From Healthy to Heart Failure in 24 Hours: Defining the upper limit of exercise induced cardiac fatigue

This study sought to investigate the cardiac consequences of undertaking 12- and 24-hours of intense cycling as part of two successful world record-setting attempts in a former professional ultra-endurance athlete (12-hour attempt: March 2017, aged 41 yrs; 24-hour attempt: March 2018, aged 42 years). The athlete was comprehensively evaluated prior to- and at several timepoints following both attempts using cardiac imaging (echocardiography, rest and exercise cardiac magnetic resonance imaging, CMR), cardiac biomarkers (B-type natriuretic peptide, BNP; cardiac troponin-I, cTnI) and clinical evaluation. Following the 12-hour attempt, the athlete was physically exhausted but demonstrated no signs of respiratory distress or heart failure. Immediately post-attempt, BNP (166 ng/L) and cTnI (64 ng/L) were moderately increased, while left- (LV) and right-ventricular (RV) strain (LV: -12.2%; RV: -13.4%) and ejection fraction (LV: 43% RV: 43%) were moderately reduced. However, all parameters recovered within 14-days of the attempt. Following the 24-hour attempt, the athlete was in acute respiratory distress and showed signs of acute pulmonary edema. This coincided with pronounced biomarker elevations (BNP: 561 ng/L; cTnI: 394 ng/L) and marked reductions in myocardial strain (LV: -14.2%; RV: -13.8%) and bi-ventricular ejection fraction (LV: 37%; RV: 32%). Cardiac function only partially recovered 18-days post-attempt but had completely normalized by 5-months post-attempt. Overall, these findings provide the most definitive illustration of an exercise dose threshold that resulted in acute heart failure in a highly trained endurance athlete. The absence of persistent myocardial injury highlights the resilience of the heart to acute stress.