WHYTE, G. P., K. GEORGE, S. SHARMA, S. LUMLEY, P. GATES, K. PRASAD, and W. J. McKENNA. Cardiac fatigue following prolonged endurance exercise of differing distances. Med. Sci. Sports Exerc., Vol. 32, No. 6, pp. 1067-1072, 2000.
Purpose: Recent echocardiographic studies have reported cardiac dysfunction following ultra-endurance exercise in trained individuals. The duration of exercise required to elicit cardiac dysfunction and the mechanisms underlying this phenomenon have not been fully elucidated. The aim of the present study was to examine the presence of cardiac dysfunction following a half - Ironman and Ironman triathlon in trained individuals.
Methods: 14 male triathletes (age: 32 ± 5 yr; height: 180 ± 8 cm; body mass: 75 ± 9 kg) completed a half-Ironman triathlon. Following a 4-wk period, 10 of the original 14 triathletes completed an Ironman triathlon. All triathletes were assessed using ECG, echocardiography, and blood analysis pre-, immediately post-, and 48 h postrace for both distances.
Results: Echocardiographic results indicated diastolic and systolic left ventricular dysfunction, for both race distances, which were associated with altered relaxation characteristics and a reduced inotropic contractility, respectively. Following 48-h recovery, all echocardiographic measures were similar to resting values. Creatine kinase MB (CKMB) was significantly elevated immediately postrace for both distances; however, it accounted for less than 5% of the total CK value and in the presence of an elevated total CK and CKMM implied that the elevated CKMB was noncardiac in origin. Troponin-T, however, was significantly elevated immediately postrace for both distances and returned to normal following 48-h recovery indicating myocardial damage.
Conclusions: Ironman and half-Ironman competition resulted in reversible abnormalities in resting left ventricular diastolic and systolic function. Results suggest that myocardial damage may be, in part, responsible for cardiac dysfunction, although the mechanisms responsible for this cardiac damage remain to be fully elucidated.
Although the cardiovascular benefits of exercise are well established (13), it is recognized that the risk of death is transiently increased during an acute exercise bout in individuals with underlying pathology (1). Recent echocardiographic studies, however, have reported cardiac dysfunction following endurance exercise in the absence of underlying cardiovascular diseases, which has been attributed to cardiac fatigue (18). Previous echocardiographic studies have reported left ventricular diastolic an systolic dysfunction following ultra-endurance exercise in trained individuals (6,11). In contrast, Seals et al. (18) demonstrated cardiac fatigue following shorter duration endurance exercise (20-km running) in untrained individuals. The duration of exercise required to induce cardiac dysfunction in trained individuals remains to be fully elucidated.
Cardiac myocyte damage has been implicated in the observed cardiac fatigue due to the presence of humoral markers of myocardial intracellular origin. Niemela et al. (12) demonstrated significant increases in creatine kinase MB fraction (CKMB) following 24-h running, a finding supported by Douglas et al. (6) following an Ironman triathlon. These studies, however, have reported significant elevations in CKMB in the presence of a significantly elevated total creatine kinase (CK) and creatine kinase MM fraction (CKMM), with CKMB constituting less than 5% of the total CK value. Furthermore, CKMB remained elevated following 2-3 d of recovery in the presence of normal cardiac function. These findings suggest that this MB fraction is noncardiac in origin (12). Conclusions regarding the role of myocardial damage in the observed cardiac dysfunction following prolonged endurance exercise are difficult to draw as a result of the relative nonspecificity of cardiac enzymes used in previous studies. Recent advances in the identification of cardiac specific enzymes may, however, allow a more detailed examination of myocardial injury following prolonged endurance exercise.
Accordingly, the purpose of the present study was twofold. In the first instance, we examined the effects of exercise duration upon left ventricular function in young well-trained individuals following Ironman and half-Ironman triathlon competition. The secondary purpose was to investigate the presence of cardiac specific humoral biochemical markers indicative of potential cardiac myocyte damage.