Sarah Chantler1,2, Alex Griffiths3, Padraic Phibbs4,5, Gregory Roe4,6, Carlos Ramírez-López4,7, Glen Davison8, Ben Jones4,9,10,11,12, Kevin Deighton13. 1. Carnegie Applied Rugby Research (CARR) Centre, Carnegie School of Sport, Leeds Beckett University, Leeds, UK. s.a.chantler@leedsbeckett.ac.uk. 2. Yorkshire Carnegie Rugby Union Club, Leeds, UK. s.a.chantler@leedsbeckett.ac.uk. 3. School of Clinical and Applied Sciences, Leeds Beckett University, Leeds, UK. 4. Carnegie Applied Rugby Research (CARR) Centre, Carnegie School of Sport, Leeds Beckett University, Leeds, UK. 5. Centre of Excellence, Leinster Rugby, Dublin, Ireland. 6. Bath Rugby Union Club, Bath, UK. 7. Scottish Rugby Union, Edinburgh, UK. 8. School of Sport and Exercise Sciences, Division of Natural Sciences, University of Kent, Canterbury, UK. 9. School of Science and Technology, University of New England, Armidale, NSW, Australia. 10. Division of Exercise Science and Sports Medicine, Department of Human Biology, Faculty of Health Sciences, the University of Cape Town and the Sports Science Institute of South Africa, Cape Town, South Africa. 11. Leeds Rhinos Rugby League Club, Leeds, UK. 12. England Performance Unit, Rugby Football League, Leeds, UK. 13. Delta Hat Limited, Tamworth Road, Nottingham, UK.
Abstract
PURPOSE: To assess indirect markers of intestinal endothelial cell damage and permeability in academy rugby players in response to rugby training at the beginning and end of preseason. METHODS: Blood and urinary measures (intestinal fatty acid binding protein and lactulose:rhamnose) as measures of gastrointestinal cell damage and permeability were taken at rest and after a standardised collision-based rugby training session in 19 elite male academy rugby players (age: 20 ± 1 years, backs: 89.3 ± 8.4 kg; forwards: 111.8 ± 7.6 kg) at the start of preseason. A subsample (n = 5) repeated the protocol after six weeks of preseason training. Gastrointestinal symptoms (GIS; range of thirteen standard symptoms), aerobic capacity (30-15 intermittent fitness test), and strength (1 repetition maximum) were also measured. RESULTS: Following the rugby training session at the start of preseason, there was an increase (median; interquartile range) in intestinal fatty acid binding protein (2140; 1260-2730 to 3245; 1985-5143 pg/ml, p = 0.003) and lactulose:rhamnose (0.31; 0.26-0.34 to 0.97; 0.82-1.07, p < 0.001). After six weeks of preseason training players physical qualities improved, and the same trends in blood and urinary measures were observed within the subsample. Overall, the frequency and severity of GIS were low and not correlated to markers of endothelial damage. CONCLUSIONS: Rugby training resulted in increased intestinal endothelial cell damage and permeability compared to rest. A similar magnitude of effect was observed after six weeks of pre-season training. This was not related to the experience of GIS.
PURPOSE: To assess indirect markers of intestinal endothelial cell damage and permeability in academy rugby players in response to rugby training at the beginning and end of preseason. METHODS: Blood and urinary measures (intestinal fatty acid binding protein and lactulose:rhamnose) as measures of gastrointestinal cell damage and permeability were taken at rest and after a standardised collision-based rugby training session in 19 elite male academy rugby players (age: 20 ± 1 years, backs: 89.3 ± 8.4 kg; forwards: 111.8 ± 7.6 kg) at the start of preseason. A subsample (n = 5) repeated the protocol after six weeks of preseason training. Gastrointestinal symptoms (GIS; range of thirteen standard symptoms), aerobic capacity (30-15 intermittent fitness test), and strength (1 repetition maximum) were also measured. RESULTS: Following the rugby training session at the start of preseason, there was an increase (median; interquartile range) in intestinal fatty acid binding protein (2140; 1260-2730 to 3245; 1985-5143 pg/ml, p = 0.003) and lactulose:rhamnose (0.31; 0.26-0.34 to 0.97; 0.82-1.07, p < 0.001). After six weeks of preseason training players physical qualities improved, and the same trends in blood and urinary measures were observed within the subsample. Overall, the frequency and severity of GIS were low and not correlated to markers of endothelial damage. CONCLUSIONS: Rugby training resulted in increased intestinal endothelial cell damage and permeability compared to rest. A similar magnitude of effect was observed after six weeks of pre-season training. This was not related to the experience of GIS.
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