title: Cardiac troponin T release and inflammation demonstrated in marathon runners.
abstract: BACKGROUND
  As shown on the basis of highly sensitive assays, cardiac troponin release is now observed after physiological heart stress and in mild heart pathologies: both are [corrected] considered unrelated to the irreversible cardiac alteration that is typically the source of release. Transitory cardiac membrane leakage was suggested as the basis. In our view, mild inflammation may drive this type of cardiac troponin release. To verify this hypothesis, marathon runners who demonstrated post-run inflammation were used as a model to correlate cTnT release and inflammation intensity.
  
  
  METHODS
  In 78 male marathon runners who participated in the BERLIN-MARATHON 2006, cardiac troponin T (cTnT) was monitored [corrected] at three time points (pre-race, post-race, and after two weeks of rest). [corrected] Measurements were done with the highly sensitive assay (hs cTnT assay) and the conventional fourth-generation cTnT assay for comparison. Concurrently, [corrected] the inflammation markers (leukocyte and neutrophil counts, CRP, IL-6) were measured.
  
  
  RESULTS
  Pre-race, the fourth-generation assay failed to demonstrate cTnT positivity (> test specific LLD). In contrast, with the [corrected] use of the highly sensitive assay, 28% of the participants were positive for cTnT (> LLD of hs cTnT assay). Post-race, cTnT as measured with the fourth-generation assay was observed to be detectable in 43% of the runners (> LLD = 99(th) percentile cut off), but all runners had detectable cTnT values (> LLD) when measured with the highly sensitive assay. Even in 94% of these cTnT-positive runners, the value exceeded the 99(th) percentile cut off determined for the highly sensitive assay (13 ng/L). cTnT release correlated significantly with inflammation intensity. Faster runners demonstrated significantly stronger cTnT releases and inflammation signs.
  
  
  CONCLUSIONS
  As demonstrated after physiological heart stress such as marathon running, transitory inflammation is evidently one of the events contributing to the cardiac troponin release under conditions suggested as unrelated to irreversible cardiac alteration.
authors.affiliation: Medizinische Klinik (Kardiologie), Charité--Universitätsmedizin Berlin, Berlin, Germany.
authors.forename: Silvia Gilka Munzoz
authors.initials: SG
authors.lastname: Saravia
authors.forename: Fabian
authors.initials: F
authors.lastname: Knebel
authors.forename: Sabrina
authors.initials: S
authors.lastname: Schroeckh
authors.forename: Reinhard
authors.initials: R
authors.lastname: Ziebig
authors.forename: Andreas
authors.initials: A
authors.lastname: Lun
authors.forename: Andreas
authors.initials: A
authors.lastname: Weimann
authors.forename: Annekathrin
authors.initials: A
authors.lastname: Haberland
authors.forename: Adrian C
authors.initials: AC
authors.lastname: Borges
authors.forename: Ingolf
authors.initials: I
authors.lastname: Schimke
mesh_terms: D001249:Asthma / Q000097:blood / Q000453:epidemiology; D056352:Athletes; D001265:Athletic Injuries / Q000097:blood*; D001794:Blood Pressure; D006339:Heart Rate; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000453:epidemiology; D007249:Inflammation / Q000097:blood / Q000209:etiology*; D008297:Male; D012420:Running / Q000502:physiology*; D012680:Sensitivity and Specificity; D020107:Troponin T / Q000097:blood*
chemical_list: D020107:Troponin T