Potential Role of Structural Variants of Circulating Lipopolysaccharide in Exercise‐Induced Heat Illness

Abstract

Previous investigations at the Falmouth Road Race (FRR; Falmouth, MA) indicated that combined exercise, heat, and dehydration stress increased gastrointestinal tract permeability. This subsequently exposed the circulatory system to components of the microbiome usually found only in the gut. Lipopolysaccharide (LPS), a component of Gram‐negative bacterial membranes, is one such element released into circulation, especially post‐exercise. LPS in circulation activates host immune cell signaling cascades that can lead to inflammatory responses (e.g. cell pyroptosis, exertional heat stroke, and sepsis) and upregulated proinflammtory gene expression (e.g. TNF‐α and IL‐1β). While subjects of the 2015 FRR (N=30) had elevated core temperature post race compared to pre (pre 36.87°C vs. post 39.87°C, p<0.05), there is unexplained variation in the relationship among the level of circulating LPS (2.90EU/ml pre vs. 3.48EU/ml post, p<0.05; Hycult Biotech, ELISA), core temperature, and subsequent heat stroke presentation. Since some strains of bacteria induce a strong immune response while others do not, it is of interest to determine if structural variations in LPS contribute to varying immune system activation during exercise‐heat stress. Diet influences the composition of the microbiome and different microbiome species have varying LPS structures. Because of this, even short‐term alterations in macronutrient consumption can alter the composition and gene expression of the microbiome. Ongoing research will utilize extraction of LPS from pre‐race and post‐race plasma and HPLC/MS to characterize structural variations in LPS in individuals of the 2015, 2016, and 2017 FRR.Support or Funding InformationNew investigator start‐up, McNair Scholar Program, FRRThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.