Ample evidence supports the notion that an acute bout of aerobic exercise and meal consumption reduces acylated ghrelin concentration. However, the mechanisms by which this exercise-and meal-induced suppression of acylated ghrelin occurs in humans is unknown. This study aimed to examine the concentration of butyrylcholinesterase (BChE), an enzyme responsible for hydrolysing ghrelin and other appetite-related hormones in response to a single bout of running and a standardised meal in young, healthy men. Thirty-three men (aged 23 ± 2 years, mean ± standard deviation) underwent two (exercise and meal conditions) 2-h laboratory-based experiments. In the exercise condition, all participants ran for 30 min at 70% of the maximum oxygen uptake (0930-1000) and rested until 1130. In the meal condition, participants reported to the laboratory at 0930 and rested until 1000. Subsequently, they consumed a standardised meal (1000-1015) and rested until 1130. Blood samples were collected at baseline ( 0930), 1000, 1030, 1100 and 1130. BChE concentration was not altered in both the exercise and meal conditions (p > 0.05). However, acylated ghrelin was suppressed after exercise (p < 0.05) and meal consumption (p < 0.05). There was no association between the change in BChE concentration and the change in acylated ghrelin before and after exercise (p = 0.571). Although des-acylated ghrelin concentration did not change during exercise (p > 0.05), it decreased after meal consumption (p < 0.05). These findings suggest that BChE may not be involved in the suppression of acylated ghrelin after exercise and meal consumption.

Purpose Although acute prolonged strenuous exercise has been shown to increase markers of gastrointestinal permeability and damage, little is known regarding the efficacy of nutritional supplement interventions on the attenuation of exercise-induced gastrointestinal syndrome. This study addressed the effects of oral amino acid supplementation on markers of gastrointestinal permeability and damage in response to exercise. Methods Sixteen active men aged 22.7 ± 2.6 years (mean ± standard deviation) completed placebo or cystine and glutamine supplementation trials in random order. Participants received either a placebo or cystine and glutamine supplements, three times a day for 5 days, separated by a 2-week washout period. On day 6, participants took their designated supplements 30 min before running at a speed corresponding to 75% of maximal oxygen uptake for 1 h, followed by a 4-h rest period. Blood samples were collected pre-exercise, immediately post-exercise, 30 min post-exercise, and 1, 2 and 4 h post-exercise on day 6. The plasma lactulose to mannitol ratio (L:M) and plasma intestinal fatty acid-binding protein (I-FABP) were used as markers of gastrointestinal permeability and damage, respectively. Results Plasma L:M (linear mixed model, coefficient ± standard error: − 0.011 ± 0.004, P = 0.0090) and changes (i.e., from pre-exercise) in plasma I-FABP (linear mixed model, − 195.3 ± 65.7 coefficient ± standard error (pg/mL), P = 0.0035) were lower in the cystine and glutamine supplementation trial than in the placebo trial. Conclusion Oral cystine and glutamine supplementation attenuated the markers of gastrointestinal permeability and damage after 1 h of strenuous running in young men. Trial registration number UMIN000026008. Date of registration 13 December 2018.

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Little is known regarding the effects of mineral-containing supplemention on oxidative stress markers, carbohydrate and lipid metabolism in response to an acute bout of exercise in humans. The present study investigated whether prior mineral-containing supplemention can improve oxidative stress status and how this supplementation influences on carbohydrate and lipid metabolism after a single bout of cycling in young men. Twelve, healthy young men (aged 22.5 ± 2.4 years, mean ± SD) underwent two, 150-min trials in a random order. Each participant received oral administration of mineral supplement containing 13.4 mg of sulphur or placebo one minute before exercise. In both trials, participants cycled at 75% of heart rate reserve for 60 minutes and then rested for 90 minutes. Blood samples were collected pre-exercise supplementation, immediately after exercise, 30 minutes after exercise, 60 minutes after exercise and 90 minutes after exercise. Circulating concentrations of derivatives of reactive oxygen metabolites, biological antioxidant potential, glucose and insulin did not differ between trials. Elevated circulating concentrations of non-esterified fatty acids were observed immediately after exercise in the supplementation trial compared with the placebo trial (mean ± SD: 1.1 ± 0.5 and 0.9 ± 0.3 mmol/L, respectively: trial × time interaction, p = 0.036). The present study showed that acute mineral-containing antioxidant supplemention appears to have no effect on improving oxidative stress markers in response to a single bout of cycling in healthy young men. In addition, the findings of this study suggested that mineral-containing supplemention may influence lipids metabolism during exercise.