title: The nutriceutical bovine colostrum truncates the increase in gut permeability caused by heavy exercise in athletes.
abstract: Heavy exercise causes gut symptoms and, in extreme cases, "heat stroke" partially due to increased intestinal permeability of luminal toxins. We examined bovine colostrum, a natural source of growth factors, as a potential moderator of such effects. Twelve volunteers completed a double-blind, placebo-controlled, crossover protocol (14 days colostrum/placebo) prior to standardized exercise. Gut permeability utilized 5 h urinary lactulose-to-rhamnose ratios. In vitro studies (T84, HT29, NCM460 human colon cell lines) examined colostrum effects on temperature-induced apoptosis (active caspase-3 and 9, Baxα, Bcl-2), heat shock protein 70 (HSP70) expression and epithelial electrical resistance. In both study arms, exercise increased blood lactate, heart rate, core temperature (mean 1.4°C rise) by similar amounts. Gut hormone profiles were similar in both arms although GLP-1 levels rose following exercise in the placebo but not the colostrum arm (P = 0.026). Intestinal permeability in the placebo arm increased 2.5-fold following exercise (0.38 ± 0.012 baseline, to 0.92 ± 0.014, P < 0.01), whereas colostrum truncated rise by 80% (0.38 ± 0.012 baseline to 0.49 ± 0.017) following exercise. In vitro apoptosis increased by 47-65% in response to increasing temperature by 2°C. This effect was truncated by 60% if colostrum was present (all P < 0.01). Similar results were obtained examining epithelial resistance (colostrum truncated temperature-induced fall in resistance by 64%, P < 0.01). Colostrum increased HSP70 expression at both 37 and 39°C (P < 0.001) and was truncated by addition of an EGF receptor-neutralizing antibody. Temperature-induced increase in Baxα and reduction in Bcl-2 was partially reversed by presence of colostrum. Colostrum may have value in enhancing athletic performance and preventing heat stroke.
authors.affiliation: Digestive Diseases, Blizard Institute of Cell and Molecular Science, Barts and The London School of Medicine, Queen Mary University of London, UK.
authors.forename: Tania
authors.initials: T
authors.lastname: Marchbank
authors.forename: Glen
authors.initials: G
authors.lastname: Davison
authors.forename: Jemma R
authors.initials: JR
authors.lastname: Oakes
authors.forename: Mohammad A
authors.initials: MA
authors.lastname: Ghatei
authors.forename: Michael
authors.initials: M
authors.lastname: Patterson
authors.forename: Mary Pat
authors.initials: MP
authors.lastname: Moyer
authors.forename: Raymond J
authors.initials: RJ
authors.lastname: Playford
mesh_terms: D000328:Adult; D000818:Animals; D017209:Apoptosis; D051017:Apoptosis Regulatory Proteins / Q000378:metabolism; D056352:Athletes; D015415:Biomarkers / Q000097:blood / Q000652:urine; D002417:Cattle; D003126:Colostrum / Q000378:metabolism*; D018592:Cross-Over Studies; D019587:Dietary Supplements; D004311:Double-Blind Method; D017097:Electric Impedance; D005260:Female; D005768:Gastrointestinal Hormones / Q000097:blood; D018840:HSP70 Heat-Shock Proteins / Q000378:metabolism; D019073:HT29 Cells; D018883:Heat Stroke / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D006358:Hot Temperature; D006801:Humans; D007408:Intestinal Absorption; D007413:Intestinal Mucosa / Q000378:metabolism*; D007422:Intestines / Q000473:pathology; D019344:Lactic Acid / Q000097:blood; D007785:Lactose / Q000652:urine; D008297:Male; D010539:Permeability; D005082:Physical Exertion; D015990:Placebo Effect; D011247:Pregnancy; D012210:Rhamnose / Q000652:urine; D055815:Young Adult
chemical_list: D051017:Apoptosis Regulatory Proteins; D015415:Biomarkers; D005768:Gastrointestinal Hormones; D018840:HSP70 Heat-Shock Proteins; D019344:Lactic Acid; D007785:Lactose; D012210:Rhamnose