Key result
Marathon running significantly increased cTnI and NT-proBNP in all runners, with marathoners having exercise-induced hypertension showing a greater increase than normotensive controls.
Why the study?
Does marathon running cause greater increases in cardiac markers and endothelin-1 in athletes with exercise-induced hypertension compared to normotensive controls?
Observational (n=20)
Does marathon running cause greater increases in cardiac markers and endothelin-1 in athletes with exercise-induced hypertension compared to normotensive controls?
Marathon running induces a greater increase in cardiac biomarkers (cTnI and NT-proBNP) in athletes with exercise-induced hypertension compared to normotensive controls, indicating a higher myocardial burden.
May indicate higher myocardial burden in exercise-induced hypertension; hypothesis-generating and should not yet change practice.
The aim of the present study was to determine the changes in cardiac makers and endothelin-1 (ET-1) in marathoners with exercise induced hypertension compared to normotensive controls before and after running a marathon. Among a total of 70 volunteers, 10 marathoners with systolic blood pressure (SBP) greater than 210 mmHg during a treadmill exercise stress test were selected as an exercise-induced hypertension group (EIH) and 10 marathoners with normal SBP were selected as a control group (CON). Blood was collected from all volunteers 2 h before and immediately after a marathon: creatinine kinase (CK), CK-MB, cardiac tropoin-I (cTnI), N-terminal pro-brain natriuretic peptide (NT-proBNP), and endothelin-1(ET-1). Cardiac markers, CK, CK-MB, and CK-MB/CK ratio significantly increased in both EIH and CON; significance was not observed between the groups. Significant increases were not observed in high sensitive-C reactive protein (hs-CRP) after the race nor between the groups. Significant increases in cTnI and NT-proBNP were observed after the race in both groups. In addition, EIH showed greater increase than CON after the race. In conclusion, increased vascular tone in EIH during a marathon increased blood pressure and myocardial burden which in turn increased myocardial cell membrane permeability to further increase myocardial tension to the point of cTnI release.
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Kim et al. (2013) conducted an observational in Exercise-induced hypertension (n=20). Marathon running vs. Normotensive marathoners was evaluated on Changes in cardiac markers (CK, CK-MB, cTnI, NT-proBNP) and endothelin-1 (ET-1). Marathon running significantly increased cTnI and NT-proBNP in all runners, with marathoners having exercise-induced hypertension showing a greater increase than normotensive controls.