title: Fibrinolytic system during long-distance running in IDDM patients and in healthy subjects.
abstract: OBJECTIVE
  Endurance exercise has been advocated in diabetes mellitus to improve both metabolic control and prevent atherosclerotic complications. The response of the fibrinolytic system during prolonged exercise has not been studied in diabetes.
  
  
  METHODS
  In seven male marathon runners with IDDM and eight healthy nondiabetic male control subjects, matched for age and degree of training, we studied fibrinolytic and coagulation parameters during a 3-h 32-km outdoor running session. Measurements included t-PA, u-PA, PAI-1, PAP (as a measure of in vivo activation of fibrinolysis), FbDPs, FGN, vWF, and VIII:C.
  
  
  RESULTS
  In both IDDM and control subjects, levels of t-PA, u-PA, PAP, vWF, and VIII:C continued to rise throughout the exercise, whereas PAI-1 showed a similar decline in both groups. FbDP rose slightly in both groups, and FGN remained unchanged. t-PA levels during exercise correlated closely with exercise intensity. These findings indicate that continued stimulation by exercise does not deplete endothelial PA stores. Differences between IDDM and control subjects were seen only for t-PA, vWF, and u-PA. The AUC during exercise (AUC0.5-3.0) of t-PA in IDDM was insignificantly lower than in control subjects (53 +/- 19 vs. 67 +/- 31 ng.ml-1.h), but the ratio of t-PA to exercise intensity was lower in IDDM (0.24 +/- 0.11 vs. 0.31 +/- 0.13, P less than 0.05). The AUC0.5-3.0 of vWF was lower in IDDM than in control subjects (569 +/- 268 vs. 880 +/- 265%.h, P less than 0.05). The AUC0.5-3.0 of u-PA was higher in IDDM than in control subjects (15.1 +/- 3.5 vs. 11.2 +/- 1.8 ng.ml-1.h, P less than 0.05).
  
  
  CONCLUSIONS
  Despite a defect in the exercise-induced endothelial release of vWF and t-PA, the overall potential to activate fibrinolysis is intact in IDDM, possibly by enhancement of u-PA after exercise. Our data suggest that in IDDM, as in nondiabetic subjects, long-distance running may slow the progression of atherosclerosis by stimulating fibrinolysis.
authors.affiliation: Department of Internal Medicine, University Hospital, Leiden, Netherlands.
authors.forename: B J
authors.initials: BJ
authors.lastname: van Loon
authors.forename: L P
authors.initials: LP
authors.lastname: Heere
authors.forename: C
authors.initials: C
authors.lastname: Kluft
authors.forename: E
authors.initials: E
authors.lastname: Briët
authors.forename: G
authors.initials: G
authors.lastname: Dooijewaard
authors.forename: A E
authors.initials: AE
authors.lastname: Meinders
mesh_terms: D000328:Adult; D001786:Blood Glucose / Q000032:analysis; D003922:Diabetes Mellitus, Type 1 / Q000097:blood* / Q000503:physiopathology; D015444:Exercise; D005169:Factor VIII / Q000032:analysis; D005338:Fibrin Fibrinogen Degradation Products / Q000032:analysis; D005342:Fibrinolysis; D006442:Glycated Hemoglobin / Q000032:analysis; D006339:Heart Rate; D006801:Humans; D015849:Plasminogen Inactivators / Q000032:analysis; D012016:Reference Values; D012420:Running; D010959:Tissue Plasminogen Activator / Q000097:blood; D014568:Urokinase-Type Plasminogen Activator / Q000097:blood; D014841:von Willebrand Factor / Q000032:analysis
chemical_list: D001786:Blood Glucose; D005169:Factor VIII; D005338:Fibrin Fibrinogen Degradation Products; D006442:Glycated Hemoglobin; D015849:Plasminogen Inactivators; D010959:Tissue Plasminogen Activator; D014568:Urokinase-Type Plasminogen Activator; D014841:von Willebrand Factor