Exertional Heat Stress Research Articles

Exertional heat stress and intestinal barrier injury: Does chronic disease add fuel to the fire?

Exertional heat stress and intestinal barrier injury: Does chronic disease add fuel to the fire?

Intestinal epithelial injury and inflammation after physical work in temperate and hot environments in older men with hypertension or type 2 diabetes.

We tested whether older adults with well-controlled type 2 diabetes or hypertension, compared with age-matched adults without chronic disease, exhibit greater intestinal damage, microbial translocation and inflammation during exertional heat stress. Twelve healthy men (age 59 years, SD 4 years), nine with type 2 diabetes (age 60 years, SD 5 years) and nine with hypertension (age 60 years, SD 4 years) walked for 180min at 200W/m2 in temperate conditions (wet-bulb globe temperature 16°C) and high-heat stress conditions (wet-bulb globe temperature 32°C). Serum intestinal fatty acid binding protein (IFABP), plasma soluble cluster of differentiation 14, lipopolysaccharide-binding protein (LBP), interleukin-6 and tumour necrosis factor-alpha were measured pre- and postexercise and after 60min recovery. Total exercise duration was lower in men with hypertension and diabetes (p≤0.049), but core temperature did not differ. All markers increased more in heat versus temperate conditions (p<0.002). In the heat, individuals with type 2 diabetes had greater postexercise increases in IFABP [+545pg/mL (95% confidence interval: 222, 869)] and LBP [+3.64µg/mL (1.73, 5.56)] relative to healthy control subjects (p<0.048), but these resolved after recovery. Despite reduced exercise duration, hypertensive individuals showed similar increases in IFABP and LBP to control subjects. Our findings suggest that older workers with well-controlled type 2 diabetes or hypertension might have greater vulnerability to heat-induced gastrointestinal barrier disturbance and downstream inflammatory responses when compared with otherwise healthy, age-matched adults during prolonged exercise in the heat.

The Effects of Prebiotic Supplementation on Markers of Exercise-Induced Gastrointestinal Syndrome in Response to Exertional Heat Stress.

Exercise perturbs various aspects of gastrointestinal integrity and function, which may lead to performance impeding gastrointestinal symptoms (GIS) and/or precipitate clinical issues warranting medical management. This study aimed to determine the impact of prebiotic supplementation on gastrointestinal integrity and functional status in response to exertional heat stress (EHS). Sixteen endurance athletes completed two trials of 3-hr running at 60% V˙O2max in 30°C at baseline (T1) and following an 8-week supplementation period (T2), with 16g/day prebiotic (PREBIOTIC) or matched placebo (PLACEBO). Blood samples were collected pre-EHS and post-EHS and in recovery for determination of stress response (cortisol), intestinal epithelial injury (intestinal fatty acid binding protein), bacterial endotoxemia (sCD14), and systemic inflammation (C-reactive protein). GIS and feeding tolerance variables were assessed throughout the EHS. Orocecal transit time was determined via a lactulose challenge given at 2.5hr into EHS. Plasma cortisol (combined mean: +252ng/ml), intestinal fatty acid binding protein (+800pg/ml), and sCD14 (+487ng/ml) concentrations increased in response to EHS in T1 (p ≤ .05), but not for C-reactive protein (+0.8μg/ml; p > .05), in both PREBIOTIC and PLACEBO. PREBIOTIC supplementation resulted in a blunted intestinal fatty acid binding protein response on T2 (+316pg/ml) compared with an increase (+1,001ng/ml) in PLACEBO (p = .005). Lower sCD14 was observed at T2 (2,799ng/ml) versus T1 (3,246ng/ml) in PREBIOTIC only (p = .039). No intervention effects were observed for C-reactive protein. No difference within or between PREBIOTIC and PLACEBO at T1 and T2 was observed for orocecal transit time, GIS, and feeding tolerance. In conclusion, 8 weeks of prebiotic supplementation modestly attenuates EHS associated perturbations to intestinal integrity, but does not further impair gastrointestinal transit and/or exacerbate EHS associated GIS or feeding tolerance.

The effect of prescription and over-the-counter medications on core temperature in adults during heat stress: a systematic review and meta-analysis

The effect of prescription and over-the-counter medications on core temperature in adults during heat stress: a systematic review and meta-analysis

Effects of Cannabidiol Ingestion on Thermoregulatory and Inflammatory Responses to Treadmill Exercise in the Heat in Recreationally Active Males.

Exertional heat stress can induce systemic endotoxin exposure and a proinflammatory cascade, likely impairing thermoregulation. Cannabidiol (CBD) is protective in preclinical models of tissue ischemia and inflammation. Therefore, this study examined the effects of CBD ingestion on exercise-induced thermoregulatory and inflammatory responses. In a randomized, double-blinded study, 13 active males (age 25 ± 5 yr; peak oxygen uptake (V̇O 2peak ) 50.4 ± 3.2 mL·kg -1 ·min -1 ) ingested 298 mg CBD or placebo 105 min before 1 h treadmill exercise (60%-65% V̇O 2peak ) in 32°C and 50% relative humidity. Core temperature, skin temperature, heart rate, subjective outcomes, and sweat loss were assessed during/after exercise. Plasma osmolality, plasma volume changes, and plasma markers of intestinal damage (I-FABP), monocyte activation (CD14), and inflammatory cytokine responses (IL-6, IL-8, and TNF-α) were assessed at baseline, pre-exercise, and 20 and 90 min post-exercise. Core temperature (∆ 1.69°C ± 0.48°C (CBD) and 1.79°C ± 0.53°C (Placebo)) and I-FABP increased during exercise, with no differences between conditions ( P > 0.050). Mean (95% confidence interval) CD14 was 1776 (463 to 3090) pg·mL -1 greater 90 min post-exercise in placebo ( P = 0.049). Median (interquartile range) peak IL-6 concentration was -0.8 (-1.1 to -0.3) pg·mL -1 less in CBD ( P = 0.050), whereas the between-condition difference in IL-6 area under curve was -113 (-172 to 27) (pg·mL -1 )·270 min ( P = 0.054). CBD did not affect thermoregulation during exertional heat stress but appeared to elicit minor immunosuppressive effects, reducing CD14 and IL-6 responses, warranting investigation in humans under more severe heat strain and other proinflammatory scenarios.

Thermal and Cardiovascular Responses during Exertional Heat Stress after Diphenhydramine Use: A Randomized Crossover Trial.

Despite sparse systematic evidence, current exercise heat safety recommendations suggest that antihistamines blunt sweating and increase the risk for heat-related injury during exertional heat stress. The primary purpose of the present study was to examine whether diphenhydramine hydrochloride (DPH), a first-generation antihistamine, affects the sweating, core temperature, and heart rate (HR) response during exertional heat stress using a double-blind randomized crossover design. On two occasions separated by >48 h, 20 healthy adults (10 females, 23 ± 3 yr, body surface area: 1.9 ± 0.2 m 2 , body mass index: 23.7 ± 2.2 kg·m -2 ) orally consumed either 50 mg of DPH or placebo (PLA), and then rested for 2 h in a climate-controlled room maintained at 30°C and 35% relative humidity (heat index of ~29°C), followed by a 60-min fixed-heat production treadmill walk (6.3 ± 1.0 W·kg -1 ). Whole-body sweat loss, local sweat rate, rectal temperature ( Trec ), and HR were measured. Whole-body sweat loss was not different between conditions (PLA: 406 ± 78 g, DPH: 396 ± 75 g; P = 0.26, treatment effect: -10 g; 95% confidence interval, -28 to 8). No differences were observed for the onset of sweating (PLA: 13.5 ± 2.4 min, DPH: 13.3 ± 2.7 min; P = 0.79) and steady-state local sweat rate (PLA: 0.83 ± 0.26 mg·cm -2 ·min -1 , DPH: 0.82 ± 0.27 mg·cm -2 ·min -1 ; P = 0.99). No difference in baseline Trec was observed (PLA: 37.09°C ± 0.35°C, DPH: 37.13°C ± 0.33°C; P = 0.68), and the 60-min Δ Trec was not different ( P = 0.99) between PLA (0.83°C ± 0.29°C) and DPH (0.81°C ± 0.30°C). HR was similar at baseline (PLA: 86 ± 13 bpm, DPH: 84 ± 11 bpm; P = 0.30) and end-exercise (PLA: 134 ± 28 bpm, DPH: 132 ± 26 bpm; P = 0.90). Fifty milligrams of DPH does not modify the sweating, core temperature, and HR response during exertional heat stress in young healthy adults.

Exertional heat stress promotes the presence of bacterial DNA in plasma: A counterbalanced randomised controlled trial

ObjectivesThe primary aim was to explore the impact of exertional-heat stress (EHS) promoted exercise-associated bacteraemia. A secondary aim was to examine if an amino acid beverage (AAB) intervention may mitigate exercise-associated bacteraemia. DesignCounterbalanced randomised control trial. MethodsTwenty endurance trained male participants completed two randomised EHS trials. On one occasion, participants consumed a 237 mL AAB twice daily for 7 days prior, immediately before and every 20 min during EHS (2 h running at 60 % V̇O2max in 35 °C). On the other occasion, a water volume control (CON) equivalent was consumed. Whole blood samples were collected pre- and immediately post-EHS, and were analysed for plasma DNA concentration by fluorometer quantification after microbial extraction, and bacterial relative abundance by next generation 16s rRNA gene sequencing. ResultsIncreased concentration of microbial DNA in plasma pre- to post-EHS was observed on CON (pre-EHS 0.014 ng/μL, post-EHS 0.039 ng/μL) (p < 0.001) and AAB (pre-EHS 0.015 ng/μL, post-EHS 0.031 ng/μL) (p < 0.001). The magnitude of change from pre- to post-exercise on AAB was 40 % lower, but no significant difference was observed versus CON (p = 0.455). Predominant bacterial groups identified included: phyla-Proteobacteria (88.0 %), family-Burkholderiaceae (59.1 %), and genus-Curvibacter (58.6 %). No significant variation in absolute and relative change in α-diversity and relative abundance for phyla, family, and genus bacterial groups was observed in AAB versus CON. ConclusionsThe increased presence of microbial-bacterial DNA in systemic circulation in response to EHS appears positive in all participants. An amino acid beverage supplementation period prior to and consumption during EHS did not provide significant attenuation of EHS-associated bacteraemia.

Does diphenhydramine exert a sex-dependent effect on sudomotor responses during exertional heat stress?

Introduction: The first-generation H1 antihistamine diphenhydramine hydrochloride (DPH) is a potent antimuscarinic agent which may compromise sweat output during heat stress. DPH consumption prior to exertional heat stress could further suppress the sweating response in females due to their lower postjunctional cholinergic sensitivity of the sweat glands relative to males. Objective and Hypothesis: The purpose of the present study was to test the hypothesis that DPH would reduce sweating to a greater extent in females relative to males due to differences in cholinergic sensitivity at the sweat gland. Methods: Equal groups (10 per group) of males (24±3 y; 82.6±10.1 kg; 182±5 cm) and females (22±3 y, 67.7±7.8 kg, 171±6 cm) completed two experimental trials presented in a randomized double-blind fashion. Upon arrival to lab, participants consumed either i) a placebo (PLA) pill or ii) 50 mg DPH and then rested in a room maintained at ~29.5°C &amp; 35% RH for 2 hours before conducting a 60-minute treadmill march at a fixed rate of heat production relative to body surface area (~245 W/m2). Rectal temperature (Trec), local sweat rate of the forearm (LSR), and whole body sweat loss (WBSL) were measured. Sex-segregated analysis was conducted for each outcome variable as the difference between PLA and DPH. Results: Baseline Trec did not differ within sex between PLA and DPH (males: -0.10±0.26°C; females: -0.05±0.33°C, P=0.70), however a higher absolute baseline Trec was observed in females compared to males (P=0.006). In comparison to PLA, DPH did not exert a sex-dependent effect on ΔTrec following 60-min of exercise (males: 0.04±0.11°C; females: 0.02±0.37°C, P=0.90). No sex-dependent effect on the onset of sweating was observed between DPH and PLA (males: -0.4±2.6 min; females: 0.6±2.4 min, P=0.34). DPH did not exert a sex-dependent effect on LSR at steady-state (males: 0.03±0.25 mg/cm2/min; females: -0.01±0.21 mg/cm2/min, P=0.71). Lastly, no sex-dependent effect on WBSL was observed between PLA and DPH (males: 14±34 g; females: 6±43 g, P=0.98). Conclusion: Current evidence suggests that sex does not independently modulate the sweating response during exertional heat stress following the consumption of 50 mg of DPH. This research is supported by Dr. Ravanelli’s Research Seed Grant from the Centre for Research in Occupational Safety &amp; Health, and Dr. Ravanelli’s Natural Sciences and Engineering Research Council of Canada Discovery Grant (PIN#2022-05096). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Effects of CurraNZ, a New Zealand Blackcurrant Extract during 1 Hour of Treadmill Running in Female and Male Marathon des Sables Athletes in Hot Conditions: Two Case Studies.

Four weeks before competition in the 2023 Marathon des Sables, a 6-stage, ~250 km running event in the Sahara Desert, we examined the effects of a 7-day intake of New Zealand blackcurrant extract (210 mg anthocyanins per day) on 1 h treadmill running-induced physiological and metabolic responses in the heat (~34 °C, relative humidity: ~30%) in non-acclimatized amateur female and male athletes (age: 23, 38 yrs, BMI: 24.2, 28.4 kg·m-2, body fat%: 29.2, 18.8%, V˙O2max: 50.1, 52.1 mL·kg-1·min-1). During the 1 h run at 50%V˙O2max (speed female: 7.3, male: 7.5 km·h-1), indirect calorimetry was used, and heart rate was recorded at 15 min intervals with core temperature monitoring (0.05 Hz). The 1 h runs took place 3 h after a light breakfast and 2 h after intake of the final dose of New Zealand blackcurrant extract with water allowed ad libitum during the run. The New Zealand blackcurrant extract had no effects on the female athlete. The respiratory exchange ratio (RER) of the female athlete in the non-supplement control condition was 0.77 ± 0.01, indicating an existing ~77% contribution of fat oxidation to the energy requirements. In the male athlete, during 1 h of running, fat oxidation was higher by 21% (p < 0.01), carbohydrate oxidation was 31% lower (p = 0.05), RER was 0.03 units lower (p = 0.04), and core temperature was 0.4 °C lower (p < 0.01) with no differences for heart rate, minute ventilation, oxygen uptake, and carbon dioxide production for the New Zealand blackcurrant condition compared to the non-supplement control condition. Seven-day intake of New Zealand blackcurrant extract (210 mg anthocyanins per day) provided beneficial physiological and metabolic responses during exertional heat stress by 1 h of indoor (~34 °C) treadmill running in a male Marathon des Sables athlete 4 weeks before competition. Future work is required to address whether New Zealand blackcurrant provides a nutritional ergogenic effect for Marathon des Sables athletes during long-duration running in the heat combined with personalized nutrition.

A novel approach to the dual sugar test for the assessment of intestinal epithelium permeability in response to exertional heat stress and nutritional intervention

An acute increase in intestinal epithelium permeability is induced by prolonged exertion in the heat, resulting in the translocation of pathogenic bacteria and endotoxins from the lumen into the circulation, causing a systemic inflammatory response and debilitating symptoms(1). Acute exercise-induced gastrointestinal syndrome mimics chronic health conditions with which an impaired intestinal barrier function is associated, including coeliac disease, inflammatory bowel disease, diabetes, Alzheimer’s and liver diseases(2). Intestinal epithelium permeability is typically assessed using a dual sugar absorption test, by administering a drink containing non-metabolisable sugars (e.g. lactulose [L] and L-rhamnose [R]) that can enter the circulation by paracellular translocation when the epithelium is compromised, and are subsequently excreted and measured cumulatively in the urine(3). We aimed to demonstrate that our recently developed ion chromatography protocol(4) can be used to accurately quantify L/R ratio in the plasma of participants exercising in hot ambient conditions and to determine the impact of nutritional intervention on intestinal epithelium permeability. Further, we hypothesised that measuring L/R in plasma collected at intervals during the post-exercise recovery period would reveal more information about intestinal permeability compared to previously published cumulative urine L/R data(3). Endurance-trained participants completed a set of randomised crossover studies, consisting of 2 h running at 60% V˙O2max in temperate, warm and hot ambient conditions (n = 8) and/or in the heat while consuming water, carbohydrate or protein (n = 9). The dual sugar solution was ingested at 90 min of exercise and blood was sampled at 0, 1, 2 and 4 h post-exercise. Plasma sugars were quantified by high-performance anion exchange chromatography with pulsed amperometric detection (HPAEC-PAD) and L/R ratios were compared by two-way repeated measures ANOVA with Tukey’s multiple comparisons. Plasma L/R increased immediately post-exercise in the heat (0.15 ± 0.11) compared with temperate (0.06 ± 0.04, p&lt;0.001) and warm (0.09 ± 0.08, p&lt;0.01) conditions, while consuming glucose before and during exercise alleviated this (0.02 ± 0.02, p&lt;0.001), and this novel information was otherwise missed when measuring urine L/R. Consuming glucose or whey protein hydrolysate during exercise attenuated intestinal permeability from exertional heat stress throughout recovery, with the mean plasma L/R over 4 h reduced from 0.11 ± 0.05 to 0.04 ± 0.03 (p&lt;0.001) and 0.06 ± 0.04 (p&lt;0.01) with glucose and protein, respectively. We recommend using the dual sugar test with quantification of plasma sugars at intervals by HPAEC-PAD to maximise intestinal permeability data collection in exercise gastroenterology research and beyond, as this gives additional acute response information compared to urinary measurements. Our approach can be employed to investigate and develop personalised nutrition strategies that prevent intestinal hyperpermeability during exertional heat stress. This has implications for athlete performance and safety, and can also build upon occupational health and safety practices and inform chronic disease management.

New Zealand blackcurrant extract modulates the heat shock response in men during exercise in hot ambient conditions

PurposeTo determine if 7d of New Zealand blackcurrant (NZBC) extract alters the heat shock, inflammatory and apoptotic response during prolonged exertional-heat stress.MethodsTen men (Age: 29 ± 2 years, Stature: 1.82 ± 0.02 m, Mass: 80.3 ± 2.7 kg, V̇O2max: 56 ± 2 mL·kg−1·min−1) ingested two capsules of CurraNZ™ (NZBC extract: 210 mg anthocyanins·day−1) or PLACEBO for 7d prior to 1 h treadmill run (65% V̇O2max) in hot ambient conditions (34 °C/40% RH). Blood samples were collected before (Pre), immediately after (Post), 1 h after (1-Post), and 4 h after (4-Post) exercise. Heat shock proteins (HSP90, HSP70, HSP32) were measured in plasma. HSP and protein markers of inflammatory capacity (TLR4, NF-κB) and apoptosis (BAX/BCL-2, Caspase 9) were measured in peripheral blood mononuclear cells (PBMC).ResultseHSP32 was elevated at baseline in NZBC(+ 31%; p < 0.001). In PLACEBO HSP32 content in PBMC was elevated at 4-Post(+ 98%; p = 0.002), whereas in NZBC it fell at Post(− 45%; p = 0.030) and 1-Post(− 48%; p = 0.026). eHSP70 was increased at Post in PLACEBO(+ 55.6%, p = 0.001) and NZBC (+ 50.7%, p = 0.010). eHSP90 was increased at Post(+ 77.9%, p < 0.001) and 1-Post(+ 73.2%, p < 0.001) in PLACEBO, with similar increases being shown in NZBC (+ 49.0%, p = 0.006 and + 66.2%, p = 0.001; respectively). TLR4 and NF-κB were both elevated in NZBC at PRE(+ 54%, p = 0.003 and + 57%, p = 0.004; respectively). Main effects of study condition were also shown for BAX/BCL-2(p = 0.025) and Caspase 9 (p = 0.043); both were higher in NZBC.Conclusion7d of NZBC extract supplementation increased eHSP32 and PBMC HSP32 content. It also increased inflammatory and apoptotic markers in PBMC, suggesting that NZBC supports the putative inflammatory response that accompanies exertional-heat stress.

Does Age Influence Gastrointestinal Status Responses to Exertional-heat Stress?

This meta-data exploration aimed to determine the impact of exertional-heat stress (EHS) on gastrointestinal status of masters age and young adult endurance athletes. Sixteen MASTERS (mean: 44y) and twenty-one YOUNG (26y) recreational endurance athletes completed 2 h of running at 60% ˙V O2max in 35˚C ambient conditions. Blood samples were collected pre-, immediately and 1 h post-EHS, and analyzed for markers of exercise-induced gastrointestinal syndrome (EIGS). Thermo-physiological measures and gastrointestinal symptoms (GIS) were recorded every 10-20 min during EHS. Peak Δ pre- to post-EHS did not substantially differ (p>0.05) between MASTERS and YOUNG for intestinal epithelial injury [I-FABP: 1652pg/ml vs. 1524pg/ml, respectively], bacterial endotoxic translocation [sCD14: -0.09µg/mL vs. 0.84µg/mL, respectively], lipopolysaccharide-binding protein [LBP: 0.26µg/mL vs. 1.76µg/mL, respectively], and systemic inflammatory response profile (SIR-Profile: 92.0arb.unit vs. 154arb.unit, respectively). A significantly higher peak Δ pre- to post-EHS in endogenous endotoxin anti-body IgM (p=0.042), and pro-inflammatory cytokine IL-1β (p=0.038), was observed in YOUNG compared to MASTERS. No difference was observed between incidence (81% and 80%, respectively) and severity (summative accumulation: 21 and 30, respectively) of reported GIS during EHS between MASTERS and YOUNG. Pathophysiology of EIGS in response to EHS does not substantially differ with age progression, since masters and younger adult endurance athletes responded comparably.

Too hot to handle? Unveiling gut permeability during exertional heat stress

Too hot to handle? Unveiling gut permeability during exertional heat stress

The increase in core body temperature in response to exertional-heat stress can predict exercise-induced gastrointestinal syndrome

ABSTRACT Utilizing metadata from existing exertional and exertional-heat stress studies, the study aimed to determine if the exercise-associated increase in core body temperature can predict the change in exercise-induced gastrointestinal syndrome (EIGS) biomarkers and exercise-associated gastrointestinal symptoms (Ex-GIS). Endurance-trained individuals completed 2 h of running exercise in temperate (21.2-30.0°C) to hot (35.0-37.2°C) ambient conditions (n = 132 trials). Blood samples were collected pre- and post-exercise to determine the change in gastrointestinal integrity biomarkers and systemic inflammatory cytokines. Physiological and thermoregulatory strain variables were assessed every 10–15 min during exercise. The strength of the linear relationship between maximal (M-Tre) and change (Δ Tre) in rectal temperature and EIGS variables was determined via Spearman’s rank correlation coefficients. While the strength of prediction was determined via simple and multiple linear regression analyses dependent on screened EIGS and Ex-GIS confounding factors. Significant positive correlations between Tre maximum (M-Tre) and change (Δ Tre) with I-FABP (rs = 0.434, p < 0.001; and rs = 0.305, p < 0.001; respectively), sCD14 (rs = 0.358, p < 0.001; and rs = 0.362, p < 0.001), systemic inflammatory response profile (SIR-Profile) (p < 0.001), and total Ex-GIS (p < 0.05) were observed. M-Tre and Δ Tre significantly predicted (adjusted R2) magnitude of change in I-FABP (R2(2,123)=0.164, p < 0.001; and R2(2,119)=0.058, p = 0.011; respectively), sCD14 (R2(2,81)=0.249, p < 0.001; and R2(2,77)=0.214, p < 0.001), SIR-Profile (p < 0.001), and total Ex-GIS (p < 0.05). Strong to weak correlations were observed between M-Tre and Δ Tre with plasma concentrations of I-FABP, sCD14, SIR-Profile, and Ex-GIS in response to exercise. M-Tre and Δ Tre can predict the magnitude of these EIGS variables and Ex-GIS in response to exercise.

Changes in surrogate markers of intestinal epithelial injury and microbial translocation in young and older men during prolonged occupational heat stress in temperate and hot conditions.

Exertional heat stress can cause damage to the intestinal epithelium and disrupt gastrointestinal barrier integrity, leading to microbial translocation (MT) linked to the development of heat stroke. This study aimed to assess age-related differences in markers of intestinal epithelial injury and MT following non-heat stress and high-heat stress exercise in healthy young and older men. Markers of intestinal epithelial injury (intestinal fatty acid-binding protein-'IFABP') and MT (soluble cluster of differentiation 14-'sCD14'; and lipopolysaccharide-binding protein-'LBP') were assessed in healthy young (18-30 y, n = 13) and older (50-70 y) men (n = 12). Blood samples were collected before, after 180min of moderate-intensity (metabolic rate: 200 W/m2) walking and following 60min recovery in either a non-heat stress [temperate: 21.9°C, 35% relative humidity (RH)] or high-heat stress (hot: 41.4°C, 35% RH) environment. There were no differences in IFABP and sCD14 between the young and older groups in the temperate condition, while LBP was greater in the older group (+ 0.66 ug/mL; + 0.08 to + 1.24 ug/mL). In the hot condition, the older group experienced greater increases in IFABP compared to the young group (+ 712pg/mL/hr; + 269 to + 1154pg/mL/hr). However, there were no clear between-group differences for sCD14 (+ 0.24 ug/mL/hr, - 0.22 to + 0.70 ug/mL/hr) or LBP (+ 0.86 ug/mL/hr, - 0.73 to + 2.46 ug/mL/hr). While older men may experience greater intestinal epithelial injury following exercise in the heat; this did not lead to a greater magnitude of microbial translocation relative to their younger counterparts.

Neurobiomarker and body temperature responses to recreational marathon running

ObjectivesTo assess how biomarkers indicating central nervous system insult (neurobiomarkers) vary in peripheral blood with exertional-heat stress from prolonged endurance exercise. DesignObservational study of changes in neuron specific enolase (NSE), S100 calcium-binding protein B (S100β), Glial Fibrillary Acid Protein (GFAP) and Ubiquitin carboxyl-terminal hydrolase isozyme L1 (UCHL1) at Brighton Marathon 2022. MethodsIn 38 marathoners with in-race core temperature (Tc) monitoring, exposure (High, Intermediate or Low) was classified by cumulative hyperthermia – calculated as area under curve of Time × Tc > 38 °C – and also by running duration (finishing time). Blood was sampled for neurobiomarkers, cortisol and fluid-regulatory stress surrogates, including copeptin and creatinine (at rested baseline; within 30 min of finishing; and at 24 h). ResultsFinishing in 236 ± 40 min, runners showed stable GFAP and UCH-L1 across the marathon and next-day. Significant (P < 0.05) increases from baseline were shown post-marathon and at 24 h for S100β (8.52 [3.65, 22.95] vs 39.0 [26.48, 52.33] vs 80.3 [49.1, 99.7] ng·L−1) and post-marathon only for NSE (3.73 [3.30, 4.32] vs 4.85 [4.45, 5.80] μg·L−1, P < 0.0001). Whilst differential response to hyperthermia was observed for cortisol, copeptin and creatinine, neurobiomarker responses did not vary. Post-marathon, only NSE differed by exercise duration (High vs Low, 5.81 ± 1.77 vs. 4.69 ± 0.73 μg·L−1, adjusted P = 0.0358). ConclusionsSuccessful marathon performance did not associate with evidence for substantial neuronal insult. To account for variation in neurobiomarkers with prolonged endurance exercise, factors additional to hyperthermia, such as exercise duration and intensity, should be further investigated.

Plasma measurements of the dual sugar test reveal carbohydrate immediately alleviates intestinal permeability caused by exertional heat stress.

The aim of this set of randomised cross-over studies was to determine the impact of progressive heat exposure and carbohydrate or protein feeding during exertional stress on small intestine permeability using a dual sugar test. In our previous work, and typically in the field, recovery of lactulose and l-rhamnose is measured cumulatively in urine. This follow-up study exploits our novel high-performance anion exchange chromatography with pulsed amperometric detection (HPAEC-PAD) protocol to accurately quantify the sugars in plasma. Endurance-trained participants completed experimental trial A (ET-A; n=8), consisting of 2h running at 60% in temperate, warm and hot ambient conditions, and/or experimental trial B (ET-B; n=9), consisting of 2h running at 60% in the heat while consuming water, carbohydrate or protein. Blood samples were collected and plasma lactulose (L) and l-rhamnose (R) appearance, after dual sugar solution ingestion at 90min of exercise, was quantified by HPAEC-PAD to measure plasma L/R and reveal new information about intestinal permeability immediately post-exercise and during recovery. In ET-A, plasma L/R increased immediately post-exercise in hot compared with temperate and warm conditions, while, in ET-B, carbohydrate alleviated this, and this information was otherwise missed when measuring urine L/R. Consuming carbohydrate or protein before and during exercise attenuated small intestine permeability throughout recovery from exertional heat stress. We recommend using the dual sugar test with quantification of plasma sugars by HPAEC-PAD at intervals to maximise intestinal permeability data collection in exercise gastroenterology research, as this gives additional information compared to urinary measurements. KEY POINTS: Intestinal permeability is typically assessed using a dual sugar test, by administering a drink containing non-metabolisable sugars (e.g. lactulose (L) and l-rhamnose (R)) that can enter the circulation by paracellular translocation when the epithelium is compromised, and are subsequently measured in urine. We demonstrate that our recently developed ion chromatography protocol can be used to accurately quantify the L/R ratio in plasma, and that measuring L/R in plasma collected at intervals during the post-exercise recovery period reveals novel acute response information compared to measuring 5-h cumulative urine L/R. We confirm that exercising in hot ambient conditions increases intestinal epithelial permeability immediately after exercise, while consuming carbohydrate or protein immediately before and during exercise attenuates this. We recommend using our dual sugar absorption test protocol to maximise intestinal epithelial permeability data collection in exercise gastroenterology research and beyond.

The Compensatory Reserve Index: Physiological Monitoring During Exertional Heat Stress

The Compensatory Reserve Index: Physiological Monitoring During Exertional Heat Stress

The Impact of a 24-h Low and High Fermentable Oligo- Di- Mono-Saccharides and Polyol (FODMAP) Diet on Plasma Bacterial Profile in Response to Exertional-Heat Stress.

Exertional-heat stress (EHS) compromises intestinal epithelial integrity, potentially leading to the translocation of pathogenic agents into circulation. This study aimed to explore the impact of EHS on the systemic circulatory bacterial profile and to determine the impact of a short-term low (LFOD) and high (HFOD) fermentable oligo- di- mono-saccharide and polyol dietary intervention before EHS on this profile. Using a double-blind randomized cross-over design, thirteen endurance runners (n = 8 males, n = 5 females), with a history of exercise-associated gastrointestinal symptoms (Ex-GIS), consumed a 24 h LFOD and HFOD before 2 h running at 60% V.O2max in 35.6 °C. Blood and fecal samples were collected pre-EHS to determine plasma microbial DNA concentration, and sample bacteria and short chain fatty acid (SCFA) profiles by fluorometer quantification, 16S rRNA amplicon gene sequencing, and gas chromatography, respectively. Blood samples were also collected post-EHS to determine changes in plasma bacteria. EHS increased plasma microbial DNA similarly in both FODMAP trials (0.019 ng·μL-1 to 0.082 ng·μL-1) (p < 0.01). Similar pre- to post-EHS increases in plasma Proteobacteria (+1.6%) and Firmicutes (+0.6%) phyla relative abundance were observed in both FODMAP trials. This included increases in several Proteobacteria genus (Delftia and Serratia) groups. LFOD presented higher fecal Firmicutes (74%) and lower Bacteroidota (10%) relative abundance pre-EHS, as a result of an increase in Ruminococcaceae and Lachnospiraceae family and respective genus groups, compared with HFOD (64% and 25%, respectively). Pre-EHS plasma total SCFA (p = 0.040) and acetate (p = 0.036) concentrations were higher for HFOD (188 and 178 μmol·L-1, respectively) vs. LFOD (163 and 153 μmol·L-1, respectively). Pre-EHS total fecal SCFA concentration (119 and 74 μmol·g-1; p < 0.001), including acetate (74 and 45 μmol·g-1; p = 0.001), butyrate (22 and 13 μmol·g-1; p = 0.002), and propionate (20 and 13 μmol·g-1; p = 0.011), were higher on HFOD vs LFOD, respectively. EHS causes the translocation of whole bacteria into systemic circulation and alterations to the plasma bacterial profile, but the FODMAP content of a 24 h diet beforehand does not alter this outcome.

Amino Acid-Based Beverage Interventions Ameliorate Exercise-Induced Gastrointestinal Syndrome in Response to Exertional-Heat Stress: The Heat Exertion Amino Acid Technology (HEAAT) Study.

The study aimed to determine the effects of two differing amino acid beverage interventions on biomarkers of intestinal epithelial integrity and systemic inflammation in response to an exertional-heat stress challenge. One week after the initial assessment, participants (n = 20) were randomly allocated to complete two exertional-heat stress trials, with at least 1 week washout. Trials included a water control trial (CON), and one of two possible amino acid beverage intervention trials (VS001 or VS006). On VS001 (4.5g/L) and VS006 (6.4g/L), participants were asked to consume two 237-ml prefabricated doses daily for 7days before the exertional-heat stress, and one 237-ml dose immediately before, and every 20min during 2-hr running at 60% maximal oxygen uptake in 35 °C ambient conditions. A water volume equivalent was provided on CON. Whole blood samples were collected pre-, immediately post-, 1 and 2hr postexercise, and analyzed for plasma concentrations of cortisol, intestinal fatty acid protein, soluble CD14, and immunoglobulin M (IgM) by ELISA, and systemic inflammatory cytokines by multiplex. Preexercise resting biomarker concentrations for all variables did not significantly differ between trials (p > .05). A lower response magnitude for intestinal fatty acid protein (mean [95% CI]: 249 [60, 437]pg/ml, 900 [464, 1,336]pg/ml), soluble CD14 (-93 [-458, 272]ng/ml, 12 [-174, 197]ng/ml), and IgM (-6.5 [-23.0, 9.9]MMU/ml, -10.4 [-16.2, 4.7]MMU/ml) were observed on VS001 and V006 compared with CON (p < .05), respectively. Systemic inflammatory response profile was lower on VS001, but not VS006, versus CON (p < .05). Total gastrointestinal symptoms did not significantly differ between trials. Amino acid beverages' consumption (i.e.,4.5-6.4g/L), twice daily for 7days, immediately before, and during exertional-heat stress ameliorated intestinal epithelial integrity and systemic inflammatory perturbations associated with exercising in the heat, but without exacerbating gastrointestinal symptoms.