Impact of marathon running on cardiac structure and function in recreational runners

The present study examined the relationship between LV (left ventricular) function, markers of cardiac-specific damage and markers of oxidative stress in recreational runners following a marathon. Runners (n=52; 43 male and nine female; age, 35±10 years; height, 1.74±0.08 m; body mass, 75.9±8.9 kg) were assessed pre- and immediately post-marathon. LV function was assessed using standard M-mode two-dimensional Doppler echocardiography and TDI (tissue-Doppler imaging) echocardiography. Serum was analysed for cTnT (cardiac troponin-T), TEAC (Trolox equivalent antioxidant capacity; a measure of total antioxidant capacity), MDA (malondealdehyde) and 4-HNE (4-hydroxynonenal). A strong relationship was observed between standard and TDI echocardiography for all functional measures. Diastolic function was altered post-marathon characterized by a reduction in E (peak early diastolic filling: 0.79±0.11 compared with 0.64±0.16 cm/s; P<0.001), an increase in A (peak late diastolic filling: 0.48±0.11 compared with 0.60±0.12 cm/s; P<0.001) and a resultant decrease in E/A (ratio of E to A; 1.71±0.48 compared with 1.10±0.31; P<0.001). Ejection fraction remained unchanged post-marathon. Thirty-two runners presented with cTnT values above the lower limit of detection for the assay (0.01 μg/l), and 20 runners presented post-marathon with cTnT values above the acute myocardial infarction cut-off value (0.05 μg/l). No significant correlations were observed between cTnT and any functional measurements. MDA (2.90±1.58 compared with 3.59±1.47 μmol/l) and TEAC (1.80±0.12 compared with 1.89±0.21 mmol/l) were significantly increased post-marathon, but were unrelated to changes in function or cTnT. In conclusion, the present study demonstrated a reduction in diastolic function and widespread evidence of minimal cardiac damage following a marathon in recreational runners. The mechanism(s) underpinning the altered function and appearance of cTnT appear unrelated to reactive oxygen species.