and N-acetyl-cysteine increases oxidative stress in humans after acute muscle injury induced by eccentric exercise. Free Radic Biol Med 31(6):745–753. doi: 10.1016/50891-5849(01)00640-2 PubMedCrossRefGoogle Scholar
- Den Broeder AA, Wanten GJA, Oyen WJG, Naber T, Van Riel PL, Barrera P (2003) Neutrophil migration and production of reactive oxygen species during treatment with a fully human anti-tumor necrosis factor-α monoclonal antibody in patients with rheumatoid arthritis. J Rheumatol 30(2):232–237Google Scholar
- German Society for Clinical Chemistry (1977) Standardization of methods for the determination of creatine kinase activity. Eur J Clin Chem Biochem 15:255–260Google Scholar
- Morabito F, Tomaino A, Cristani M, Cimino F, Martino A, Minciullo PL, Calabro C, Saija A, Gangemi S (2005) Modification of the content of plasma protein carbonyl groups in donors after granulocyte colony stimulating factor-induced stem cell mobilization. Trans Aphereis Sci 33:141–146. doi: 10.1016/j.transci.2005.05.003 CrossRefGoogle Scholar