title: Endothelial function after high-sugar-food ingestion improves with endurance exercise performed on the previous day.
abstract: BACKGROUND
  Endothelial function deteriorates after glucose ingestion. This may be attributed to hyperglycemia-induced oxidative stress. Acute endurance exercise might improve postprandial endothelial function by enhancing glucoregulation and reducing postprandial hyperglycemia.
  
  
  OBJECTIVE
  The objective was to determine whether endurance exercise performed 17 h before high-sugar-food ingestion attenuates postprandial impairment in endothelial function.
  
  
  METHODS
  Healthy men and women (n = 13; age: 48 +/- 17 y) were studied on 2 occasions: after > or = 48 h with no exercise and 17 h after a 60-min bout of endurance exercise. During each trial, brachial artery flow mediated dilation (FMD) was used to assess endothelial function before and after the ingestion of a candy bar and soft drink. Glucose, insulin, and thiobarbituric acid-reactive substances (TBARS), a marker of oxidative stress, were measured in blood obtained during each FMD measurement. The insulin sensitivity index was calculated from the glucose and insulin data.
  
  
  RESULTS
  FMD decreased significantly after food ingestion in both trials. However, prior exercise shifted the entire FMD curve upward (main treatment effect: P = 0.0002), which resulted in a greater area under the curve for FMD (774 +/- 122%.min) than did no exercise (607 +/- 122%.min) (P = 0.01). Prior exercise shifted the glucose and insulin curves downward (main treatment effects: P = 0.05 and P = 0.0007, respectively) and resulted in a significantly greater insulin sensitivity index (10.8 +/- 0.7) than did no exercise (9.2 +/- 0.7) (P = 0.01). TBARS did not differ significantly between trials.
  
  
  CONCLUSIONS
  Postprandial endothelial function was improved by endurance exercise performed approximately 17 h earlier. This effect was accompanied by exercise-induced improvements in insulin action and reductions in glycemia, but did not correspond with reductions in oxidative stress, as assessed by TBARS.
authors.affiliation: Department of Internal Medicine, Washington University School of Medicine, Saint Louis, MO, USA. eweiss4@slu.edu
authors.forename: Edward P
authors.initials: EP
authors.lastname: Weiss
authors.forename: Hassan
authors.initials: H
authors.lastname: Arif
authors.forename: Dennis T
authors.initials: DT
authors.lastname: Villareal
authors.forename: Emanuele
authors.initials: E
authors.lastname: Marzetti
authors.forename: John O
authors.initials: JO
authors.lastname: Holloszy
mesh_terms: D000328:Adult; D000368:Aged; D019540:Area Under Curve; D001783:Blood Flow Velocity; D001786:Blood Glucose / Q000378:metabolism*; D002153:Calorimetry, Indirect; D018592:Cross-Over Studies; D019422:Dietary Sucrose / Q000494:pharmacology*; D004730:Endothelium, Vascular / Q000187:drug effects*; D005260:Female; D005951:Glucose Tolerance Test; D006801:Humans; D007328:Insulin / Q000097:blood*; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000187:drug effects; D010101:Oxygen Consumption; D010807:Physical Endurance / Q000502:physiology*; D019518:Postprandial Period; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis; D014664:Vasodilation / Q000187:drug effects
chemical_list: D001786:Blood Glucose; D019422:Dietary Sucrose; D007328:Insulin; D017392:Thiobarbituric Acid Reactive Substances