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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.

Purpose: The core temperature responses during exercise and effects of different cooling strategies on endurance performance under heat stress have been investigated in recreational athletes. This investigation aimed to determine peak rectal temperatures during elite racewalking competitions and to detail any cooling strategies used. Methods: Rectal temperature was measured in 14 heat-adapted elite/preelite race walkers (9 females) via a telemetric capsule across 4 outdoor events, including the 2018 Commonwealth Games (race 1: 20 km, 25°C, 74% relative humidity [RH], n = 2) and 3 International Association of Athletics Federations–sanctioned 10-km events (race 2: 19°C, 34% RH, n = 2; race 3: 29°C, 47% RH, n = 14; and race 4: 23°C, 72% RH, n = 11). All athletes completed race 3, and a subsample completed the other events. Their use of cooling strategies and symptoms of heat illness were determined. Results: Peak rectal temperatures >40°C were observed in all events. The highest rectal temperature observed during an event was 41.2°C. These high rectal temperatures were observed without concomitant heat illness, with the exception of cramping in one athlete during race 1. The rectal temperatures tended to reach a steady state in the second half of the 20-km event, but no steady state was observed in the 10-km events. The athletes used cooling strategies in race 1 only, implementing different combinations of cold-water immersion, ice-slurry ingestion, ice-towel application, ice-vest application, and facial water spraying. Conclusions: Elite/preelite race walkers experience rectal temperatures >40°C during competition despite only moderate-warm conditions, and even when precooling and midcooling strategies are applied.

Purpose: To investigate whether including heat and altitude exposures during an elite team-sport training camp induces similar or greater performance benefits. Methods: The study assessed 56 elite male rugby players for maximal oxygen uptake, repeated-sprint cycling, and Yo-Yo intermittent recovery level 2 (Yo-Yo) before and after a 2-week training camp, which included 5 endurance and 5 repeated-sprint cycling sessions in addition to daily rugby training. Players were separated into 4 groups: (1) control (all sessions in temperate conditions at sea level), (2) heat training (endurance sessions in the heat), (3) altitude (repeated-sprint sessions and sleeping in hypoxia), and (4) combined heat and altitude (endurance in the heat, repeated sprints, and sleeping in hypoxia). Results: Training increased maximal oxygen uptake (4% [10%], P = .017), maximal aerobic power (9% [8%], P < .001), and repeated-sprint peak (5% [10%], P = .004) and average power (12% [14%], P < .001) independent of training conditions. Yo-Yo distance increased (16% [17%], P < .001) but not in the altitude group (P = .562). Training in heat lowered core temperature and increased sweat rate during a heat-response test (P < .05). Conclusion: A 2-week intensified training camp improved maximal oxygen uptake, repeated-sprint ability, and aerobic performance in elite rugby players. Adding heat and/or altitude did not further enhance physical performance, and altitude appears to have been detrimental to improving Yo-Yo.

Purpose: Hot-water immersion (HWI) after training in temperate conditions has been shown to induce thermophysiological adaptations and improve endurance performance in the heat; however, the potential additive effects of HWI and training in hot outdoor conditions remain unknown. Therefore, this study aimed to determine the effect of repeated postexercise HWI in athletes training in a hot environment. Methods: A total of 13 (9 female) elite/preelite racewalkers completed a 15-day training program in outdoor heat (mean afternoon high temperature = 34.6°C). Athletes were divided into 2 matched groups that completed either HWI (40°C for 30–40 min) or seated rest in 21°C (CON), following 8 training sessions. Pre–post testing included a 30-minute fixed-intensity walk in heat, laboratory incremental walk to exhaustion, and 10,000-m outdoor time trial. Results: Training frequency and volume were similar between groups (P = .54). Core temperature was significantly higher during immersion in HWI (38.5 [0.3]) than CON (37.8°C [0.2°C]; P < .001). There were no differences between groups in resting or exercise rectal temperature or heart rate, skin temperature, sweat rate, or the speed at lactate threshold 2, maximal O₂ uptake, or 10,000-m performance (P > .05). There were significant (P < .05) pre–post differences for both groups in submaximal exercising heart rate (∼11 beats·min⁻¹), sweat rate (0.34–0.55 L·h⁻¹) and thermal comfort (1.2–1.5 arbitrary units), and 10,000-m racewalking performance time (∼3 min). Conclusions: Both groups demonstrated significant improvement in markers of heat adaptation and performance; however, the addition of HWI did not provide further enhancements. Improvements in adaptation appeared to be maximized by the training program in hot conditions.

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 [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). 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.