title: Relationship between Inflammatory Cytokines and Indices of Cardiac Dysfunction following Intense Endurance Exercise.
abstract: OBJECTIVE
  Pro-inflammatory cytokines have been noted to increase following exercise but their relationship to exercise-induced cardiac dysfunction has not previously been investigated. We sought to evaluate whether exercise-induced cardiac dysfunction was associated with increases in cytokines, particularly the pro-inflammatory cytokines IL-1β, IL-12p70 and TNFα, which have been most implicated in cardiac pathology.
  
  
  METHODS
  40 well-trained endurance athletes underwent evaluation prior to and immediately following one of four endurance sporting events ranging from 3 to 11 hours duration. Cytokines (IL-1β, IL-6, IL-8, IL-10, IL-12p70 and TNFα) were analyzed by flow cytometry from serum samples collected within 50 minutes of race completion. Cardiac troponin (cTnI) and B-type natriuretic peptide were combined with an echocardiographic assessment of cardiac function, and a composite of cTnI > 0.04 μg/L, BNP increase > 10 ng/L and a decrease in right ventricular ejection (RVEF) > 10% were prospectively defined as evidence of myocardial dysfunction.
  
  
  RESULTS
  Relative to baseline, IL-6 IL-8 and IL-10 increased 8.5-, 2.9-, and 7.1-fold, respectively, P<0.0001. Thirty-one (78%), 19 (48%) and 18 (45%) of the athletes met the pre-specified criteria for significant cTnI, BNP and RVEF changes, respectively. TNFα, IL-12p70 were univariate predictors of ΔRVEF and ΔBNP whilst none of the anti-inflammatory cytokines were significantly associated with these measures. Ten athletes (25%, all athletes competing in the endurance event of longest duration) met criteria for exercise-induced myocardial dysfunction. In these 10 athletes with myocardial dysfunction, as compared to those without, there was significantly greater post-race expression of the pro-inflammatory cytokines IL-12p70 (8.1±3.8 pg/ml vs. 2.5±2.6 pg/ml, P<0.0001) and TNFα (6.5±3.1 pg/ml vs. 2.0±2.5 pg/ml, P<0.0001).
  
  
  CONCLUSIONS
  Cardiac dysfunction following intense endurance exercise was associated with increased expression of pro-inflammatory cytokines. This does not prove a causal relationship but provides rationale for further investigations into whether inflammation mediates exercise-induced myocardial dysfunction.
authors.affiliation: Baker IDI Heart and Diabetes Institute, Melbourne, Australia; St Vincent's Hospital Melbourne, Fitzroy, Australia; University Hospitals Leuven, KU Leuven, Belgium.
authors.forename: Andre
authors.initials: A
authors.lastname: La Gerche
authors.affiliation: University of Queensland, and Princess Alexandra Hospital, Brisbane, Australia.
authors.forename: Warrick J
authors.initials: WJ
authors.lastname: Inder
authors.affiliation: St Vincent's Hospital Melbourne, Fitzroy, Australia; St Vincent's Department of Medicine, University of Melbourne, Fitzroy, Australia.
authors.forename: Timothy J
authors.initials: TJ
authors.lastname: Roberts
authors.affiliation: St Vincent's Hospital Melbourne, Fitzroy, Australia; St Vincent's Department of Medicine, University of Melbourne, Fitzroy, Australia.
authors.forename: Maria J
authors.initials: MJ
authors.lastname: Brosnan
authors.affiliation: Hasselt University and Heart Center, Jessa Hospital, Hasselt, Belgium.
authors.forename: Hein
authors.initials: H
authors.lastname: Heidbuchel
authors.affiliation: St Vincent's Hospital Melbourne, Fitzroy, Australia; St Vincent's Department of Medicine, University of Melbourne, Fitzroy, Australia.
authors.forename: David L
authors.initials: DL
authors.lastname: Prior
mesh_terms: D000328:Adult; D056352:Athletes; D015415:Biomarkers / Q000097:blood; D001772:Blood Cell Count; D016207:Cytokines / Q000097:blood*; D003710:Demography; D015444:Exercise; D006321:Heart / Q000503:physiopathology*; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism*; D008297:Male; D009206:Myocardium / Q000473:pathology; D010807:Physical Endurance; D013318:Stroke Volume
chemical_list: D015415:Biomarkers; D016207:Cytokines; D018836:Inflammation Mediators