over the years , researchers have investigated to describe the changes in biomarkers of cardiac damage during recovery from strenuous and prolonged exercise events .
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 .
however , triathletes may experience a variety of medical problems during training and competition , including hyponatremia , hemolysis , immunosuppression , and muscle damage .
exercise - induced skeletal muscle damage is the most interesting adverse consequence in triathlon competition which is related with exercise performance and cardiac health .
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 .
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 .
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 . 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 .
although previous studies revealed that increased level of the biochemical indexes of muscle injury following strenuous exercise , especially marathon running   or ultra - triathlon   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 .
the 15 participants who completed olympic triathlon were classified as well - trained national team triathletes ( elite group [ eg ] , n=7 ) or amateur non - elite triathletes ( non - elite group [ neg ] , n=8 ) .
none of the participants suffered from any acute or chronic disease , and reported medication intake , including antioxidants and nicotine abuse .
all participants agreed and signed an informed consent approved by the institutional human research ethics committee .
we have read and understood the ethical standards document and confirmed that our study meets the ethical standards ( dirb-201309-hr - r-005 ) .
subjects were permitted to drink and eat ad libitum during their performance and no particular conduct was given to participants .
three days before the race , baseline blood samples were collected after an overnight fasting ( 8 hours ) .
post race blood samples were collected in the supine position immediately , 2 hours , and 7 days following the triathlon .
ldh and total ck were evaluated by the modular system p ( roche diagnostics gmbh , germany ) .
cardiac troponin t ( ctnt ) , ck - mb and myoglobin were assayed by the elecsys 1010 ( roche ) .
although the detection limit for ctnt is 0.01 ng / ml , the recommended diagnostic threshold for myocardial damage is > 0.03 ng / ml . hemoglobin and hematocrit were measured on advia 120 ( bayer diagnostics , newbury , uk ) .
biochemical data were summarized and expressed as meansd . utilizing the statistical package spss ( version 15.0 )
, we analyzed the effects of triathlon race on groups and periods by two - way anova with repeated measures and the point of statistical significance was set at p<.05 .
the 15 participants who completed olympic triathlon were classified as well - trained national team triathletes ( elite group [ eg ] , n=7 ) or amateur non - elite triathletes ( non - elite group [ neg ] , n=8 ) .
none of the participants suffered from any acute or chronic disease , and reported medication intake , including antioxidants and nicotine abuse .
all participants agreed and signed an informed consent approved by the institutional human research ethics committee .
we have read and understood the ethical standards document and confirmed that our study meets the ethical standards ( dirb-201309-hr - r-005 ) .
subjects were permitted to drink and eat ad libitum during their performance and no particular conduct was given to participants .
three days before the race , baseline blood samples were collected after an overnight fasting ( 8 hours ) .
post race blood samples were collected in the supine position immediately , 2 hours , and 7 days following the triathlon .
ldh and total ck were evaluated by the modular system p ( roche diagnostics gmbh , germany ) .
cardiac troponin t ( ctnt ) , ck - mb and myoglobin were assayed by the elecsys 1010 ( roche ) .
although the detection limit for ctnt is 0.01 ng / ml , the recommended diagnostic threshold for myocardial damage is > 0.03 ng / ml . hemoglobin and hematocrit were measured on advia 120 ( bayer diagnostics , newbury , uk ) .
biochemical data were summarized and expressed as meansd . utilizing the statistical package spss ( version 15.0 )
, we analyzed the effects of triathlon race on groups and periods by two - way anova with repeated measures and the point of statistical significance was set at p<.05 .
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 .
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 .
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 .
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 .
transient cardiac ventricular dysfunction or sudden cardiac death has been reported in male athletes participating in marathon racing .
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 .
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 . in ctnt change after marathon race , 55 ( 11% ) among 482 participant
had significant increases and young age ( < 30 years ) were associated with elevated troponins .
myocardial injury after strenuous exercise in healthy individuals is well indicated and may be the result of exercise - induced production of free radicals .
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 .
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 . 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 .
however , the significant increase in ck levels are usually found in non - trained than in trained subjects .
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 .
this suggests that the release of these biochemical markers into the circulation may be stabilized in ultra - endurance events . 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 . 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 .
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 .
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 .
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 can not be determined to the specific indicator of myocardial damage induced in athletes following olympic triathlon . 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 .
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 . 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 .
several other studies have reported no evidence of cardiac muscle damage after prolonged endurance exercise .
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 .
in contrast , leetmaa et al . reported that ctnt increased immediately , but decreased to normal limits within 12 - 24 hours post - triathlon race . 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 .
it has a key role in the regulation of the calcium mediated muscle contraction through an interaction with actin and myosin . after myocardial damage ,
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 .
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 .
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 can not 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 .
hct increase during exercise due to a decrease in plasma volume when fluid replacement during exercise is insufficient . 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 .
 the purpose of the present study was to investigate cardiac damage biomarkers after a triathlon race in elite and non - elite athlete groups . 
 fifteen healthy men participated in the study . 
 based on performance , they were divided into elite athlete group ( eg : n=7 ) and non - elite athlete group ( neg : n=8 ) . 
 participants ' blood samples were obtained during four periods : before , immediately , 2 hours and 7 days after finishing the race . 
 creatine kinase ( ck ) , creatine kinase - myoglobin ( ck - mb ) , myoglobin , and lactate dehydrogenase ( ldh ) were significantly increased in both groups immediately after , and 2 hours after finishing the race ( p<.05 ) . 
 ck , ck - mb , and myoglobin were completely recovered after 7 days ( p<.05 ) . 
 hematocrit ( hct ) was significantly decreased in both groups ( p<.05 ) 7 days after the race . 
 ldh was significantly decreased in the eg ( p<.05 ) only 7 days after the race . 
 homoglobin ( hb ) was significantly decreased in the neg ( p<.05 ) only 2 hours after the race . 
 although cardiac troponin t ( ctnt ) was significantly increased in the eg but not in the neg 2hours after the race ( p<.05 ) , there was no group - by - time interaction . 
 ctnt was completely recovered in both groups 7 days after the race . in conclusion , 
 cardiac damage occurs during a triathlon race and , is greater in elite than in non - elite . 
 however , all cardiac damage markers return to normal range within 1 week . 
INTRODUCTION
METHODS
Subjects
Data collection
Statistical analysis
RESULTS
DISCUSSION