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2011 Publications

Antioxidant supplementation does not attenuate exercise-induced cardiac troponin Howatson G, Goodall S, Hill J, Brouner J, Gaze D, McHugh M, Shave R. - last modified 2013-07-29 09:53
Int J Cardiol. 2011 Oct 6;152(1):101-2. doi: 10.1016/j.ijcard.2011.07.006. Epub 2011 Aug 3.


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 [4–6]. 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 associatedwith prolonged exercisemay damage the

cardiomyocyte membrane, resulting in cTn release from the cytosol.

Antioxidant supplementation has been shown to attenuate oxidative

stress, in!ammation 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