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First published online on January 23, 2006.
Experimental Physiology (2006)
DOI: 10.1113/expphysiol.2005.032631
© The Physiological Society 2006

A more recent version of this article appeared on May 1, 2006
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Received October 19, 2005
Revised December 12, 2005
Accepted after revision January 13, 2006


Human, Environmental & Exercise [250]

Novel application of flow propagation velocity and ischaemia modified albumin in analysis of post-exercise cardiac function

Natalie Middleton 1*, Rob Shave 1, Keith George 2, Gregory Whyte 3, Jan Forster 4, David Oxborough 4, David Gaze 5, Paul Collinson 5

1 Brunel University
2 Liverpool John Moores University
3 English Institute of Sport
4 Leeds General Infirmary
5 St Georges Healthcare NHS Trust

* To whom correspondence should be addressed. E-mail: natalie.middleton{at}brunel.ac.uk.


   Abstract
The present study employed novel echocardiographic tools and cardiac markers to obtain a greater understanding of the aetiology and time course of altered cardiac function and cardiac damage following prolonged exercise, and in particular, the possible role of transient ischaemia within these phenomena. Fourteen runners in the 2004 London Marathon were assessed pre-, post-,1 h post-, and 24 h post-completion of the race. Left ventricular function was examined echocardiographically using 2-D, M-mode, tissue Doppler imaging and flow propagation velocity (Vp). Venous blood samples were analysed for N-terminal pro-B-type natriuretic peptide (proBNP), cardiac troponin T (cTnT), and ischaemia-modified albumin (IMA). Left ventricular (LV) diastolic filling was altered on completion of the race indicated by significant decreases in mean E':A' and Vp (1.82 ± 0.9 to 1.32 ± 0.32, and 67.5 ± 9.3 cm·sec-1 to 60.2 ± 8.2 cm·sec-1 respectively, P < 0.05), accompanied by an increase in proBNP (21.6 ± 11 pg/L to 47.08 ± 19.5 pg/L, P < 0.05). The observed reduction in LV diastolic filling following completion of a marathon, unrelated to changes in heart rate or loading parameters, indicate an intrinsically mediated change in diastolic filling. Exercise-induced elevations in cTnT in nine individuals (range: 0.023 - 0.37 µg/L) were indicative of minor cardiac damage. A significant reduction in IMA was observed after the marathon (63.68 ± 9.83 KU/L to 44.94 ± 16.13 KU/L, P < 0.05), unrelated to the alterations in cardiac function, proBNP, or cTnT. The absence of an elevation in IMA suggests that exercise-induced myocardial ischaemia did not occur, and therefore could not explain the changes in cardiac function or biomarkers. Future studies in this area should investigate alternative diagnostic tools for the detection of transient ischaemia, and other potential mechanisms in order to extend the understanding of this phenomenon.

Key Words: Cardiac muscle, Exercise, Ischaemia




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