Running at Increasing Intensities in the Heat Induces Transient Gut Perturbations

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 exercise under heat stress.

A total of 12 well-trained male runners (age 37 [7] y, maximal oxygen uptake [VO2max] 61.0 [6.8] mL·min-1·kg-1) undertook 2 treadmill runs of 2 × 15-minutes at 60% and 75% VO2max and up to 8 × 1-minutes at 95% VO2max 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).

The increase in LPS binding protein following each exercise intensity in the HOT condition 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 the COOL condition. LPS was 69% higher than baseline following running at 75% VO2max in the HOT condition (0.2 endotoxin units·mL-1, 0.1-0.4; P = .011). Intestinal fatty acid-binding protein increased 43% (2.1 ng·mL-1, 0.1-4.2; P = .04) 1 hour postexercise in HOT compared with the COOL condition.

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.