Myocardial damages and left and right ventricular strains after an extreme mountain ultra-long duration exercise
Résumé
Running a marathon or a long-distance triathlon [1–3] induces transient ventricular dysfunctions associated in some subjects with an increase in cardiac troponin I (cTnI), a biomarker of myocardial damages [1,2,4]. Ultra-long duration exercise (ULDE, i.e. N24 h) is getting more and more popular. However, little information is available about the potential cardiovascular alterations induced by such race. The present study described for the first time ULDE-induced acute cardiovascular perturbations through simultaneous 2D-strain echocardiography, cTnI and blood and plasma volume evaluations. Twenty-one experienced ultramarathon male runners (age: 40±8 yr) participated in the Ultra-Trail du Mont-Blanc (UTMB®), a 166-km race with 9600 m of positive altitude change across France, Italy and Switzer-land (race duration: 38 ± 5 h). The protocol was part of a larger experiment [5,6] and was approved by the local Ethics Committee. All subjects gave written informed consent. Heart rate (HR) was continuously monitored during the race (Garmin Forerunner-310XT, Olathe, USA). Before and after the race, left and right ventricular (LV and RV, respectively) evaluations included standard echocardiography, tissue Doppler imaging and 2D-strain echocardiogra-phy (Vivid Q, GE-Healthcare, Horten, Norway) as previously described [7]. RV longitudinal strains (S) and strain rates (SR) were assessed on the free wall, from an apical 4-chambers view. CTnI were analyzed from peripheral venous blood samples before and immediately after the race [4]. The conventional upper cutoff level of normal and acute myocardial infarction risk (i.e. 0.03 μg/L) [4] was used to identify subjects with elevated cTnI. Blood (BV) and plasma (PV) volumes were assessed by a carbon monoxide re-breathing method [6]. Data were analyzed using one-way repeated measures analysis of variance. In athletes with elevated cTnI (n=7), Wilcoxon signed rank tests were used to compare pre and post values. Regression analysis between finishing time and pre-post changes for echocardiographic and biochemical data were examined using Pearson correlations. Data are expressed as mean±standard deviation and statistical significance was assumed if Pb 0.05. HR decreased regularly during the race so that first and second half of the race were run respectively at 59% and 39% of the reserve HR (mean : 117 ± 7 bpm). After the race, cTnI were significantly increased (from 0.010 ±0.001 to 0.038 ± 0.055 μg/L pre-post race) and seven of the twenty-one athletes (including the fastest runners of the study) had increased cTnI above the cutoff level of myocardial infarction risk. PV and BV were higher after the ULDE (+20% and +12%, respectively) [6], but no significant correlations were found with changes in LV and RV functional parameters. LV global diastolic (i.e. Peak E and Peak A velocities) and systolic functions (i.e. ejection fraction) were respectively enhanced and unchanged after the race (Table 1). LV S did not change post-race, except radial apical S which was increased. LV longitudinal and apical radial systolic and diastolic SR were higher post-race. Similar results were obtained on all parameters of the LV on the seven athletes with elevated cTnI. Concerning RV data (Table 2), RV annular end-diastolic diameter, RA end-diastolic area and peak E m recorded at the free wall level were increased post-race. The increase in RA end-diastolic area was positively correlated with finishing times (P b 0.05), the fastest participants demonstrating the highest increases. Longitudinal S and systolic and diastolic SR were unchanged post-race and fractional area shortening (FAC) tended to decrease. Interestingly, when considering only the athletes with elevated cTnI, results indicated higher RV basal