Running at Increasing Intensities in the Heat Induces Transient Gut Perturbations

Purpose: The risk of exercise-induced endotoxemia is increased in the heat and is primarily attributable to changes in gut permeability resulting in the translocation of lipopolysaccharides (LPS) into the circulation. The purpose of this study was to quantify the acute changes in gut permeability and LPS translocation during submaximal continuous and high-intensity interval Q exercise under heat stress. Methods: A total of 12 well-trained male runners (age 2 37 [7] y, maximal oxygen uptake 61.0 [6.8] mL· min−1·kg−1) undertook 2 treadmill runs of 2 × 15 minutes at 60% and 75% maximal oxygen uptake and up to 8 × 1 minutes at 95% maximal oxygen uptake in HOT (34°C, 68% relative humidity) and COOL (18°C, 57% relative humidity) conditions. Venous blood samples were collected at the baseline, following each running intensity, and 1-hour postexercise. Blood samples were analyzed for markers of intestinal permeability (LPS, LPS binding protein, and intestinal fatty acid–binding protein). Results: The increase in the LPS binding protein following each exercise intensity in HOT was 4% (5.3 μg·mL−1, 2.4–8.4; mean, 95% confidence interval, P < .001), 32% (4.6 μg·mL−1, 1.8–7.4; P = .002), and 30% (3.0 μg·mL−1, 0.03–5.9; P = .047) greater than in COOL. LPS was 69% Q higher than the baseline 3 following 75% running in HOT (0.2 EU·mL−1, 0.1–0.4; P = .011). The intestinal fatty acid–binding protein increased 43% (2.1 ng·mL−1 Q , 0.1–4.2; P = .04) 1-hour post exercise in HOT compared with COOL. 4 Conclusions: Small increases in LPS concentration during exercise in the heat and subsequent increases in intestinal fatty acid–binding protein and LPS binding protein indicate a capacity to tolerate acute, transient intestinal disturbance in well-trained endurance runners.