The nutriceutical bovine colostrum truncates the increase in gut permeability caused by heavy exercise in athletes.
Am J Physiol Gastrointest Liver Physiol 300: G477–G484, 2011.
First published December 9, 2010; doi:10.1152/ajpgi.00281.2010.
—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, Bax, 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 Bax and reduction in Bcl-2 was partially reversed by presence of colostrum. Colostrum may have value in enhancing athletic performance and preventing heat stroke.
Tania Marchbank,1 Glen Davison,2 Jemma R. Oakes,2 Mohammad A. Ghatei,3 Michael Patterson,3 Mary Pat Moyer,4 and Raymond J. Playford1 1 Digestive Diseases, Blizard Institute of Cell and Molecular Science, Barts and The London School of Medicine, Queen Mary University of London, London; 2 Department of Sport and Exercise Science, Aberystwyth University, Aberystwyth; 3 Department of Metabolic Medicine, Hammersmith Hospital, Imperial College London, London, United Kingdom; and 4 INCELL Corporation, San Antonio, Texas