P4425The exercise-induced troponin I elevation is highly correlated with power output during exercise in recreational cyclists with coronary atherosclerosis

Abstract

Abstract Background Following strenuous exercise there is an increase cardiac Troponins (cTn) elevation considered being a physiological response. During prolonged strenuous physical activity, high work-loads may induce demand myocardial ischemia due to an oxygen demand/supply mismatch in susceptible subjects, causing an excessive cTn elevation. Purpose This study aimed to assess the relationship between exercise-induced cTnI elevation and direct measurement of work performed during prolonged strenuous exercise in subjects with and without atherosclerotic CAD. Methods Work during a 91 km mountain bike race was quantified by Stages™ power meters. Power (Watt) and heart rate data were stored in Garmin™ Forerunner 935 monitors. Coronary computed tomography angiography was performed after the race. Blood pressure was measured 4 times during the race. Blood samples (hs-cTnI from Abbot Diagnostics) were obtained one day prior to the race and at 3 and 24 h after the race. Data are presented as mean±SD or median (25th and 75th percentile). Results 40 subjects (10 women) were included in the final analysis. 15 Participants (4 women) had atherosclerosis, none had obstructive CAD. These participants were significantly older (55±8 years vs. 46±8 years p=0.007) and had higher training volumes (METS: 69 (64–102) hrs/week) compared with normal subjects (METS: 51 (33–88) hrs/week) (p=0.03). Baseline cTnI was higher (p=0.04) in the atherosclerotic group (4.5 (3.4–8.8) ng/L) compared with normals (2.6 (1.6–4.8) ng/L). There were no differences in baseline blood pressure, peak VO2 max, heart rate or BMI. There was no significant difference in race duration between normals (3.9 (3.5–4.5) hrs) and subjects with atherosclerosis (4.1 (3.6–4.5) hrs). During the race there were no differences in peak power or peak Watt/kg. cTnI increased after the race in all participants, but there were no differences between groups: 3h: atherosclerosis: 89 (27–131) ng/L vs. normal 77 (36–104) ng/L, 24h: atherosclerosis: 13 (6.3–23.7) ng/L vs. normal: 17 (12–37) ng/L. There were no significant difference between the groups in average power during the race: atherosclerosis: 167±50 Watt vs. 174 (±50) Watt or ratio: 2.0±0.49 Watt/kg vs 2.2±0.58 Watt/kg during the race. Maximal systolic and diastolic blood pressures during the race were higher (p=0.002) in the atherosclerotic group: SBP: 241±14 mmHg vs. 219±26 mmHg, DBP: 107±8 vs 95±8 mmHg. In atherosclerotic subjects cTnI both at 3h and 24 h were highly correlated (p<0.001) with Watt/kg ratio during the race in contrast to no correlations in the normal group (Figure). Conclusions Our findings suggest that the presence of coronary atherosclerosis, even in the absences of significant stenosis, alters the relationship between workload and the troponin response. This indicates different release kinetics in exercise-induced cTn in participants with and without CAD, with prolonged elevation in cTnI in CAD subjects exceeding the highest work-intensities. Acknowledgement/Funding Grant Western Norway Health service, Grant ConocoPhillips, Grant Simon Fougner Hartmanns Familyfund