Cardiovascular Consequences of Completing a 160-km Ultramarathon


Medicine & Science in Sports & Exercise: January 2009 - Volume 41 - Issue 1 - pp 25-33
doi: 10.1249/MSS.0b013e31818313ff
Clinical Sciences

Purposes: To comprehensively investigate the cardiovascular consequences of a 160-km ultramarathon using traditional echocardiography, speckle tracking imaging, cardiac biomarkers, and heart rate variability (HRV) and to examine the relationship between the changes in these variables.

Methods: We examined athletes before an ultramarathon and reassessed all finishers immediately after the race. Left ventricular (LV) systolic (ejection fraction [EF], systolic blood pressure/end-systolic volume [SBP/ESV] ratio) and diastolic (ratio of early [E] to late [A], filling E:A) measurements were assessed using traditional echocardiography, whereas myocardial peak strain and strain rate were analyzed using speckle tracking. Cardiac biomarkers measured were cardiac troponin T (cTnT) and N-terminal pro-brain natriuretic peptide (NT-pro-BNP). HRV indices were assessed using standard frequency and time domain measures.

Results: Twenty-five athletes successfully completed the race (25.5 ± 3.2 h). Significant pre- to postrace changes in EF (66.8 ± 3.8 to 61.2 ± 4.0 %, P < 0.05) and E:A ratio (1.62 ± 0.37 to 1.35 ± 0.33, P < 0.05) were reported. Peak strain was significantly decreased in all planes, with the largest reduction occurring circumferentially. NT-pro-BNP concentrations increased significantly (28 ± 17.1 vs 795 ± 823 ng·L−1, P < 0.05), whereas postrace cTnT were elevated in just five athletes (20%). No significant alterations in HRV were noted postrace. Reductions in LV function were not significantly associated with changes in cardiac biomarkers and/or HRV.

Conclusions: Although the stress of an ultramarathon resulted in a mild reduction in LV function and biomarker release, the mechanisms behind such consequences remain unknown. It is likely that factors other than myocardial damage or strong vagal reactivation contributed to postexercise decreases in LV function after an ultramarathon.

1University of British Columbia, Vancouver, BC, CANADA; 2Brunel University, Uxbridge, Middlesex, UNITED KINGDOM; 3St. George's Hospital, London, UNITED KINGDOM; and 4Liverpool John Moores University, Liverpool, UNITED KINGDOM

Address for correspondence: Jessica M. Scott, MSc, Cardiovascular Physiology and Rehabilitation Laboratory, Rm. 128, Unit II Osborne Centre, 6108 Thunderbird Blvd., University of British Columbia, Vancouver, BC, Canada V6T 1Z3; E-mail:

Submitted for publication February 2008.

Accepted for publication June 2008.

© 2009 American College of Sports Medicine