SHAVE, R., E. DAWSON, G. WHYTE, K. GEORGE, D. BALL, P. COLLINSON, and D. GAZE. The cardiospecificity of the third-generation cTnT assay after exercise-induced muscle damage. Med. Sci. Sports Exerc., Vol. 34, No. 4, pp. 651–654, 2002.
Purpose: The purpose of the present study was to examine the cardiospecificity of cTnI and the new third-generation cTnT assay, in the presence of exercise-induced muscle damage in highly trained individuals, and to examine the impact of a maximal-ramping treadmill test on cardiac function.
Methods: Eight highly trained male triathletes (mean ± SD; age: 29 ± 9 yr; height: 1.79 ± 0.10 m; body mass: 77 ± 10 kg; V̇O2max: 67.4 ± 6.3 mL·kg−1·min−1) completed two bouts of exercise. On the first occasion, subjects completed a maximal-ramping treadmill test. On a separate occasion, the subjects completed 30 min of downhill running (15% gradient) at a speed equivalent to 70% of maximal running velocity attained during the maximal-ramping treadmill test. All subjects were assessed using ECG, echocardiography, and blood analysis. Measurements were taken at rest, immediately after, and 48 h postexercise for each bout of exercise. Echocardiographic analysis was used to determine left ventricular systolic and diastolic function. Blood samples were analyzed for markers of myocyte damage.
Results: Echocardiographic results indicated normal left ventricular function before and after both exercise bouts. Total CK and CKMB were significantly elevated 48 h after the downhill run. cTnT and cTnI were not elevated at any stage of the study.
Conclusions: Neither the maximal-ramping treadmill test nor the 30-min downhill run produced cardiac dysfunction or myocardial damage in young, healthy trained subjects. The elevated total CK and CKMB within the downhill study are noncardiac in origin as demonstrated by the lack of cTnT and cTnI. The cTnI and new third-generation cTnT assays may be used to detect cardiac damage in the presence of elevated total CK and CKMB associated with exercise-induced skeletal muscle damage.
British Olympic Medical Centre, Northwick Park, Harrow, London, UNITED KINGDOM; Department of Sports Science, Manchester Metropolitan University, Alsager Campus, Alsager, UNITED KINGDOM; and Department of Chemical Pathology, St. George’s Hospital Medical School, London, UNITED KINGDOM
Submitted for publication October 2000.
Accepted for publication July 2001.