title: Exercise-induced splanchnic hypoperfusion results in gut dysfunction in healthy men.
abstract: BACKGROUND
  Splanchnic hypoperfusion is common in various pathophysiological conditions and often considered to lead to gut dysfunction. While it is known that physiological situations such as physical exercise also result in splanchnic hypoperfusion, the consequences of flow redistribution at the expense of abdominal organs remained to be determined. This study focuses on the effects of splanchnic hypoperfusion on the gut, and the relationship between hypoperfusion, intestinal injury and permeability during physical exercise in healthy men.
  
  
  RESULTS
  Healthy men cycled for 60 minutes at 70% of maximum workload capacity. Splanchnic hypoperfusion was assessed using gastric tonometry. Blood, sampled every 10 minutes, was analyzed for enterocyte damage parameters (intestinal fatty acid binding protein (I-FABP) and ileal bile acid binding protein (I-BABP)). Changes in intestinal permeability were assessed using sugar probes. Furthermore, liver and renal parameters were assessed. Splanchnic perfusion rapidly decreased during exercise, reflected by increased gap(g-a)pCO(2) from -0.85±0.15 to 0.85±0.42 kPa (p<0.001). Hypoperfusion increased plasma I-FABP (615±118 vs. 309±46 pg/ml, p<0.001) and I-BABP (14.30±2.20 vs. 5.06±1.27 ng/ml, p<0.001), and hypoperfusion correlated significantly with this small intestinal damage (r(S) = 0.59; p<0.001). Last of all, plasma analysis revealed an increase in small intestinal permeability after exercise (p<0.001), which correlated with intestinal injury (r(S) = 0.50; p<0.001). Liver parameters, but not renal parameters were elevated.
  
  
  CONCLUSIONS
  Exercise-induced splanchnic hypoperfusion results in quantifiable small intestinal injury. Importantly, the extent of intestinal injury correlates with transiently increased small intestinal permeability, indicating gut barrier dysfunction in healthy individuals. These physiological observations increase our knowledge of splanchnic hypoperfusion sequelae, and may help to understand and prevent these phenomena in patients.
authors.affiliation: Top Institute Food and Nutrition, Wageningen, The Netherlands.
authors.forename: Kim
authors.initials: K
authors.lastname: van Wijck
authors.forename: Kaatje
authors.initials: K
authors.lastname: Lenaerts
authors.forename: Luc J C
authors.initials: LJ
authors.lastname: van Loon
authors.forename: Wilbert H M
authors.initials: WH
authors.lastname: Peters
authors.forename: Wim A
authors.initials: WA
authors.lastname: Buurman
authors.forename: Cornelis H C
authors.initials: CH
authors.lastname: Dejong
mesh_terms: D001419:Bacteria / Q000378:metabolism; D015444:Exercise; D041981:Gastrointestinal Tract / Q000382:microbiology / Q000473:pathology / Q000503:physiopathology*; D006262:Health; D006801:Humans; D007249:Inflammation / Q000473:pathology; D007668:Kidney / Q000473:pathology; D008099:Liver / Q000473:pathology; D008297:Male; D010477:Perfusion; D010539:Permeability; D013152:Splanchnic Circulation / Q000502:physiology*; D055815:Young Adult