The effect of exercise and heat stress on indirect blood markers of gastrointestinal damage in well-trained populations

  • Alice Wallett

    Student thesis: Doctoral Thesis


    Prolonged exercise, particularly in the heat, results in gastrointestinal hypoperfusion and oxidative damage, compromising gastrointestinal tight junction proteins and intestinal mucosa wall integrity, increasing epithelial permeability and the potential for translocation of luminal endotoxins into the circulation. The aim of this thesis was to determine the effects of exercise intensity and duration, coupled with environmental heat stress, as well as short-term nutritional interventions, on blood markers of gastrointestinal damage and immune/inflammatory response in well-trained and elite athletes. A systematic review evaluated the effects of exercise in the heat on blood markers of gastrointestinal epithelial disturbance in well-trained individuals (Chapter 3). The findings of the review indicate that prolonged high-intensity (>70% 饾憠虈O2max) exercise in the heat acutely increases biomarkers of gastrointestinal permeability (e.g. lipopolysaccharide endotoxin [LPS]) and damage (e.g. IFABP, sCD14) compared to exercise in cooler conditions. The first experimental study (Chapter 4) found that treadmill running at increasing intensities (i.e. 60, 75 and 95% 饾憠虈O2max) led to transient perturbations in gastrointestinal permeability in well-trained athletes, as indicated by a 69% increase (0.2 EU路mL-1, 0.1 to 0.4; P=0.011) in LPS, irrespective of exercising in hot (34掳C, 68% RH) or cool (18掳C, 57% RH) conditions. However, LPS binding protein (LBP) was 4% (5.3 渭g路mL-1, 2.4 to 8.4; P<0.001), 32% (4.6 渭g路mL-1, 1.8 to 7.4; P=0.002) and 30% (3.0 渭g路mL-1, 0.03 to 5.9; P=0.047) higher in the hot condition following exercise at 60%, 75% and 95% 饾憠虈O2max, respectively, compared to the cooler condition. Moreover, intestinal fatty acid binding protein (IFABP) was 43% (2.1 ng路mL-1, 0.1 to 4.2; P=0.04) higher 1h post-exercise in the hot compared to the cool condition. Self-reported gastrointestinal discomfort between the HOT and COOL conditions did not differ (P=0.597). These data suggest that running at increasing intensities in the heat resulted in acute but transient changes in gastrointestinal perturbations, which were well-tolerated by the endurance-trained cohort, as indicated by the lack of reported gastrointestinal discomfort (i.e. symptoms). In the second experimental study (Chapter 5), non-heat acclimated male team-sport athletes completed a 5-session, repeated-sprint training regimen over seven days in either HOT (40掳C and 40% RH) or COOL (20掳C and 40% RH) conditions. In the heat, IFABP increased by 593 pg路mL-1 (254 to 932 pg路mL-1; 95% CI; P<0.001) immediately post-exercise and was 454 pg路mL-1 (115 to 793 pg路mL-1; P<0.004) higher 1 h post-exercise, relative to baseline. Soluble CD14 (sCD14) increased by 398 ng路mL-1 (149 to 647 ng路mL-1; P=0.001) following exercise in the heat compared to the cool condition on Day 1 and by 308 ng路mL-1 (59 to 557 ng路mL-1; P=0.010) on Day 5. LBP increased by 1694 ng路mL-1 (424 to 2964 ng路mL-1; P=0.005) immediately post-exercise in the heat on Day 1 and remained unchanged in the cooler condition. These findings indicated that exercise under heat stress, rather than exercise alone, exacerbates gastrointestinal disturbances and immune activation when performing maximal repeated-sprint efforts. Finally, the third experimental study (Chapter 6) compared the effects of short-term (i.e. five days) low carbohydrate high fat (LCHF) and high carbohydrate (HCHO) dietary interventions on blood markers of gastrointestinal damage during a 25-km race walk in warm conditions in elite athletes. The results showed that the LCHF diet increased IFABP concentration by 1822 pg路mL-1 (1205 to 2438; P<0.001) and 662 pg路mL-1 (160 to 1163; P=0.010) post and 1 h post 25-km race walk, relative to the HCHO diet. sCD14 was 0.9 渭g路mL-1 (0.2 to 1.7; P=0.013) higher pre-exercise, 1.9 渭g路mL-1 (1.2 to 2.6; P<0.001) higher post-exercise, and 2.5 渭g路mL-1 (1.8 to 3.2; P<0.001) higher 1 h post-exercise after consuming the LCHF diet, compared to HCHO diet. Interleukin (IL)-1Ra increased by 57.5 pg路mL-1 (23.8 to 91.1; P<0.001) and 84.7 pg路mL-1 (51.0 to 118.4; P<0.001) post- and 1 h post-exercise, and IL-10 increased by 77.5 pg路mL-1 (59.2 to 95.9; P<0.001) and 83.4 pg路mL-1 (65.1 to 101.8; P<0.001) post- and 1 h post-exercise in LCHF diet. While IFABP is commonly used as a marker of gastrointestinal damage, its greater concentration in the blood following the LCHF diet suggests that it may have a protective function in cells under metabolic stress, and therefore represent a marker of increased lipid intake and oxidation. Furthermore, the increased cytokines (i.e. IL-1Ra, IL-10) may suggest a regulatory macrophage response in the LCHF group. The results of this thesis suggest that: 1) well-trained and elite athletes experience transient perturbations in blood markers of gastrointestinal damage when exercising in the heat; 2) maximal repeated-sprint exercise in the heat acutely increases gastrointestinal damage and immune activation compared to sprinting in the cool; and 3) LCHF diets increase IFABP concentration, which is typically indicative of gastrointestinal damage, however, may also act as a marker of increased lipid intake and alter the systemic immune inflammatory response to strenuous exercise in elite athletes. Furthermore, it appears that most of the current research is focused on healthy or trained individuals, leaving a gap in knowledge regarding the acute and chronic responses of well-trained and elite populations. Therefore, further investigation is required to determine whether well-trained individuals have an enhanced capacity to overcome gastrointestinal disturbances during exercise in the heat compared to untrained individuals.
    Date of Award2022
    Original languageEnglish
    SupervisorAndrew Mckune (Supervisor), Julien Periard (Supervisor) & David Pyne (Supervisor)

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