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Naroa Etxebarria, Nicole A. Beard, Maree Gleeson, Alice Wallett, Warren A. McDonald, Kate L. Pumpa, and David B. Pyne

for biomarkers, which represent GI permeability, included lipopolysaccharide (LPS), lipopolysaccharide-binding protein, and intestinal fatty-acid-binding protein (i-FABP). All biomarkers were analyzed in duplicate, as previously described ( Wallett et al., 2020 ). Statistical Analysis The descriptive

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Alice M. Wallett, Naroa Etxebarria, Nicole A. Beard, Philo U. Saunders, Marijke Welvaert, Julien D. Périard, Andrew J. McKune, and David B. Pyne

), an acute phase response protein that mediates the rise in LPS, and intestinal fatty acid–binding protein (I-FABP), an early GI-ischemia marker. 10 While there is evidence supporting the premise that heat stress mediates exercise-induced endotoxemia, specific GI responses to exercise in the heat at

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Ricardo J.S. Costa, Vera Camões-Costa, Rhiannon M.J. Snipe, David Dixon, Isabella Russo, and Zoya Huschtscha

fatty acid binding protein (I-FABP) concentration ( Costa et al., 2019b ; Costa et al., 2017b ). In addition, exercise stress has the potential to reduce gastrointestinal transit and enterocyte cell activity through mesenteric and submucosal plexus deactivation linked with the natural stress response

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SILVA. Blood samples were collected pre- and post-exercise to determine I-FABP, cortisol, and cytokine profiles. Markers of physiological and thermoregulatory strain, and gastrointestinal symptoms (GIS) were measured throughout. Correlations and β-diversity analysis between amplicon sequence variants

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Isabella Russo, Paul A. Della Gatta, Andrew Garnham, Judi Porter, Louise M. Burke, and Ricardo J.S. Costa

, intestinal fatty-acid-binding protein [I-FABP] and sCD14 enzyme-linked immunosorbent assay [ELISA], and multiplex system for systemic inflammatory profile) as previously reported. 6 , 15 , 22 The CVs for ELISAs were ≤6.1%, and for cytokine, profile multiplex was 16.0%. Breath samples (20 mL) were analyzed

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samples were collected pre- and post-exercise, and during recovery to determine plasma I-FABP and cortisol. Breath samples were collected every 30 min in recovery for 3 h to determine H 2 (malabsorption marker) responses. DEH resulted in higher heart rate (p = .038; 158 vs 152 bpm), RPE (p = .001; 15 vs

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. Immediately after exercise (or the equivalent time-period during the resting trial), participants underwent a 2-h oral glucose tolerance test (OGTT) with dual-stable isotope tracers to assess plasma glucose kinetics. Plasma concentrations of intestinal fatty acid binding protein (I-FABP) were assessed as a

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lactulose to L -rhamnose (L:R) in serum. Plasma glutamine concentrations were measured at 2 h pre, post, and 1 h post heat stress and plasma intestinal fatty acid binding protein (I-FABP) concentrations were determined pre and post heat stress. Subjective heat illness symptoms were assessed throughout hot