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Malabsorption of fermentable oligo-, di-, mono-saccharides and polyols (FODMAPs) in response to prolonged exercise may increase incidence of upper and lower gastrointestinal symptoms (GIS), which are known to impair exercise performance. This case study aimed to explore the impact of a low-FODMAP diet on exercise-associated GIS in a female ultraendurance runner diagnosed with irritable bowel syndrome, competing in a 6-day 186.7-km mountainous multistage ultramarathon (MSUM). Irritable bowel syndrome symptom severity score at diagnosis was 410 and following a low-FODMAP diet (3.9 g FODMAPs/day) it reduced to 70. The diet was applied 6 days before (i.e., lead-in diet), and maintained during (5.1 g FODMAPs/day) the MSUM. Nutrition intake was analyzed through dietary analysis software. A validated 100-mm visual analog scale quantified GIS incidence and severity. GIS were modest during the MSUM (overall mean ± SD: bloating 27 ± 5 mm and flatulence 23 ± 8 mm), except severe nausea (67 ± 14 mm) experienced throughout. Total daily energy (11.7 ± 1.6 MJ/day) intake did not meet estimated energy requirements (range: 13.9–17.9 MJ/day). Total daily protein [1.4 ± 0.3 g·kg body weight (BW)⁻¹·day⁻¹], carbohydrate (9.1 ± 1.3 g·kg BW⁻¹·day⁻¹), fat (1.1 ± 0.2 g·kg BW⁻¹·day⁻¹), and water (78.7 ± 6.4 ml·kg BW⁻¹·day⁻¹) intakes satisfied current consensus guidelines, except for carbohydrates. Carbohydrate intake during running failed to meet recommendations (43 ± 9 g/hr). The runner successfully implemented a low-FODMAP diet and completed the MSUM with minimal GIS. However, suboptimal energy and carbohydrate intake occurred, potentially exacerbated by nausea associated with running at altitude.

There is little information describing how endurance athletes perceive sodium intake in relation to training and competition. Using an online questionnaire, this study assessed the beliefs, information sources, and intended practices regarding sodium ingestion for training and competition. Endurance athletes (n = 344) from six English-speaking countries completed the questionnaire and were included for analysis. The most cited information sources were social supports (63%), self-experimentation (56%), and media (48%). Respondents generally believed (>50% on electronic visual analog scale) endurance athletes require additional sodium on a daily basis (median 67% [interquartile range: 40–81%]), benefit from increased sodium in the days preceding competition (60% [30–77%]), should replace sodium losses during training (69% [48–83%]) and competition (74% [54–87%]), and would benefit from sweat composition testing (82% [65–95%]). Respondents generally believed sodium ingestion during endurance exercise prevents exercise-associated muscle cramps (75% [60–88%]) and exercise-associated hyponatremia (74% [62–89%]). The majority (58%) planned to consciously increase sodium or total food intake (i.e., indirectly increasing sodium intake) in the days preceding competition. Most (79%) were conscious of sodium intake during competition, but only 29% could articulate a specific intake plan. A small minority (5%) reported using commercial sweat testing services, of which 75% believed it was beneficial. We conclude that endurance athletes commonly perceive sodium intake as important for their sporting activities. Many intend to consciously increase sodium intake in the days preceding and during competition, although these views appear informed mostly by nonscientific and/or non-evidence-based sources.

The aims of this study were to assess the dietary intake and monitor self-reported recovery quality and clinical symptomology of a male ultra-endurance runner who completed a multiday ultra-endurance running challenge covering 4,254 km from North Scotland to the Moroccan Sahara desert over 78 consecutive days. Food and fluid intakes were recorded and analyzed through dietary analysis software. Body mass (BM) was determined before and after running each day, and before sleep. Clinical symptomology and perceived recovery quality were recorded each day. Whole blood hemoglobin and serum ferritin were determined before and after the challenge. Total daily energy (mean ± SD: 23.2 ± 3.2MJ·day⁻¹) and macronutrient intake (182 ± 31g·day⁻¹ protein, 842 ± 115g·day⁻¹ carbohydrate, 159 ± 55 g·day⁻¹ fat) met consensus nutritional guidelines for endurance performance. Total daily water intake through foods and fluids was 4.8 ± 2.0L·day⁻¹. Water and carbohydrate intake rates during running were 239 ± 143ml·h⁻¹ and 56 ± 19g·h⁻¹, respectively. Immediately after running, carbohydrate and protein intakes were 1.3 ± 1.0g·kg BM⁻¹ and 0.4 ± 0.2g·kg BM⁻¹, respectively. Daily micronutrient intakes ranged from 109 to 662% of UK RNIs. Prerunning BM was generally maintained throughout. Overall exercise-induced BM loss averaged 0.8 ± 1.0%; although BM losses of ≥ 2% occurred in the latter stages, a reflection of the warmer climate. Varying degrees of self-reported perceived recovery quality and clinical symptomology occurred throughout the challenge. This case study highlights oscillations in dietary habits along 78 consecutive days of ultra-endurance running, dependent on changes in ambient conditions and course topography. Nevertheless, nutrition and hydration status were maintained throughout the challenge. Despite dietary iron intake above RNI and iron supplementation, this alone did not prevent deficiency symptoms.

The purpose of the study was to determine the effects of carbohydrate (CHO) intake, with and without protein (PRO), immediately after prolonged strenuous exercise on circulating bacterially stimulated neutrophil degranulation. Twelve male runners completed 3 feeding interventions, 1 week apart, in randomized order after 2 hr of running at 75% VO_2max. The feeding interventions included a placebo solution, a CHO solution equal to 1.2 g CHO^~/kg body mass (BM), and a CHO-PRO solution equal to 1.2 g CHO/kg BM and 0.4 g PRO/kg BM (CHO+PRO) immediately postexercise. All solutions were flavor and water-volume equivalent (12 ml/kg BM). Circulating leukocyte counts, bacterially stimulated neutrophil degranulation, plasma insulin, and cortisol were determined from blood samples collected preexercise, immediately postexercise, and every 30 min until 180 min postexercise. The immediate postexercise circulating leukocytosis, neutrophilia, and lymphocytosis (p < .01 vs. preexercise) and the delayed lymphopenia (90 min postexercise, p < .05 vs. preexercise) were similar on all trials. Bacterially stimulated neutrophil degranulation decreased during recovery in control (23% at 180 min, p < .01 vs. preexercise) but remained above preexercise levels with CHO and CHO+PRO. In conclusion, CHO ingestion, with or without PRO, immediately after prolonged strenuous exercise prevented the decrease in bacterially stimulated neutrophil degranulation during recovery.

The impact of a carbohydrate-electrolyte solution with sodium alginate and pectin for hydrogel formation (CES-HGel), was compared to a standard CES with otherwise matched ingredients (CES-Std), for blood glucose, substrate oxidation, gastrointestinal symptoms (GIS; nausea, belching, bloating, pain, regurgitation, flatulence, urge to defecate, and diarrhea), and exercise performance. Nine trained male endurance runners completed 3 hr of steady-state running (SS) at 60% $\dot{\mathrm{V}}{\mathrm{O}}_2\text{max}$ , consuming 90 g/hr of carbohydrate from CES-HGel or CES-Std (53 g/hr maltodextrin, 37 g/hr fructose, 16% w/v solution) in a randomized crossover design, followed by an incremental time to exhaustion (TTE) test. Blood glucose and substrate oxidation were measured every 30 min during SS and oxidation throughout TTE. Breath hydrogen (H₂) was measured every 30 min during exercise and every 15 min for 2 hr postexercise. GIS were recorded every 15 min throughout SS, immediately after and every 15-min post-TTE. No differences in blood glucose (incremental area under the curve [mean ± SD]: CES-HGel 1,100 ± 96 mmol·L⁻¹·150 min⁻¹ and CES-Std 1,076 ± 58 mmol·L⁻¹·150 min⁻¹; p = .266) were observed during SS. There were no differences in substrate oxidation during SS (carbohydrate: p = .650; fat: p = .765) or TTE (carbohydrate: p = .466; fat: p = .633) and no effect of trial on GIS incidence (100% in both trials) or severity (summative rating score: CES-HGel 29.1 ± 32.6 and CES-Std 34.8 ± 34.8; p = .262). Breath hydrogen was not different between trials (p = .347), nor was TTE performance (CES-HGel 722 ± 182 s and CES-Std: 756 ± 187 s; p = .08). In conclusion, sodium alginate and pectin added to a CES consumed during endurance running does not alter the blood glucose responses, carbohydrate malabsorption, substrate oxidation, GIS, or TTE beyond those of a CES with otherwise matched ingredients.

Considering the recent growth of exercise gastroenterology research focusing on exercise-induced gastrointestinal syndrome mechanisms, response magnitude, prevention and management strategies, the standardized assessment of gastrointestinal symptoms (GIS) is warranted. The current methodological study aimed to test the reliability of a modified visual analog scale for assessing GIS during exercise, in response to a variety of exertional-stress scenarios, with and without dietary intervention. Recreational endurance runners (n = 31) performed one of the three exercise protocols, which included: 2-hr running at 70% $\dot{\mathrm{V}}{\mathrm{O}}_2\max$ in temperate (24.7 °C) ambient conditions, with fluid restriction; 2-hr running at 60% $\dot{\mathrm{V}}{\mathrm{O}}_2\max$ in hot (35.1 °C) ambient conditions, while consuming chilled water immediately before and every 15 min during exercise; and 2-hr running at 60% $\dot{\mathrm{V}}{\mathrm{O}}_2\max$ in temperate (23.0 °C) ambient conditions, while consuming 30 g/20 min carbohydrate (2∶1 glucose∶fructose, 10% temperate w/v), followed by a 1-hr distance test. GIS was monitored pre-exercise, periodically during exercise, and immediately postexercise. After wash out, participants were retested in mirrored conditions. No significant differences (p > .05) were identified between test–retest using Wilcoxon signed-rank test for all GIS (specific and categorized), within each exercise protocol and the combined protocols. Strong correlations were observed for gut discomfort, total GIS, upper GIS, and nausea (r _s = .566 to r _s = .686; p < .001), but not for lower GIS (r _s = .204; p = .232). Cohen’s magnitude of difference was minimal for all GIS (specific δ < 0.14 and categorized δ < 0.08). The modified visual analog scale for assessing GIS during exercise appears to be a reliable tool for identifying incidence and severity of GIS in cohort populations and is sensitive enough to detect exertional and intervention differences.

The study aimed to determine the impact of a dairy milk recovery beverage immediately after endurance exercise on leukocyte trafficking, neutrophil function, and gastrointestinal tolerance markers during recovery. Male runners (N = 11) completed two feeding trials in randomized order, after 2 hr of running at 70% $\dot{\mathrm{V}}{\mathrm{O}}_2\text{max}$ , fluid restricted, in temperate conditions (25 °C, 43% relative humidity). Immediately postexercise, the participants received a chocolate-flavored dairy milk beverage equating to 1.2 g/kg body mass carbohydrate and 0.4 g/kg body mass protein in one trial, and water volume equivalent in another trial. Venous blood and breath samples were collected preexercise, postexercise, and during recovery to determine the leukocyte counts, plasma intestinal fatty acid binding protein, and cortisol concentrations, as well as breath H₂. In addition, 1,000 µl of whole blood was incubated with 1 μg/ml Escherichia coli lipopolysaccharide for 1 hr at 37 °C to determine the stimulated plasma elastase concentration. Gastrointestinal symptoms and feeding tolerance markers were measured preexercise, every 15 min during exercise, and hourly postexercise for 3 hr. The postexercise leukocyte (mean [95% confidence interval]: 12.7 [11.6, 14.0] × 10⁹/L [main effect of time, MEOT]; p < .001) and neutrophil (10.2 [9.1, 11.5] × 10⁹/L; p < .001) counts, as well as the plasma intestinal fatty acid binding protein (470 pg/ml; +120%; p = .012) and cortisol (236 nMol/L; +71%; p = .006) concentrations, were similar throughout recovery for both trials. No significant difference in breath H₂ and gastrointestinal symptoms was observed between trials. The total (Trial × Time, p = .025) and per cell (Trial × Time, p = .001) bacterially stimulated neutrophil elastase release was greater for the chocolate-flavored dairy milk recovery beverage (+360% and +28%, respectively) in recovery, compared with the water trial (+85% and −38%, respectively). Chocolate-flavored dairy milk recovery beverage consumption immediately after exercise prevents the decrease in neutrophil function during the recovery period, and it does not account for substantial malabsorption or gastrointestinal symptoms over a water volume equivalent.

The aim of the study was to determine the influence of immediate and 1-hr-delayed carbohydrate (CHO) and protein (PRO) feeding after prolonged exercise on leukocyte trafficking, bacterially stimulated neutrophil degranulation, saliva secretory IgA (S-IgA) responses, and circulating stress hormones. In randomized order, separated by 1 wk, 9 male runners completed 3 feeding interventions after 2 hr of running at 75% VO_2max. During control (CON), participants received water (12 ml/kg body mass [BM]) immediately and 1 hr postexercise. During immediate feeding (IF), participants received a CHO-PRO solution equal to 1.2 g CHO/kg BM and 0.4 g PRO/kg BM immediately postexercise and water 1 hr postexercise. During delayed feeding (DF), participants received water immediately postexercise and CHO-PRO solution 1 hr postexercise. Unstimulated saliva and venous blood samples were collected preexercise, immediately postexercise, and every 20 min until 140 min postexercise. No significant interactions were observed for circulating leukocytes and T-lymphocyte subset counts, S-IgA secretion rate, or plasma cortisol, epinephrine, or norepinephrine concentration. Bacterially stimulated neutrophil degranulation decreased during recovery on CON and DF (24% and 31%, respectively, at 140 min; p < .01) but not on IF. Compared with CON, neutrophil degranulation was higher on IF at 100 min postexercise and higher on IF than DF at 80 min and 100 min onward postexercise (p < .05). Ingestion of a CHO-PRO solution immediately after, but not 1 hr after, prolonged strenuous exercise prevented the decrease in neutrophil degranulation but did not alter circulating stress hormone, leukocyte trafficking, or S-IgA responses. Further research should identify the independent effect of different quantities of CHO and PRO ingestion during recovery on neutrophil responses and other aspects of immune function.