ORCID Profile
0000-0002-9858-0538
Current Organisation
Maastricht University
Does something not look right? The information on this page has been harvested from data sources that may not be up to date. We continue to work with information providers to improve coverage and quality. To report an issue, use the Feedback Form.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 03-2019
DOI: 10.1249/MSS.0000000000001800
Abstract: 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. In a randomized crossover manner, 16 well-trained male athletes (age, 28 ± 7 yr W max , 5.0 ± 0.3 W·kg −1 ) cycled 60 min at 70% W max after acute ingestion of sodium nitrate (NIT 800 mg NO 3 ), sucrose (SUC 40 g), or a water placebo (PLA). Splanchnic perfusion was assessed by determining the gap between gastric and arterial pCO 2 (gap g-a pCO 2 ) 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. The exercise protocol resulted in splanchnic hypoperfusion, as gap g-a pCO 2 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 (AUC 0–120 ) was significantly lower in SUC versus PLA (57,270 ± 77,425 vs 114,907 ± 91,527 pg·mL −1 per 120 min, P = 0.002). No differences were observed between NIT and PLA ( P = 0.99). 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.
Publisher: Frontiers Media SA
Date: 17-03-2020
Publisher: Frontiers Media SA
Date: 15-04-2020
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 12-2012
Publisher: American Physiological Society
Date: 03-2013
DOI: 10.1152/AJPREGU.00294.2012
Abstract: 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 H 5 ]phenylalanine were employed, and blood s les 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 ( r S = −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.
Publisher: Public Library of Science (PLoS)
Date: 21-07-2011
Publisher: MDPI AG
Date: 13-04-2016
DOI: 10.3390/NU8040221
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 11-2014
Publisher: MDPI AG
Date: 03-01-2019
DOI: 10.3390/NU11010077
Abstract: Serum vitamin D levels negatively correlate with obesity and associated disorders such as non-alcoholic steatohepatitis (NASH). However, the mechanisms linking low vitamin D (VD) status to disease progression are not completely understood. In this study, we analyzed the effect of VD treatment on NASH in mice. C57BL6/J mice were fed a high-fat/high-sugar diet (HFSD) containing low amounts of VD for 16 weeks to induce obesity, NASH and liver fibrosis. The effects of preventive and interventional VD treatment were studied on the level of liver histology and hepatic/intestinal gene expression. Interestingly, preventive and to a lesser extent also interventional VD treatment resulted in improvements of liver histology. This included a significant decrease of steatosis, a trend towards lower non-alcoholic fatty liver disease (NAFLD) activity score and a slight non-significant decrease of fibrosis in the preventive treatment group. In line with these changes, preventive VD treatment reduced the hepatic expression of lipogenic, inflammatory and pro-fibrotic genes. Notably, these beneficial effects occurred in conjunction with a reduction of intestinal inflammation. Together, our observations suggest that timely initiation of VD supplementation (preventive vs. interventional) is a critical determinant of treatment outcome in NASH. In the applied animal model, the improvements of liver histology occurred in conjunction with reduced inflammation in the gut, suggesting a potential relevance of vitamin D as a therapeutic agent acting on the gut–liver axis.
Publisher: American Physiological Society
Date: 15-07-2012
Abstract: 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 in idual athlete's GI tract are discussed. In addition, we elaborate on several promising components that could be exploited for preventive interventions.
No related grants have been discovered for Kaatje Lenaerts.