Previously, we demonstrated that exercise can cause small intestinal injury, leading to loss of gut barrier function. The functional consequences of such exercise-induced intestinal injury on subsequent food digestion and absorption are unclear. The present study determined the impact of resistance-type exercise on small intestinal integrity and in vivo dietary protein digestion and absorption kinetics. Twenty-four young males ingested 20 g specifically produced intrinsically l-[1-(13)C]phenylalanine-labeled protein at rest or after performing a single bout of resistance-type exercise. Continuous intravenous infusions with l-[ring-(2)H5]phenylalanine were employed, and blood samples were collected regularly to assess in vivo protein digestion and absorption kinetics and to quantify plasma levels of intestinal fatty-acid binding protein (I-FABP) as a measure of small intestinal injury. Plasma I-FABP levels were increased after exercise by 35%, reaching peak values of 344 ± 53 pg/ml compared with baseline 254 ± 31 pg/ml (P < 0.05). In resting conditions, I-FABP levels remained unchanged. Dietary protein digestion and absorption rates were reduced during postexercise recovery when compared with resting conditions (P < 0.001), with average peak exogenous phenylalanine appearance rates of 0.18 ± 0.04 vs. 0.23 ± 0.03 mmol phenylalanine·kg lean body mass(-1)·min(-1), respectively. Plasma I-FABP levels correlated with in vivo rates of dietary protein digestion and absorption (rS = -0.57, P < 0.01). Resistance-type exercise induces small intestinal injury in healthy, young men, causing impairments in dietary protein digestion and absorption kinetics during the acute postexercise recovery phase. To the best of our knowledge, this is first evidence that shows that exercise attenuates dietary protein digestion and absorption kinetics during acute postexercise recovery.
To improve diagnosis of necrotizing enterocolitis (NEC) by noninvasive markers representing gut wall integrity loss (I-FABP and claudin-3) and gut wall inflammation (calprotectin). Furthermore, the usefulness of I-FABP to predict NEC severity and to screen for NEC was evaluated.Urinary I-FABP and claudin-3 concentrations and fecal calprotectin concentrations were measured in 35 consecutive neonates suspected of NEC at the moment of NEC suspicion. To investigate I-FABP as screening tool for NEC, daily urinary levels were determined in 6 neonates who developed NEC out of 226 neonates included before clinical suspicion of NEC.Of 35 neonates suspected of NEC, 14 developed NEC. Median I-FABP, claudin-3, and calprotectin levels were significantly higher in neonates with NEC than in neonates with other diagnoses. Cutoff values for I-FABP (2.20 pg/nmol creatinine), claudin-3 (800.8 INT), and calprotectin (286.2 microg/g feces) showed clinically relevant positive likelihood ratios (LRs) of 9.30, 3.74, 12.29, and negative LRs of 0.08, 0.36, 0.15, respectively. At suspicion of NEC, median urinary I-FABP levels of neonates with intestinal necrosis necessitating surgery or causing death were significantly higher than urinary I-FABP levels in conservatively treated neonates. Of the 226 neonates included before clinical suspicion of NEC, 6 developed NEC. In 4 of these 6 neonates I-FABP levels were not above the cutoff level to diagnose NEC before clinical suspicion.Urinary I-FABP levels are not suitable as screening tool for NEC before clinical suspicion. However, urinary I-FABP and claudin-3 and fecal calprotectin are promising diagnostic markers for NEC. Furthermore, urinary I-FABP might also be used to predict disease severity.
Physical exercise places high demands on the adaptive capacity of the human body.Strenuous physical performance increases the blood supply to active muscles, cardiopulmonary system, and skin to meet the altered demands for oxygen and nutrients.The redistribution of blood flow, necessary for such an increased blood supply to the periphery, significantly reduces blood flow to the gut, leading to splanchnic hypoperfusion and gastrointestinal (GI) compromise.A compromised GI system can have a negative impact on exercise performance and subsequent post-exercise recovery due to abdominal distress and impairments in the uptake of fluid, electrolytes, and nutrients.In addition, strenuous physical exercise leads to loss of epithelial integrity, which may give rise to increased intestinal permeability with bacterial translocation and inflammation.Ultimately, these effects can deteriorate post-exercise recovery and disrupt exercise training routine.This review provides an overview on the recent advances in our understanding of GI physiology and pathophysiology in relation to strenuous exercise.Various approaches to determine the impact of exercise on the individual athlete's GI tract will be discussed.In addition, we will elaborate on several promising components that could be exploited for preventive interventions.Lumen Bloodvessel Mucosa Tonometer course also be related to the fact that in general, absolute workloads of young athletes are substantially higher than for the elderly, leading to more profound circulatory changes.Another explanation for the less extensive splanchnic hypoperfusion observed in the elderly is their reduced muscle mass.In conclusion, exercise leads to redistribution of blood away from the splanchnic area, resulting in intestinal hypoperfusion and rapid reperfusion, which may contribute to GI distress in symptomatic athletes.22 PART I -CHAPTER 2 -1.5 -1.0 -0.5 0.0 0.5 1.0 1.5 Time (min) gap g-a pCO 2 (kPa) cycling 70% Wmax cycling 70% W max
Physical exercise places high demands on the adaptive capacity of the human body. Strenuous physical performance increases the blood supply to active muscles, cardiopulmonary system, and skin to meet the altered demands for oxygen and nutrients. The redistribution of blood flow, necessary for such an increased blood supply to the periphery, significantly reduces blood flow to the gut, leading to hypoperfusion and gastrointestinal (GI) compromise. A compromised GI system can have a negative impact on exercise performance and subsequent postexercise recovery due to abdominal distress and impairments in the uptake of fluid, electrolytes, and nutrients. In addition, strenuous physical exercise leads to loss of epithelial integrity, which may give rise to increased intestinal permeability with bacterial translocation and inflammation. Ultimately, these effects can deteriorate postexercise recovery and disrupt exercise training routine. This review provides an overview on the recent advances in our understanding of GI physiology and pathophysiology in relation to strenuous exercise. Various approaches to determine the impact of exercise on the individual athlete's GI tract are discussed. In addition, we elaborate on several promising components that could be exploited for preventive interventions.
