KÖNIG, D., Y. O. SCHUMACHER, L. HEINRICH, A. SCHMID, A. BERG, and H.-H. DICKHUTH. Myocardial Stress after Competitive Exercise in Professional Road Cyclists. Med. Sci. Sports Exerc., Vol. 35, No. 10, pp. 1679–1683, 2003.
Purpose: Based on the determination of cardiac troponin (cTnT), brain natriuretic peptide (BNP), and echocardiographic measurements, recent investigations have reported myocardial damage and reversible cardiac dysfunction after prolonged endurance exercise in apparently healthy subjects. In the present study, we investigated the myocardial stress reaction in professional endurance athletes after strenuous competitive physical exercise.
Methods: Eleven highly trained male professional road cyclists (age 27 ± 4 yr; V̇O2peak 67 ± 5 mL·kg−1·min−1; training workload 34,000 ± 2,500 km·yr−1) were examined. The following parameters were determined before and after one stage of a 5-d professional cycling race: BNP, cTnT (third-generation assay that shows no cross reactivity with skeletal TnT), creatine kinase (CK), creatine kinase MB (CKMB), myoglobin (Myo), and urea. All participants were submitted to a careful cardiac examination including echocardiography and stress ECG.
Results: None of the athletes showed pathological findings in the cardiac examination. CK (P < 0.01), CKMB (P < 0.05), and Myo (P < 0.01) were increased after the race. Normal postexercise cTnT levels indicate that the increase in CK, CKMB, and Myo was of noncardiac origin. In contrast, BNP rose significantly from 47.5 ± 37.5 to 75.3 ± 55.3 pg·mL−1 (P < 0.01). Pre- and postexercise values of BNP as well as the individual exercise-induced increase in BNP were significantly correlated with age (R2 = 0.68, R2 = 0.66, and R2 = 0.58, respectively; P < 0.05).
Conclusion: Strenuous endurance exercise in professional road cyclists does not result in structural myocardial damage. The rise in BNP in older athletes may reflect a reversible, mainly diastolic left ventricular dysfunction. This needs to be confirmed by larger trials including different intensities, sports, and age groups.
The question whether strenuous endurance exercise is associated with structural or functional damage of the human heart is of utmost importance for physicians involved in the medical care and guidance of endurance athletes. The determination of cardiac Troponin T (cTnT) and brain natriuretic peptide (BNP) as indicators of myocardial damage (cTnT) and cardiac dysfunction (BNP) has reactivated the discussion about possible negative effects of prolonged, exhaustive exercise on the heart. In the past years, several studies have suggested myocardial damage after extreme endurance exercise due to increased postexercise levels of cTnT (2,4,11,15,18,20,28). This finding, however, could not be ascertained by other investigators (9,12,22). It has to be emphasized that most previous studies have applied cTnT assays of the first and second generation that show a considerable cross-reactivity with skeletal TnT. Therefore, the exercise-induced increase in TnT observed in these studies could well be derived from skeletal muscle cells (24,25). The highly cardiospecific third-generation cTnT assay does not show this cross-reactivity (7) and is thus most suitable for a clear differentiation between the cardiac and noncardiac origin of postexercise increases in creatine kinase (CK) and particularly creatine kinase MB (CKMB) (22). Skeletal muscle contains approximately 5% CKMB; this percentage can be higher in endurance trained athletes due to the larger amount of CKMB in slow-twitch fibers. Most recently, Shave et al. (23) have reported a slight increase in cTnT (third-generation assay) together with signs of reversible systolic and diastolic exercise-induced cardiac dysfunction. However, in all subjects, cTnT values were beyond the threshold indicating substantial myocardial damage. In addition, subjects investigated were relatively old (42 ± 11 yr), and both exercise intensity (Alpine Mountain Marathon) and duration (approximately 10 h) were extreme (23).
In the past years, BNP has turned out to be an excellent humoral marker for beginning or manifest cardiac dysfunction (13,14,21,26). This natriuretic peptide, mainly secreted from ventricular cells, has shown to be closely associated with increased left ventricular end diastolic pressure and impaired diastolic filling (1,6). Baseline levels of BNP and particularly the exercise-induced rise in BNP were proportional to the severeness of heart failure (10).
A marked increase in BNP has been described after a 100-km ultramarathon in apparently healthy athletes (18). In contrast, only small alterations in BNP were observed after symptom-limited bicycle exercise in healthy subjects (1,14,16,26). Recent echocardiographic investigations have shown a reversible diastolic and systolic dysfunction after long-lasting endurance events in trained individuals (20,28). It can be speculated that this exercise-induced myocardial dysfunction is pathogenetically responsible for an increase in BNP after such types of exercise.
Thus, there is a reasonable background to claim for more information regarding the exercise-induced myocardial stress reaction in athletes, particularly with the third-generation assay for cTnT. Moreover, different exercise intensities and durations have to be considered. Aside from the already mentioned problem regarding the cross-reactivity of the cTnT assay, an increase in postexercise cTnT levels or the marked rise in BNP were mostly observed after extreme ultra-endurance events (2,4,11,20,23,28). Although the authors reported that the majority of subjects investigated were well-trained endurance athletes, the question arises in how far any form of training can prepare the human organism and particularly the heart for such forms of exercise. In addition, some events took place under extreme environmental conditions (Hawaii Ironman triathlon (20)) or high altitude (Alpine bicycle ultramarathon (15,23)), thereby imposing additional cardiovascular stress.
In the present study, we investigated myocardial stress factors in highly trained professional road cyclists after long-lasting competitive endurance exercise. The hypothesis was that these athletes, training 34,000 ± 2,500 km·yr−1, would not show any form of myocardial damage or dysfunction because they were accustomed to this type of exercise.