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Indexed/Abstracted in: Chemical Abstracts, CINAHL, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,111
Online ISSN 1827-1928
(Biochemistry, Immunology, Kinanthropometry, Neurology, Neurophysiology, Ophtalmology, Pharmacology, Phlebology, etc.)
Spagnuolo P. A., Hoffman-Goetz L.
Department of Health Studies and Gerontology Faculty of Applied Health Sciences University of Waterloo, Waterloo, ON, Canada
Aim. Athletes may experience gastrointestinal disturbances during intense exercise. Using a mouse model, we determined the influence of acute exercise (AE) and dextran sulfate sodium (DSS), a chemical known to induce intestinal inflammation, on: 1) inflammatory changes within small and large intestine, 2) extent of cell death as measured by cytochrome c levels in intestinal lymphocytes (IL) and 3) the effects of bovine lactoferrin (bLf), a dietary protein with anti-inflammatory properties, on these parameters.
Methods. DSS was given as 5% w/v in water for 4 days. AE consisted of 3 bouts of 90 min of exhaustive treadmill exercise, each separated by 24 h, with sacrifice before, immediately after, or 24 h after the final exercise bout. Mice were fed 2% bLf or control diet for 2 weeks before AE or DSS. Tissue inflammation was determined by histology and IL cytochrome c levels by Western blotting.
Results. AE increased plasma 8-iso-PGF2a, a marker of oxidative stress, immediately after relative to before exercise (P<0.01). Cytochrome c levels were elevated following bLf (P<0.01) and DSS (P<0.05) treatment whereas AE had no significant effect. DSS, but not AE, produced histological changes suggestive of intestinal inflammation with no attenuation by bLf.
Conclusion. Three bouts of AE were not associated with intestinal inflammation or IL death in this animal model. Gastrointestinal disturbances arising from intense exercise in humans may not be due to direct inflammatory damage although this remains to be determined clinically.