Along with digestion and absorption of nutrients, the gastrointestinal epithelium acts as a primary intestinal defense layer, preventing luminal pathogens from entering the circulation. During exercise in the heat, epithelial integrity can become compromised, allowing bacteria and bacterial endotoxins to translocate into circulation, triggering a systemic inflammatory response and exacerbating gastrointestinal damage. While this relationship seems clear in the general population in endurance/ultraendurance exercise, the aim of this systematic review was to evaluate the effect of exercise in the heat on blood markers of gastrointestinal epithelial disturbance in well-trained individuals. Following the 2009 Preferred Reporting Items for Systematic Reviewed and Meta-Analyses guidelines, five electronic databases were searched for appropriate research, and 1,885 studies were identified. Five studies met the inclusion criteria and were subject to full methodological appraisal by two reviewers. Critical appraisal of the studies was conducted using the McMasters Critical Review Form. The studies investigated changes in markers of gastrointestinal damage (intestinal fatty acid–binding protein, endotoxin, and/or lipopolysaccharide-binding protein) following acute exercise in warm to hot conditions (≥ 30 °C) and included trained or well-trained participants with direct comparisons to a control temperate condition (≤ 22 °C). The studies found that prolonged submaximal and strenuous exercise in hot environmental conditions can acutely increase epithelial disturbance compared with exercise in cooler conditions, with disturbances not being clinically relevant. However, trained and well-trained populations appear to tolerate exercise-induced gastrointestinal disturbance in the heat. Whether this is an acquired tolerance related to regular training remains to be investigated.
Alice Wallett, Julien D. Périard, Philo Saunders, and Andrew McKune
Alice M. Wallett, Amy L. Woods, Nathan Versey, Laura A. Garvican-Lewis, Marijke Welvaert, and Kevin G. Thompson
Studies examining pacing strategies during 4000-m cycling time trials (TTs) typically ensure that participants are not prefatigued; however, competitive cyclists often undertake TTs when already fatigued. This study aimed to determine how TT pacing strategies and sprint characteristics of cyclists change during an intensified training period (mesocycle). Thirteen cyclists regularly competing in A- and B-grade cycling races and consistently training (>10 h/wk for 4  y) completed a 6-wk training mesocycle. Participants undertook individually prescribed training, using training stress scores (TrainingPeaks, Boulder, CO), partitioned into a baseline week, a build week, 2 loading weeks (designed to elicit an overreached state), and 2 recovery weeks. Laboratory-based tests (15-s sprint and TT) and Recovery-Stress Questionnaire (RESTQ-52) responses were repeatedly undertaken over the mesocycle. TT power output increased during recovery compared with baseline and loading weeks (P = .001) with >6-W increases in mean power output (MPO) detected for 400-m sections (10% bins) from 1200 to 4000 m in recovery weeks. Decreases in peak heart rate (P < .001) during loading weeks and postexercise blood lactate (P = .005) during loading week 2 and recovery week 1 were detected. Compared with baseline, 15-s sprint MPO declined during loading and recovery weeks (P < .001). An interaction was observed between RESTQ-52 total stress score with a 15-s sprint (P = .003) and with a TT MPO (P = .04), indicating that participants who experienced greater stress during loading weeks exhibited reduced performance. To conclude, intensified endurance training diminished sprint performance but improved 4000-m TT performance, with a subtle change in MPO evident over the last 70% of TTs.
Naroa Etxebarria, Nicole A. Beard, Maree Gleeson, Alice Wallett, Warren A. McDonald, Kate L. Pumpa, and David B. Pyne
Gastrointestinal disturbances are one of the most common issues for endurance athletes during training and competition in the heat. The relationship between typical dietary intake or nutritional interventions and perturbations in or maintenance of gut integrity is unclear. Twelve well-trained male endurance athletes (peak oxygen consumption = 61.4 ± 7.0 ml·kg−1·min−1) completed two trials in a randomized order in 35 °C (heat) and 21 °C (thermoneutral) conditions and kept a detailed nutritional diary for eight consecutive days between the two trials. The treadmill running trials consisted of 15 min at 60% peak oxygen consumption, 15 min at 75% peak oxygen consumption, followed by 8 × 1-min high-intensity efforts. Venous blood samples were taken at the baseline, at the end of each of the three exercise stages, and 1 hr postexercise to measure gut integrity and the permeability biomarker concentration for intestinal fatty-acid-binding protein, lipopolysaccharide, and lipopolysaccharide-binding protein. The runners self-reported gut symptoms 1 hr postexercise and 3 days postexercise. The heat condition induced large (45–370%) increases in intestinal fatty-acid-binding protein, lipopolysaccharide-binding protein, and lipopolysaccharide concentrations compared with the baseline, but induced mild gastrointestinal symptoms. Carbohydrate and polyunsaturated fat intake 24 hr preexercise were associated with less lipopolysaccharide translocation. Protein, carbohydrate, total fat, and polyunsaturated fat intake (8 days) were positively associated with the percentage increase of intestinal fatty-acid-binding protein in both conditions (range of correlations, 95% confidence interval = .62–.93 [.02, .98]). Typical nutrition intake partly explained increases in biomarkers and the attenuation of symptoms induced by moderate- and high-intensity exercise under both heat and thermoneutral conditions.
Alice M. Wallett, Naroa Etxebarria, Nicole A. Beard, Philo U. Saunders, Marijke Welvaert, Julien D. Périard, Andrew J. McKune, and David B. Pyne
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 exercise under heat stress. Methods: A total of 12 well-trained male runners (age 37  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). Results: 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. 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.