Over the years, researchers have investigated to describe the changes in biomarkers of cardiac damage during recovery from strenuous and prolonged exercise events [1,2,3,4,5,6,7]. A triathlon is an endurance sport-event, which includes swimming, cycling and running with various distances. Olympic triathlon involving swim 1.5 km, bike 40 km, and run 10 km (total 51.5 km) and Ironman triathlon involving swim 3.8 km, cycle 180 km, and marathon 42 km (total 226 km) have recently become also popular in Korea.

Exercise-mediated physical treatment has attracted much interest in recent years. In particular, swimming and cycling are considered as effective exercise mode for patients with muscular and cardiovascular diseases [8]. However, triathletes may experience a variety of medical problems during training and competition, including hyponatremia [5], hemolysis [9], immunosuppression [10], and muscle damage [11].

Exercise-induced skeletal muscle damage is the most interesting adverse consequence in triathlon competition which is related with exercise performance and cardiac health [4,12,13]. Previous studies have found that serum creatine kinase(CK), hydroxybutyrate dehydrogenase(HBD), and lactate dehydrogenase (LDH) are traditional markers of myocardial damage in both pathological and physiological conditions [14,15]. However, recent studies have suggested that CK-MB isoenzyme, myoglobin, and cTnT are better markers of exercise-induced myocardial injury. Creatine isoenzymes (CK-MB, CK-MM) are markers of muscle and liver damage. Troponins(cTnI, cTnT) are markers that are used in a clinical setting to detect minor cardiac damage [11].

It has been demonstrated that strenuous, long-lasting exercise is associated with an increase in biomarkers of myocardial damage such as cTnT even in healthy trained subjects without signs of myocardial disease [13,16]. The reason why apparently healthy subjects exhibit increased concentrations of cTnT is not yet fully understood. The amounts and release time of plasma biochemical markers of muscle damage rely on the type, intensity, level of exercise, and the time of recovery [17].

Although previous studies revealed that increased level of the biochemical indexes of muscle injury following strenuous exercise, especially marathon running [11,15,17,18] or ultra-triathlon [7] such as Ironman triathlon, less is revealed about the acute changes of these indexes in elite and non-elite triathletes following Olympic triathlon competition.

The different performance level in athlete and the different distance of competition may also be valuable, as a multi-sport events such as triathlon may cause more cardiac muscle damage compared to the individual events such as swimming, cycling and running, and therefore, the comparisons between these different events may be inappropriate.

Accordingly, the aim of present study was to examine the effects of Olympic triathlon on specific cardiac biomarkers in elite and non-elite triathletes following a triathlon competition.

All the athletes completed Olympic triathlon event successfully. Table 2 shows biomarkers of myocardial damage before, immediately, 2 hours and 7 days after finishing the race.

There were no significant differences between the groups in any variable at baseline. CK-MB, CK, myoglobin, and LDH were significantly increased in both groups immediately and 2 hours after the event (p<.05). CK, CK-MB, and myoglobin were completely recovered after the post 7 days (p>.05), whereas, Hct was significantly decreased 7 days after the performance in both groups (p<.05). LDH was significantly decreased 7 days after the performance in the EG (p<.05).

The cTnT was unchanged immediately after the triathlon race in both groups, but it was significantly increased 2 hours after the race in the EG (p<.05), but not in the NEG group. cTnT was also completely recovered 7 days after the race in both groups.

Hct was unchanged immediately after the triathlon race in both groups, but it was significantly decreased in both groups at 2 hours and 7 days after the race (p<.05). Hemoglobin was unchanged immediately after the triathlon race in both groups (p<.05), but it significantly decreased at 2 hours after the race in the NEG (p<.05), but not in the EG. Hemoglobin was recovered 7 days after the race in both groups.

Cardiac injury after strenuous physical exercise in healthy individuals is relatively well known, however the effect of Olympic triathlon on cardiac damage in elite and non-elite athletes has not been evaluated. In the present study, we found that cardiac damage occurs during a triathlon race and elite triathletes had more improvement than the non-elite triathletes. However, all cardiac damage markers return to normal range within 1 week.

Young athletes are widely regarded as a unique subgroup of healthy individuals. However, sudden death of young athletes was regarded as a mysterious and undefined syndrome [20]. Transient cardiac ventricular dysfunction or sudden cardiac death has been reported in male athletes participating in marathon racing [1,2,21,22]. Vigorous exercise is associated with a transient increase in risk of sudden cardiac death. For young athletes (12 to 35 years) participating in competitive sports, the total relative risk of sudden cardiac death is approximately 2.5 times higher than in nonathletes [22]. The incidence of sudden cardiac death in older athletes (>35 years old) is reportedly more frequent than in the young, with an estimated annual incidence of approximately 1:11,000 to 1:80,000 in men [21]. In cTnT change after marathon race, 55 (11%) among 482 participant had significant increases and young age (<30 years) were associated with elevated troponins [2].

Myocardial injury after strenuous exercise in healthy individuals is well indicated and may be the result of exercise-induced production of free radicals [23]. Muscle soreness results from skeletal muscle damage and prolonged and intense training induces a subsequent release of biochemical indexes, including CK-MB, CK, LDH and myoglobin [24,25]. One possible explanation for endurance performance is that less muscle activation would be needed to perform a task when a muscle is stronger, hence delaying fatigue [26]. In response to exercise, skeletal muscle is a highly adaptable tissue and capable of regeneration in response to injury. The adaptation of skeletal muscles is governed by three major processes: satellite cell activity, gene transcription, and protein translation. Exercise parameters such as intensity, duration or average energy expenditure increase typical markers of skeletal muscle damage. Previous study indicated that the post-training elevations of CK values are higher in elite athletes [27]. However, the significant increase in CK levels are usually found in non-trained than in trained subjects [28].

Myoglobin, in fact, is released from the injured tissue more rapidly, which explains an earlier peak in plasma and faster return to baseline levels than CK-MB, CK and LDH. In the present study, CK and myoglobin increased in both groups immediately and 2 hours after the race. We found that the transient increase in CK was higher in NEG than in the EG. However, despite the great severity of the triathlon, these results are comparable to the results observed in marathon runners [15]. This suggests that the release of these biochemical markers into the circulation may be stabilized in ultra-endurance events [18,29]. In previous studies CK and myoglobin have decreased after five days post-race in the Ironman triathlon, but were still significantly elevated compared to the levels observed immediately after the event [4]. However, in the present study revealed that CK, CK-MB, myoglobin and LDH level were completely recovered 7 days after the race.

The time of CK release into and clearance from plasma depends on the type, duration and level of training [29]. The peak levels of serum CK, which are about 2-fold above baseline, occurs 8 hours after exhaustive acute exercise. Increased CK levels after muscle damage induced by eccentric exercise are elevated between 2 and 7 days after exercise. Previous study indicated that CK-MB is a more sensitive indicator induced by myocardial damage than the level of CK itself activity, because it has a lower level and has a much narrow range [29].

It is known that CK-MB values are elevated during 4 to 6 hours, peak at 10 to 24 hours, and return to normal levels within 3 to 4 days after an acute myocardial infarction [25]. We found that CK-MB concentrations were also significantly increased in both groups immediately and 2 hours after the race. Although CK-MB is a more specific marker of myocardial necrosis, its specificity decreases in the presence of significant skeletal muscle damage. Therefore, CK-MB cannot be determined to the specific indicator of myocardial damage induced in athletes following olympic triathlon [25].

A reduction in left ventricular systolic and diastolic function subsequent to prolonged exercise in healthy humans, often called exercise-induced cardiac fatigue (EICF), has been reported in the literature [7,13,39]. If myocardial damage occurs with prolonged exercise such as marathon, cycling and triathlon, this would result in the release of myocardial cellular proteins into the general circulation, where they can be detected.

Several previous studies have indicated that the release of cardiac troponins as they are considered to be more specific markers of myocardial damage occurs after prolonged and strenuous endurance exercise [4,6,7,11,15,17,18]. However, there are some opposite results about the appearance of cardiac troponins. There is some evidence that intensive swimming for 5 hours could cause necrosis of myocardial cells [31]. Several other studies have reported no evidence of cardiac muscle damage after prolonged endurance exercise [31,32]. Although there is exercise-induced skeletal muscle damage shown by increased CK and CK-MB, cTnT was not increased and left ventricular function was unaffected [33]. In contrast, Leetmaa et al. reported that cTnT increased immediately, but decreased to normal limits within 12-24 hours post-triathlon race [34]. In the current study, we found that the cTnT remained unchanged immediately after the triathlon race in both groups, but it was significantly increased 2 hours after the race in the elite group. It appears that the high exercise intensity explains in part the myocardial injury, as race time is inversely associated with cTnT after a triathlon [35]. Troponin is a contractile protein and comprises 5 percent of muscle proteins. It has a key role in the regulation of the calcium mediated muscle contraction through an interaction with actin and myosin [36]. After myocardial damage, troponins released from cardiomyocytes are detectable in peripheral blood within 3~10 hours [27]. Myocardial damage could be induced by various factors, including coronary artery spasms, wall stress, increased stress on atherosclerotic plaques, ischemia, and strenuous exercise. The mechanism of cTnT release after exhaustive exercise and myocardial infarction may somewhat be different. A possible role of catecholamine-induced myocardial damage after triathlon has been proposed [33].

The physiologic stress imposed by the triathlon race resulted in increased CK, CK-MB, myoglobin and LDH levels in elite and non-elite male triathletes. CK, CK-MB, myoglobin and LDH are associated with exercise-induced skeletal muscle damage and cTnT may be used to find myocardial damage following triathlon race. But the mechanisms behind such altered cardiac damage after triathlon race are yet to be found.

In this study, although there is exercise-induced skeletal muscle damage shown by increased CK and CK-MB, cTnT was not increased in both groups immediately after the race. But there was the significant increase in cTnT after 2 hours in EG. We can suggest that it was due to the enormous exercise stress for high performance imposed in EG.

However, the main limitation of the present study is that we cannot absolutely sure that without the investigation of left ventricular function during triathlon. The underlying mechanisms responsible for the myocardial damage observed in the present study remain to be fully elucidated and warrant further investigation.

There are many mechanisms that contribute to an increased tissue oxygen supply during exercise. Generally, it was well known that training increase total Hb mass by stimulating erythropoiesis. The main function of erythrocytes is to transport the oxygen carrier, Hb. For the most part, Hb and Hct are associated with sports anemia. Previous study had reported that Hb and Hct values were increased immediately after Ironman triathlon, but these responses did not occur immediately after Olympic triathlon [37]. Hct increase during exercise due to a decrease in plasma volume when fluid replacement during exercise is insufficient [37]. In this study, Hb was unchanged immediately after the race in both groups, but it decreased at 2 hours after the race in the NEG. The reason for the different result of Hb between both groups at 2 hours after the race is that Hb was influenced by training status, which is probably one important reason for their high performance in endurance athletes.