Cardiac damage has recently been implicated in the aetiology of
“exercise induced cardiac dysfunction”. The humoral markers of
cardiac damage that have been utilised to date are not sufficiently
cardio-specific to investigate this hypothesis. The aim of the present study
was to examine cardiac function following prolonged exercise, and investigate
the contention of cardiac damage utilising a new highly cardio-specific marker.
Thirty-seven competitors in the 2-day Lowe Alpine Mountain Marathon 2000
volunteered for the study. Competitors were sub-divided into 2 groups. Group 1
(n = 11) were examined using echocardiography pre and post
the event, examining left ventricular diastolic and systolic function. Group 2
(n = 26) had venous blood samples drawn prior to the event
and immediately following day-1 and day-2. Blood samples were analysed for
total creatine kinase activity (CK), creatine kinase isoenzyme
MBmass (CK-MBmass), and cardiac troponin T.
Echocardiographic results indicated left ventricular diastolic and systolic
dysfunction following cessation of exercise. CK and CK-MBmass were
both elevated following day-1, and immediately following race completion.
Cardiac troponin T levels were below the 99th percentile
(0.01 µg/L) in all subjects prior to the event, following day-1
cTnT was elevated above 0.01 µg/L in 13 subjects, but returned to
below 0.01 µg/L following race completion on day-2. However, no
individual data reached clinical cut-off levels for acute myocardial infarction
(AMI) (0.1 µg/L). Two days arduous exercise over mountainous
terrain resulted in cardiac dysfunction, and significant skeletal muscular
degradation. The elevation of cTnT above the 99th percentile in the present
study is suggestive of minimal myocardial damage. The clinical significance of
and exact mechanism responsible for such damage remains to be elucidated.
Key words
cTnT - cardiac dysfunction - endurance exercise
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