The increase in core body temperature in response to exertional-heat stress can predict exercise-induced gastrointestinal syndrome

Abstract

Utilizing metadata from existing exertional and exertional-heat stress studies, the study aimed to determine if the exercise-associated increase in core body temperature can predict the change in exercise-induced gastrointestinal syndrome (EIGS) biomarkers and exercise-associated gastrointestinal symptoms (Ex-GIS). Endurance-trained individuals completed 2 h of running exercise in temperate (21.2-30.0°C) to hot (35.0-37.2°C) ambient conditions (n = 132 trials). Blood samples were collected pre- and post-exercise to determine the change in gastrointestinal integrity biomarkers and systemic inflammatory cytokines. Physiological and thermoregulatory strain variables were assessed every 10–15 min during exercise. The strength of the linear relationship between maximal (M-Tre) and change (Δ Tre) in rectal temperature and EIGS variables was determined via Spearman’s rank correlation coefficients. While the strength of prediction was determined via simple and multiple linear regression analyses dependent on screened EIGS and Ex-GIS confounding factors. Significant positive correlations between Tre maximum (M-Tre) and change (Δ Tre) with I-FABP (rs = 0.434, p < 0.001; and rs = 0.305, p < 0.001; respectively), sCD14 (rs = 0.358, p < 0.001; and rs = 0.362, p < 0.001), systemic inflammatory response profile (SIR-Profile) (p < 0.001), and total Ex-GIS (p < 0.05) were observed. M-Tre and Δ Tre significantly predicted (adjusted R2) magnitude of change in I-FABP (R2(2,123)=0.164, p < 0.001; and R2(2,119)=0.058, p = 0.011; respectively), sCD14 (R2(2,81)=0.249, p < 0.001; and R2(2,77)=0.214, p < 0.001), SIR-Profile (p < 0.001), and total Ex-GIS (p < 0.05). Strong to weak correlations were observed between M-Tre and Δ Tre with plasma concentrations of I-FABP, sCD14, SIR-Profile, and Ex-GIS in response to exercise. M-Tre and Δ Tre can predict the magnitude of these EIGS variables and Ex-GIS in response to exercise.

Does Age Influence Gastrointestinal Status Responses to Exertional-heat Stress?

“…Interestingly, the incidence of total GIS during EHS was considerably high among both MASTERS and YOUNG athletes (81% and 80%, respectively) in spite of rigorous control of confounding factors known to reduce exercise-associated GIS (i. e. 24 h low FODMAP diet and euhydration maintenance) and absence of factors recognized to exacerbate the neuroendocrine-gastrointestinal pathway of EIGS 14 . Incidence of upper-GIS was reported highest among both age groups, which is in accordance with recent research reporting a correlation between EHS and upper-GIS 17 . The only observed difference between groups was in the predominating lower-GIS, with MASTERS reporting highest incidence of lower abdominal pain versus YOUNG athletes reporting highest incidence in urge to defecate.…”

“…On this occasion, the 2-h EHS protocol was also insufficient in causing a significant increase in circulating sCD14 concentrations in both age groups. This may be explained by the peak T re (≤39.0˚C) failing to meet the minimum threshold of≥39.5˚C, recently associated with increased probability of gastrointestinal perturbations of clinical significance 14 17 . Subsequently, there was no difference in the change in circulating sCD14 concentrations between YOUNG and MASTERS.…”

“…Within the EIGS pathogenic model, both extrinsic and intrinsic exacerbation factors have been described to influence the incidence and severity of EIGS and associated Ex-GIS in response to exercise [1,2,14]. Notably, it has consistently been reported that substantial rises in core body temperature in response to EHS profoundly exacerbates intestinal epithelial disturbances to levels of clinical significance, in comparison to exertional stress or EHS models with more modest rises in core body temperature [5,6,[15][16][17]. This provides support for heat exposure during exercise as a primary and potent extrinsic factor in the exacerbation of EIGS and Ex-GIS over other documented extrinsic exacerbation factors (e. g. exercise duration, intensity, modality) [1,2,14].…”

Exertional Stress-induced Pathogenic Luminal Content Translocation – Friend or Foe?

“…1, 2). EHS has recently been confirmed to initiate the greatest disturbance to gastrointestinal status, with two circulatory mechanisms of action underpinning the gastrointestinal perturbations that occur in response to EHS [11]. First, skeletal muscle contraction during exercise diverts blood flow to the working muscles to allow for optimal myofibril function [12].…”

“…As previously discussed, epithelial damage has been demonstrated to occur in response to prolonged exertional activity with subsequent translocation of pathogenic agents such as bacterial endo-toxins (e. g. lipopolysaccharide), and also whole bacteria, to occur significantly, as demonstrated in plasma samples pre-to post-exercise [19][20][21][22]. These observations are indicative of the epithelial injury resulting from exertional activity, consequently allowing for unrestricted translocation to occur, acknowledging that heat exposure during exertional activity substantially exacerbates these responses proportionally [11].…”