No abstract

Debilitating gastrointestinal symptoms is a common feature of endurance running and may be exacerbated by and/or limit the ability to tolerate carbohydrate intake during exercise. The study aimed to determine whether two weeks of repetitive gut-challenge during running can reduce exercise-associated gastrointestinal symptoms and carbohydrate malabsorption. Endurance runners (n=18) performed an initial gut-challenge trial (GC1) comprising 2-hour running exercise at 60% VO (steady state) while consuming a formulated gel-disk containing 30 g carbohydrates (2:1 glucose-fructose, 10% w/v) every 20 minutes, followed by a 1-hour running effort bout. Gastrointestinal symptoms, feeding tolerance, and breath hydrogen (H ) were determined along the gut-challenge trial. After GC1, participants were randomly assigned to a blinded carbohydrate (CHO, 90 gCHO hour ) or placebo (PLA, 0 gCHO hour ) gut-training group. This comprised of consuming the group-specific feeding intervention during 1-hour running exercise at 60% VO equivalent, daily over a period of two weeks. Participants then repeated the gut-challenge trial (GC2). In GC2, a reduced gut discomfort (P=.012), total (P=.009), upper- (P=.015), and lower-gastrointestinal (P=.008) symptoms, and nausea (P=.05) were observed on CHO, but not PLA. Feeding tolerance did not differ between GC1 and GC2 on CHO and PLA. H peak was attenuated in GC2 (6±3 ppm) compared to GC1 (13±6 ppm) on CHO (P=.004), but not on PLA (GC1 11±7 ppm, and GC2 10±10 ppm). The effort bout distance was greater in GC2 (12.3±1.3 km) compared with GC1 (11.7±1.5 km) on CHO (P=.035) only. Two weeks of repetitive gut-challenge improve gastrointestinal symptoms and reduce carbohydrate malabsorption during endurance running, which may have performance implications.

Weight loss was achieved in overweight and obese adults following IER and this loss was comparable to a DER diet. IER may be an effective alternative strategy for health practitioners to promote weight loss for selected overweight and obese people.

Purpose: The study aimed to determine the effect of diurnal versus nocturnal exercise on gastrointestinal integrity and functional responses, plasma lipopolysaccharide binding protein (LBP) and soluble CD14 (sCD14) concentrations (as indirect indicators of endotoxin responses), systemic inflammatory cytokine profile, gastrointestinal symptoms, and feeding tolerance. Methods: Endurance runners (n = 16) completed 3 h of 60% V ˙O2max (22.7°C, 45% relative humidity) running, on one occasion performed at 0900 h (400 lx; DAY) and on another occasion at 2100 h (2 lx; NIGHT). Blood samples were collected pre-and postexercise and during recovery to determine plasma concentrations of cortisol, catecholamines, claudin-3, I-FABP, LBP, and sCD14 and inflammatory cytokine profiles by ELISA. Orocecal transit time (OCTT) was determined by lactulose challenge test given at 150 min, with concomitant breath hydrogen (H 2 ) and gastrointestinal symptom determination. Results: Cortisol increased substantially pre-to postexercise on NIGHT (+182%) versus DAY (+4%) (trial-time, P = 0.046), with no epinephrine (+41%) and norepinephrine (+102%) trial differences. I-FABP, but not claudin-3, increased pre-to postexercise on both trials (mean = 2269 pg•mL −1 , 95% confidence interval = 1351-3187, +143%) (main effect of time [MEOT], P < 0.001). sCD14 increased pre-to postexercise (trial-time, P = 0.045, +5.6%) and was greater on DAY, but LBP decreased (MEOT, P = 0.019, −11.2%) on both trials. No trial difference was observed for systemic cytokine profile (MEOT, P = 0.004). Breath H 2 responses (P = 0.019) showed that OCTT was significantly delayed on NIGHT (>84 min, with n = 3 showing no breath H 2 turning point by 180 min postexercise) compared with DAY (mean = 54 min, 95% confidence interval = 29-79). NIGHT resulted in greater total gastrointestinal symptoms (P = 0.009) compared with DAY. No difference in feeding tolerance markers was observed between trials. Conclusion: Nocturnal exercise instigates greater gastrointestinal functional perturbations and symptoms compared with diurnal exercise. However, there are no circadian differences to gastrointestinal integrity and systemic perturbations in response to the same exertional stress and controlled procedures.

This translational research case series describes the implementation of a gastrointestinal assessment protocol during exercise (GastroAxEx) to inform individualised therapeutic intervention of endurance athletes affected by exercise-induced gastrointestinal syndrome (EIGS) and associated gastrointestinal symptoms (GIS). A four-phase approach was applied. Phase 1: Clinical assessment and exploring background history of exercise-associated gastrointestinal symptoms. Phase 2: Individual tailored GastroAxEx laboratory simulation designed to mirror exercise stress, highlighted in phase 1, that promotes EIGS and GIS during exercise. Phase 3: Individually programmed therapeutic intervention, based on the outcomes of Phase 2. Phase 4: Monitoring and readjustment of intervention based on outcomes from field testing under training and race conditions. Nine endurance athletes presenting with EIGS, and two control athletes not presenting with EIGS, completed Phase 2. Two athletes experienced significant thermoregulatory strain (peak core temperature attained &gt; 40°C) during the GastroAxEx. Plasma cortisol increased substantially pre- to post-exercise in n = 6/7 (Δ &gt; 500 nmol/L). Plasma I-FABP concentration increased substantially pre- to post-exercise in n = 2/8 (Δ &gt; 1,000 pg/ml). No substantial change was observed in pre- to post-exercise for systemic endotoxin and inflammatory profiles in all athletes. Breath H2 responses showed that orocecal transit time (OCTT) was delayed in n = 5/9 (90–150 min post-exercise) athletes, with the remaining athletes (n = 4/9) showing no H2 turning point by 180 min post-exercise. Severe GIS during exercise was experienced in n = 5/9 athletes, of which n = 2/9 had to dramatically reduce work output or cease exercise. Based on each athlete’s identified proposed causal factors of EIGS and GIS during exercise (i.e., n = 9/9 neuroendocrine-gastrointestinal pathway of EIGS), an individualised gastrointestinal therapeutic intervention was programmed and advised, adjusted from a standard EIGS prevention and management template that included established strategies with evidence of attenuating EIGS primary causal pathways, exacerbation factors, and GIS during exercise. All participants reported qualitative data on their progress, which included their previously presenting GIS during exercise, such as nausea and vomiting, either being eliminated or diminished resulting in work output improving (i.e., completing competition and/or not slowing down during training or competition as a result of GIS during exercise). These outcomes suggest GIS during exercise in endurance athletes are predominantly related to gastrointestinal functional and feeding tolerance issues, and not necessarily gastrointestinal integrity and/or systemic issues. GastroAxEx allows for informed identification of potential causal pathway(s) and exacerbation factor(s) of EIGS and GIS during exercise at an individual level, providing a valuable informed individualised therapeutic intervention approach.