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Published on: February 9, 2016
Cardiovascular consequences of completing a 160-km ultramarathon
Jessica M Scott1, Ben T A Esch, Rob Shave
1Cardiovascular Physiology and Rehabilitation Laboratory, 6108 Thunderbird Blvd., University of British Columbia,Vancouver, BC, Canada. jmscott@interchange.ubc.ca
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 x L, 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.
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