Lewis J. James’s research while affiliated with Loughborough University and other places

INTRODUCTION: Exogenous carbohydrate oxidation (i.e., from drinks) is reduced in hot conditions (1,2). Increased thermal and cardiovascular strain and reduced gastrointestinal (GI) integrity (3) may impair glucose uptake and transport, gastric emptying, and intestinal absorption. However, dehydration, often resulting from heat exposure, may also contribute to these impairments by reducing blood volume and altering blood flow distribution. As previous studies in hot conditions have not controlled hydration status, the impact of dehydration on reduced exogenous carbohydrate oxidation is unclear. Therefore, this study aimed to investigate the effect of hydration status on exogenous carbohydrate oxidation during running in a hot environment. METHODS: Ten trained male runners (21 ± 2 y; 68.9 ± 7.6 kg; V̇O2peak: 67 ± 6 mL/kg/min) completed a preliminary session (V̇O2peak and sweat rate testing) and two experimental trials [100 min of steady state running at ~65% V̇O2peak in hot conditions (32°C) with hydration (water intake to replace 90% of mass losses; HYD) or to induce dehydration (minimal fluid provided; DEH)]. In each trial, participants consumed 60 g/h (bolus every 20 min) of a 35% dextrose solution enriched with [U-13C] glucose (145 ± 2 δ‰ enrichment). Expired breath (analysed for 13C:12C ratio using GC-IRMS), venous blood samples and subjective scales of GI comfort were collected at rest and every 20 min during exercise. Data were analysed using linear mixed models with significance at P < 0.05. Results presented as mean ± SD. RESULTS: Average (40-100 min) and peak exogenous carbohydrate oxidation rates were 29% (DEH: 0.35 ± 0.15 vs. HYD: 0.50 ± 0.13 g/min; P = 0.016) and 24% (DEH: 0.54 ± 0.19 vs. HYD: 0.71 ± 0.13 g/min; P = 0.017) lower in DEH than HYD, respectively. Total (DEH: 2.52 ± 0.47 vs. HYD: 2.56 ± 0.26 g/min; P = 0.737) and endogenous carbohydrate oxidation (DEH: 2.17 ± 0.36 vs. HYD: 2.06 ± 0.30 g/min; P = 0.188) were not different between trials. GI temperature (DEH: 39.4 ± 0.5°C; HYD: 39.2 ± 0.4°C; P = 0.380) and heart rate (DEH: 173 ± 11 bpm; HYD: 169 ± 12 bpm; P = 0.124) at the end of trials were not different between conditions. Body mass loss (-2.7 ± 0.5% vs. -0.4 ± 0.5%; P < 0.001) and changes in plasma volume from baseline (-9.3 ± 4.1% vs.-2.5 ± 5.1%; P < 0.001) were greater in DEH. No differences in GI symptoms, including stomach bloatedness, were observed between conditions (P > 0.05). CONCLUSION: Prolonged exercise in the heat, with minimal fluid intake leading to dehydration, impaired exogenous carbohydrate oxidation. These findings underscore the importance of hydration and fluid delivery for optimising exogenous carbohydrate utilisation, particularly for athletes aiming to sustain endurance performance in hot conditions. REFERENCES: (1) Jentjens et al. 2002. JAP 92:1562–1572 (2) Reynolds et al. 2025. MSSE Epub ahead of print. (3) Snipe et al. 2018. EJAP 118:389-400

Macrae, HZ, Reynolds, KM, Cable, TG, Barutcu, A, Hansell, EJ, Mears, SA, Midwood, KL, Mould, C, Funnell, MP, Goosey-Tolfrey, VL, and James, LJ. Twice a day lacrosse training in temperate conditions results in a negative 24-hour sodium balance in male and female university lacrosse players. J Strength Cond Res XX(X): 000-000, 2025-This study measured 24-hour fluid and sodium balance in 27 university lacrosse players (13 males, 14 females; 21 ± 1 years). For 24 hours, participants maintained their usual fluid and food intake, completed a weighed food diary, and collected all urine produced. Participants completed 2 bouts of 1.5 hours (males) or 2 hours (females) lacrosse training (16.0 ± 3.9°C, 62.3 ± 11.7% relative humidity) separated by 2-2.5 hours rest. Nude body mass was measured at baseline (0 hour), 24 hours later, before and after training, and corrected for food/fluid consumed and urine/feces produced during training to determine sweat losses. A sweat patch was applied (scapula) and analyzed for sweat sodium concentration. Data are mean ± standard deviation or median (Q1-Q3), p < 0.05. Sodium balance at 24 hours was negative for both male (-0.76 ± 1.31 g) and female (-0.47 ± 0.70 g) players but was not different between sexes ( p = 0.350). Body mass at 0 hour and 24 hours was not different for male (79.99 ± 10.02 kg vs 79.69 ± 10.15 kg) or female (65.68 ± 10.17 kg vs 65.82 ± 10.21 kg; both p > 0.05) players. Sweat rates were relatively low and not different between male (0.39 ± 0.23 L/h) and female (0.33 ± 0.18 L/h; p = 0.286) players. There was no difference in sweat sodium concentration (male players: 27 (23-28) mmol/L; female players: 27 (23-31) mmol/L; p = 0.786). Ad libitum drinking, combined with low sweat rates, generally prevented dehydration accruing to a level that might impair performance. Sodium balance deficit was small (∼0.61 g) but may require investigation to understand whether daily deficits accumulate.

INTRODUCTION: Exogenous carbohydrate oxidation (i.e., from drinks) is reduced in hot conditions1,2. Increased thermal and cardiovascular strain and reduced gastrointestinal (GI) integrity3 may impair glucose uptake, gastric emptying, and absorption. Dehydration resulting from heat exposure, can also contribute to these impairments by reducing blood volume and altering blood flow distribution. As previous studies in hot conditions have not controlled hydration status, it remains unclear whether increased exogenous carbohydrate oxidation was due to increased core temperature or dehydration. Therefore, this study investigated the effect of running in a hot compared to temperate environment on exogenous carbohydrate oxidation, whilst maintaining a state of euhydration. METHODS: Ten trained runners (24 ± 6 y; 72.7 ± 8.3 kg; V̇O2peak: 63 ± 6 mL/kg/min) completed a preliminary session (V̇O2peak and sweat rate testing) and two experimental trials [100 minutes of steady state running at ~65% V̇O2peak in either a temperate (19°C; TEMP) or a hot environment (32°C; HOT)]. Water was provided every 20 min to replace ~90% of body mass losses (TEMP: 795 ± 213 mL; HOT: 1665 ± 437 mL). In each trial, participants consumed 60 g/h (bolus every 20 min) of a 35% dextrose solution enriched with [U-13C] glucose (145 ± 2 δ‰ enrichment). Expired breath (analysed for 13C:12C), blood samples and subjective scales of GI comfort were collected at rest and every 20 min during exercise. Data were analysed using linear mixed models (significance at P < 0.05). Results presented as mean ± SD. Institutional ethical approval was granted (LEON 16408). RESULTS: Average (40-100 min) and peak exogenous carbohydrate oxidation rates were 20% (HOT: 0.43 ± 0.09 vs. TEMP: 0.54 ± 0.12 g/min; P = 0.006) and 18% (HOT: 0.67 ± 0.10 vs. TEMP: 0.81 ± 0.11 g/min; P = 0.002) lower in HOT than in TEMP respectively. Total carbohydrate oxidation (HOT: 2.72 ± 0.40 g/min vs. TEMP: 2.57 ± 0.34; P = 0.111) was not different between trials resulting in a greater contribution from endogenous sources in HOT (2.28 ± 0.38 vs. 2.03 ± 0.33 g/min; P = 0.020). Gastrointestinal temperature (HOT: 39.2 ± 0.4°C; TEMP: 37.9 ± 0.3°C; P < 0.001) and heart rate (HOT: 166 ± 14 bpm; TEMP: 137 ± 16 bpm; P < 0.001) at the end of trials were greater in HOT. In both trials body mass loss remained in a state of euhydration (± 1% body mass loss4) but was greater in HOT (-0.47 ± 0.51% vs. -0.04 ± 0.33%; P = 0.004). No difference was reported for changes in plasma volume (HOT: -9.0 ± 6.8%; TEMP: -10.3 ± 4.4%; P = 0.621). No differences in GI symptoms, including stomach bloatedness, were observed between conditions (P > 0.05). CONCLUSION: Even with adequate hydration (within ± 1% body mass loss), running in a hot environment reduces exogenous carbohydrate oxidation likely due to impaired muscle glucose uptake, decreased intestinal absorption and slower gastric emptying. This led to a compensatory increase in endogenous carbohydrate oxidation to maintain similar total oxidation rates.

Purpose: This study aimed to evaluate the effect of telemetric-pill ingestion timing on gastrointestinal temperature measurements during exercise with tepid fluid intake. Methods: Twelve participants swallowed temperature pills 12, 3, or 0.5 hours before completing 60 minutes of treadmill running, consuming 200 mL of room-temperature water every 15 minutes. Results: Pills ingested 0.5 or 3 hours before exercise resulted in significantly lower gastrointestinal temperature compared with those ingested 12 hours prior. Conclusions: These results indicate that ingesting pills closer to exercise with fluid ingestion may confound gastrointestinal temperature measurements, underlining the need for sufficient ingestion time before exercise to avoid interference with fluid intake.

Purpose Exercise-induced hypohydration exacerbates biomarkers of renal injury, but studies isolating the effects of hypohydration without exercise have produced mixed findings. This study investigated the effects of 24-h severe fluid restriction on biomarkers of renal injury and glucose tolerance. Methods Fifteen males (age: 27 ± 5 y; BMI: 24.1 ± 3.8 kg/m²) completed two randomised trials, involving consuming either 40 mL/kg body mass water to maintain euhydration (EU) or severe fluid restriction via limiting water consumption to 100 mL (HYP). A standardised dry food diet was consumed in both trials (~ 300 g water). At baseline and 24 h post-baseline, nude body mass, and blood and urine samples (additional urine sample at 12 h) were collected. An oral glucose tolerance test was conducted after 24-h post-baseline measurements (n = 12). Results At 24 h, body mass loss (HYP: − 1.52 ± 0.34%, EU: − 0.24 ± 0.40%), plasma volume loss, serum, and urine osmolality were greater in HYP than EU (P ≤ 0.004). Osmolality-corrected urinary kidney injury molecule-1 (uKIM-1) concentrations were greater in HYP at 12 (HYP: 1.097 ± 0.587 ng/mOsm, EU: 0.570 ± 0.408 ng/mOsm; P < 0.001) and 24-h (HYP: 1.932 ± 1.173 ng/mOsm, EU: 1.599 ± 1.012 ng/mOsm; P = 0.01). There was no trial-by-time interactions for osmolality-corrected urinary neutrophil gelatinase-associated lipocalin concentrations (P = 0.781) or plasma glucose (P = 0.550) and insulin (P = 0.193) concentrations. Conclusion Hypohydration produced by 24-h fluid restriction increased proximal tubular injury but did not affect glucose tolerance.

This study compared oxygen consumption and substrate oxidation while exercising in hot and temperate conditions in individuals with different physical activity status (i.e., inactive individuals vs. trained runners). 10 inactive individuals (IA: 26 ± 6 y; 79.1 ± 14.1 kg; 40.7 ± 5.1 ml·kg ⁻¹ ·min ⁻¹ ) and 10 trained runners (TR: 25 ± 6 y; 69.5 ± 9.1 kg; 63.1 ± 5.1 ml·kg ⁻¹ ·min ⁻¹ ) completed two incremental exercise tests (4 min stages) until exhaustion in temperate (TEMP: 18.7 ± 0.1 °C; 43.2 ± 4.1% relative humidity) and hot (HOT: 34.4 ± 0.2 °C and 42.6 ± 1.6% relative humidity) conditions. Expired gas and blood lactate concentrations were measured at the end of each stage. Peak oxygen consumption similarly decreased in HOT compared to TEMP for IA and TR (-13.2 ± 4.5% vs. -15.2 ± 7%; p=0.571; ES=0.25). In HOT compared to TEMP, lipid oxidation, from 30 to 70% of V̇O 2peak , was reduced for both groups (IA: p=0.023, ES=0.43; TR: p<0.001, ES=0.72) while carbohydrate oxidation was increased for TR ( p=0.011; ES=0.45) but not for IA ( p=0.268; ES=0.21). Core temperature was different between conditions for TR (higher in HOT, p=0.017; ES=0.66) but not for IA ( p=0.901; ES=0.25). Despite reduced physiological capacities in IA, both populations demonstrated reductions in lipid utilisation and peak oxygen consumption in hot compared to temperate conditions. However, the increased carbohydrate oxidation in HOT for TR were not observed in IA, potentially explained by lower thermal strain.

Purpose 7 days L-citrulline supplementation has been reported to improve blood pressure, $\mathop {\text{V}}\limits^{.}$ V . O 2 kinetics, gastrointestinal (GI) perfusion and endurance cycling performance through increasing arterial blood flow. In situations where blood volume is compromised (e.g., hyperthermia/hypohydration), L-citrulline may improve thermoregulation and exercise performance by redistributing blood flow to aid heat loss and/or muscle function. This study assessed 7 days L-citrulline supplementation on running performance in the heat, whilst mildly hypohydrated. Methods 13 endurance runners (2 female, 31 ± 8 y, $\mathop {\text{V}}\limits^{.}$ V . O 2 peak 60 ± 6 mL/kg/min) participated in a randomised crossover study with 7 days L-citrulline (CIT; 6 g/d) or placebo (maltodextrin powder; PLA) supplementation. Participants completed a 50 min running ‘preload’ at 65% $\mathop {\text{V}}\limits^{.}$ V . O 2 peak (32 °C, 50% relative humidity) to induce hyperthermia and hypohydration before a 3 km running time trial (TT). Body mass and blood samples were collected at baseline, pre-preload, post-preload and post-TT, whilst core and skin temperature, heart rate and perceptual responses were collected periodically throughout. Results TT performance was not different between trials (CIT 865 ± 142 s; PLA 892 ± 154 s; P = 0.437). Core and skin temperature and heart rate ( P ≥ 0.270), hydration (sweat rate, plasma volume, osmolality) indices ( P ≥ 0.216), GI damage ( P ≥ 0.260) and perceptual responses ( P ≥ 0.610) were not different between trials during the preload and TT. Conclusions 7 days of L-citrulline supplementation had no effect on 3 km running performance in the heat or any effects on thermoregulation or GI damage in trained runners in a hypohydrated state.

Exercise in warm environments increases thermal/cardiovascular strain and decreases gastrointestinal (GI) integrity and endurance performance. However, laboratory-based studies have provided little to/no facing airflow, potentially exacerbating these effects, particularly for cycling, where convective cooling may be a major contributor to thermal balance. Purpose This study investigated the effect of cycling in a warm vs temperate environment with sufficient facing airflow on exogenous glucose use, performance, and GI responses. Methods Ten trained male cyclists/triathletes (36 ± 6 y; 55 ± 6 mL/kg/min) completed V̇ O 2peak and familiarisation trials, and two experimental trials in 19 °C (TEMP) and 32 °C (WARM). Experimental trials involved 2 h cycling at ~50% W peak (preload) and an ~15 min time trial (TT) with fan-provided airflow covering the cyclist (preload: ~29 km/h, TT: ~35 km/h). A glucose drink containing [U- ¹³ C]-glucose was consumed every 20 min during the preload (72 g/h). Results Average 40-120 min (TEMP 0.56 ± 0.13 g/min; WARM 0.48 ± 0.12 g/min; 15%; P = 0.015) and peak (TEMP 0.79 ± 0.18 g/min; WARM 0.68 ± 0.14 g/min; 14%; P = 0.008) exogenous glucose oxidation were reduced in WARM. TT performance was 15% slower in WARM (TEMP 819 ± 47 s; WARM 961 ± 130 s; P = 0.002). GI temperature ( P = 0.007), heart rate ( P < 0.001), and RPE ( P = 0.046) were greater during WARM. GI comfort ( P = 0.659) and Intestinal Fatty Acid Binding Protein (IFABP) ( P = 0.094) were not different between trials. Conclusions These data demonstrate that ability to use glucose provided in drinks was impaired during prolonged cycling in WARM. WARM ambient conditions impaired laboratory-based cycling performance, even with facing airflow approximating outdoor conditions, likely via impairments of thermoregulatory, cardiovascular, and metabolic function.

Acetate, propionate, and butyrate are naturally-occurring short-chain fatty acids (SCFAs) derived from bacterial metabolism of dietary fibre and have been associated with numerous positive health outcomes. All three acids have...