|Authors||Howatson, G., Goodall, S., Hill, J., Brouner, J., Gaze, D.C., McHugh, J and Shave, R.|
Clinically, cardiac troponins (cTn) are used as sensitive markers of cardiomyocyte damage [ 1 , 2 ] with any elevation in cTn being related to poor prognosis [ 3 ]. Recently, however, exercise has also been shown to stimulate the release of cTn [ 4 , 5 , 6 ]. The mechanism responsible for exercise-induced cTn release is not known, and is currently a matter of debate [ 7 ]. Notwithstanding this, it has been proposed, due to the relatively low post-exercise cTn concentrations and its rapid clearance, that cTn is likely released from the cytosolic pool and not from the breakdown of contractile apparatus. Previous authors [ 8 ] have suggested that oxidative stress associated with prolonged exercise may damage the cardiomyocyte membrane, resulting in cTn release from the cytosol. Antioxidant supplementation has been shown to attenuate oxidative stress, inflammation and muscle damage indices following strenuous exercise [ 9 ]; therefore, if post-exercise cTn release is related to cardiomyocyte membrane damage we hypothesised that antioxidant supplementation would reduce cTn release following marathon running.