Abstract

The aim of this study was to investigate the expression of cardiac strain and damage in 18 male marathoners with average age of 52.8±5.0 years running at a 308 km ultra-marathon. Blood samples were collected at pre-race, 100 km, 200 km and 308 km check points for the analysis of cardiac muscle injury markers, creatine kinase (CK), creatine kinase–myocardial band (CK–MB), cardiac troponin I (cTnI) and cardiac muscle strain marker, N-terminal pro-brain natriuretic peptide (NT-proBNP). The CK levels increased 1127.2±507.9 IU/L, 5133.8±2492.7 IU/L and 4958.4±2087.9 IU/L at 100 km, 200 km and 308 km, respectively, compared to the pre-race levels. The CK–MB levels increased 20.2±11.2 ng/mL, 73.3±35.6 ng/mL and 68.6±42.6 ng/mL at 100, 200 and 308 km, respectively, compared to the pre-race levels. The CK–MB/CK ratio showed that the CK–MB mass index was within the normal range (<2.5%) at 100 km, 200 km and 308 km. The cTnI levels showed no significant difference in all check points. The NT-proBNP levels increased 146.55±92.7 pg/mL, 167.95±111.9 pg/mL and 241.23±121.2 pg/mL at 100, 200 and 308 km, respectively, compared to the pre-race levels. The normal CK–MB mass index (<5.0 ng/mL) and the absence of an increase in the cTnI levels during the 308 km ultra-marathon suggested that no myocardial injury despite an elevation in CK–MB. The increase in NT-proBNP levels probably resulted from continuous hemodynamic cardiac stress and represents a transient physiological myocardial protective response.

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