Sucrose but Not Nitrate Ingestion Reduces Strenuous Cycling-induced Intestinal Injury.

Purpose: Strenuous exercise induces intestinal injury, which is likely related to splanchnic hypoperfusion and may be associated with gastrointestinal complaints commonly reported during certain exercise modalities. Increasing circulating nitric oxide (NO) levels or inducing postprandial hyperemia may improve splanchnic perfusion, thereby attenuating intestinal injury during exercise. Therefore, we investigated the effects of both dietary nitrate ingestion and sucrose ingestion on splanchnic perfusion and intestinal injury induced by prolonged strenuous cycling.

Methods: In a randomized crossover manner, 16 well-trained male athletes (age, 28 ± 7 yr; Wmax, 5.0 ± 0.3 W·kg) cycled 60 min at 70% Wmax after acute ingestion of sodium nitrate (NIT; 800 mg NO3), sucrose (SUC; 40 g), or a water placebo (PLA). Splanchnic perfusion was assessed by determining the gap between gastric and arterial pCO2 (gapg-apCO2) using gastric air tonometry. Plasma intestinal fatty acid-binding protein (I-FABP) concentrations, reflecting enterocyte damage, were assessed every 20 min during and up to 60 min of postexercise recovery.

Results: The exercise protocol resulted in splanchnic hypoperfusion, as gapg-apCO2 levels increased during exercise (P < 0.001), with no differences between treatments (P = 0.47). Although plasma I-FABP concentrations increased during exercise and postexercise recovery for all treatments (P < 0.0001), the increase was different between treatments (P < 0.0001). Post hoc comparisons showed an attenuated increase in I-FABP in SUC versus PLA (P = 0.020). In accordance, I-FABP area under the curve (AUC0-120) was significantly lower in SUC versus PLA (57,270 ± 77,425 vs 114,907 ± 91,527 pg·mL per 120 min, P = 0.002). No differences were observed between NIT and PLA (P = 0.99).

Conclusion: Sucrose but not nitrate ingestion lowers intestinal injury evoked during prolonged strenuous cycling. These results suggest that sucrose ingestion, but not nitrate, prevents hypoperfusion-induced gastrointestinal damage during exercise and, as such, may help to lower exercise-related gastrointestinal complaints.