Intestinal damage following short-duration exercise at the same relative intensity is similar in temperate and hot environments

Increasing temperature and exercise disrupt tight junctions of the gastrointestinal tract although the contribution of environmental temperature to intestinal damage when exercising is unknown. This study investigated the effect of 2 different environmental temperatures on intestinal damage when exercising at the same relative intensity. Twelve men (mean +/- SD; body mass, 81.98 +/- 7.95 kg; height, 182.6 +/- 7.4 cm) completed randomised cycling trials (45 min, 70% maximal oxygen uptake) in 30 degrees C/40% relative humidity (RH) and 20 degrees C/40%RH. A subset of participants (n = 5) also completed a seated passive trial (30 degrees C/40%RH). Rectal temperature and thermal sensation (TSS) were recorded during each trial and venous blood samples collected at pre- and post-trial for the analysis of intestinal fatty acid-binding protein (I-FABP) level as a marker of intestinal damage. Oxygen uptake was similar between 30 degrees C and 20 degrees C exercise trials, as intended (p = 0.94). I-FABP increased after exercise at 30 degrees C (pre-exercise: 585 +/- 188 pg.mL(-1); postexercise: 954 +/- 411 pg.mL(-1)) and 20 degrees C (pre-exercise: 571 +/- 175 pg.mL(-1); postexercise: 852 +/- 317 pg.mL(-1)) (p < 0.0001) but the magnitude of damage was similar between temperatures (p = 0.58). There was no significant increase in I-FABP concentration following passive heat exposure (p = 0.59). Rectal temperature increased during exercise trials (p < 0.001), but not the passive trial (p = 0.084). TSS increased more when exercising in 30 degrees C compared with 20 degrees C (p < 0.001). There was an increase in TSS during the passive heat trial (p = 0.03). Intestinal damage, as measured by I-FABP, following exercise in the heat was similar to when exercising in a cooler environment at the same relative intensity. Passive heat exposure did not increase I-FABP. It is suggested that when exercising in conditions of compensable heat stress, the increase in intestinal damage is predominantly attributable to the exercise component, rather than environmental conditions.