Abstract
ObjectivesThe effects of ultra-distance on cardiac remodeling and fibrosis are unclear. Moreover, there are no data reporting the kinetics of cardiac alterations throughout the event and during recovery. Our aim was to investigate the kinetics of biological markers including new cardiac fibrosis biomarkers suppression of tumorigenicity 2 (ST2) and galectin-3 (Gal-3) during and after an extreme mountain ultramarathon.MethodsFifty experienced runners participating in one of the most challenging mountain ultramarathons (330 km, D+ 25,000 m) were enrolled in our study. Blood samples were collected at four time points: before (Pre-), at 148 km (Mid-), at the finish line (Post-), and 3 days after the recovery period (Recov-).ResultsThe cardiac fibrosis biomarkers (ST2 and Gal-3) increased from Pre- to Mid-. During the second half, ST2 remained higher than pre-values as opposed to Gal-3. Necrosis, ischemia, and myocyte injury biomarkers increased until Mid- then decreased but remained higher at Recov- than Pre-values. Oxidative stress appeared at Mid-. Lipid peroxides remained higher at Recov- compared to Pre-. The maximal value in most of these biomarkers was observed at Mid- and not at Post-.ConclusionsThe present study supports biphasic kinetics of cardiac fibrosis biomarkers, with a relative recovery during the second half of the event that seems specific to this extreme event. Overall, performing at such an extreme ultramarathon seems less deleterious for the heart than shorter events.
Highlights
Cardiovascular incidents during physical activity known as “sudden cardiac death” (SCD) [1] are rare but can be associated with right ventricular dysfunction, arrhythmia, or dysplasia [2, 3]
It is assumed that if at rest under normal conditions, the Cardiac and Fibrosis Biomarkers in Ultramarathon values of these biomarkers are higher than the cut-off limits; the subject presents an acute risk of developing cardiovascular disease [4]
We found a significant increase for hsTnT (165 ± 136%), heart-fatty acid-binding protein (HFABP) (1,815 ± 2,245%), creatine kinase (CK) (8,760 ± 9,323%), CKMB (3,890 ± 3,982%), and MYO (5,203 ± 6,128%) from Preto Mid
Summary
Cardiovascular incidents during physical activity known as “sudden cardiac death” (SCD) [1] are rare but can be associated with right ventricular dysfunction, arrhythmia, or dysplasia [2, 3]. It is assumed that if at rest under normal conditions, the Cardiac and Fibrosis Biomarkers in Ultramarathon values of these biomarkers are higher than the cut-off limits; the subject presents an acute risk of developing cardiovascular disease [4]. A non-optimal level of physical activity is among the SCD risk factors for athletes. There is vigorous debate on a potential ceiling, where above a maximal volume of exercise, there is an increased incidence of SCD [5, 6]. One way to explore how extreme exercise loads may affect SCD is to assess ultraendurance athletes [7]. In recent years, ultra-endurance events have become increasingly popular [8], and so, there is an emerging clinical urgency to clarify any relationship between exercise volume and SCD
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
