Acute _L‐glutamine supplementation does not improve gastrointestinal permeability, injury or microbial translocation in response to exhaustive high intensity exertional‐heat stress

Abstract

Purpose: Exertional-heat stress adversely distrupts (GI) barrier integrity and, through subsequent microbial translocation (MT), can result in potentially fatal exertional-heat stroke. Acute glutamine (GLN) supplementation is a potential nutritional countermeasure, although the practical value of current supplementation regimens is questionable. Method: Ten males completed two high-intensity exertional-heat stress tests (EHST) involving running in the heat (40°C and 40% relative humidity) at lactate threshold to volitional exhaustion. Participants ingested GLN (0.3 g kg FFM −1 ) or a non-calorific placebo (PLA) one hour prior to the EHST. Venous blood was drawn pre-, post-and one-hour post-EHST. GI permeability was assessed using a serum dual-sugar absorption test (DSAT) and small intestinal epithelial injury using plasma Intestinal Fatty-Acid Binding Protein (I-FABP). MT was assessed using the Bacteroides/total 16S DNA ratio. Results: Volitional exhaustion occurred after 22:19 ± 2:22 (minutes: seconds) in both conditions, during which whole-body physiological responses and GI symptoms were not different (p > 0.05). GI permeability (serum DSAT) was greater following GLN (0.043 ± 0.020) than PLA (0.034 ± 0.019) (p = 0.02; d = 0.47), but small intestine epithelial injury (I-FABP) increased comparably (p = 0.22; h 2 p = 0.16) following the EHST in both trials (GLN Δ = 1.25 ± 0.63 ng ml −1 ; PLA Δ = 0.92 ± 0.44 ng ml −1 ). GI MT (Bacteroides/total 16S DNA ratio) was unchanged in either condition following the EHST (p = 0.43). Conclusion: Acute low-dose (0.3 g kg −1 fat free mass) GLN supplementation ingested one hour before high-intesity exertional-heat stress worsened GI permeability, but did not influence either small intestinal epithilial injury or microbial translocation.

Reliability of pathophysiological markers reflective of exercise-induced gastrointestinal syndrome (EIGS) in response to 2-h high-intensity interval exercise: A comprehensive methodological efficacy exploration

“…Although there is substantial research exploring the impact of exercise stress on direct or indirect markers of bacterial endotoxin translocation [e.g., plasma lipopolysaccharides (LPS), LBP, sCD14, and/or EndoCAb concentration], research into exercise-associated whole bacterial luminal to systemic translocation (i.e., bacteremia) is scarce ( Costa et al, 2022 ). Some previous studies have attempted to detect whole bacteria presence in circulation (e.g., total 16S bacteria: Bacteroides ratio) in response to prolonged low intensity exercise (i.e., 80 min fixed-intensity treadmill walking- 6 km/h and 7% gradient) ( Ogden et al, 2020a ; Ogden et al, 2020b ), and higher intensity of shorter duration exercise (i.e., 60 min running at 70% V̇ O 2peak ) ( March et al, 2019 ; Ogden et al, 2022 ), with findings modest and inconsistent. Variability of bacterial translocation in response to these exercise bouts may be explained by the application of insufficient exertional stress among studies, a lack of control of confounding factors within experimental procedures, and/or the biomarker selected to represent whole bacterial translocation into systemic circulation (i.e., Bacteriodes /total bacterial DNA) ( Costa et al, 2022 ).…”

Alteration of gut microbiota after heat acclimation may reduce organ damage by regulating immune factors during heat stress

“…After HAT, biomarkers of organ injury and inflammatory factors showed significant changes, including alpha-tumor necrosis factor (TNF-α), interleukin-6 (IL-6), IL-10, IL-18, intestinal fatty acid-binding protein (I-FABP), neutrophil gelatinase-associated lipocalin (NGAL), heat shock protein 72 (HSP72), and kidney injury molecule-1 (KIM-1) (Dolci et al, 2015;Lee and Thake, 2017;Chapman et al, 2021;Osborne et al, 2021). The pathophysiology of HS is caused, at least in part, by a systemic inflammatory response induced by gastrointestinal microbe leakage into the bloodstream (Ogden et al, 2021). Cao et al demonstrated that a 28-day HAT improved the structure of the gut microbiome community and the fecal metabolome in rats, providing novel insights into improving the gut microbiome and its functions as a potential mechanism for HA's protective properties under heat stress (Cao et al, 2022).…”