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Letters |
1
Middlemore Hospital Laboratory, Auckland, NZ
2
University of Auckland, School of Medicine, Auckland, NZ
3
Department of General Practice, and Primary Care, University of Auckland, Auckland, NZ
a Address correspondence to this author at: Laboratory, Middlemore Hospital, Private Bag 93311, Otahuhu, Auckland, NZ. Fax 64-9-270-4761; e-mail drb{at}med.co.nz.
To the Editor:
The New Zealand Ironman competition is an international ultradistance triathlon in which each athlete swims 3.8 km, cycles 180 km, and runs 42.2 km on the same day, completing the event in a time ranging from 9 to 16 h. In 1998, the race was held on March 15. A summary of the medical complications of the race and their treatment has been published separately (1). During and immediately after the race, 134 of the 650 starting athletes presented to the race medical facility for advice and treatment. Of these, 64 underwent venipuncture for measurement of plasma electrolytes because of clinical suspicion of acute hyponatremia (2). The residual blood from these tests was used in the study reported here.
Athletes withdrew from the race because of injury or exhaustion when necessary. Those who presented for medical treatment were asked for informed consent, either at presentation or after recovery, for use of their clinical records and use of residual blood for assays of markers of myocardial injury. The study protocol was approved by the North Health Ethics Committee.
The first blood specimen was drawn 
11 h, and the last 16 h after
the race starting time. Whole blood drawn into lithium heparin
evacuated tubes was used for urgent measurement of sodium, potassium,
and glucose. After these tests, and within 20 min of venipuncture, the
residual blood was centrifuged and the plasma separated and stored at
0 °C for further analysis within 18 h.
Total creatine kinase (CK) was measured with a Boehringer-Hitachi 717 analyzer. Cardiac troponin T (cTnT) was measured with a Boehringer Elecsys 1010 analyzer using the "second-generation" dual monoclonal antibody assay. Cardiac troponin I (cTnI) was measured with an Abbott AxSYM analyzer. In all cases, the reagents and analytical protocols provided by the equipment manufacturers were used. Correlation analysis was performed with Microsoft Excel. In the statistical analysis, cTnT concentrations reported as <0.01 µg/L were represented as 0.005 µg/L.
A total of 64 athletes underwent venipuncture. One sample had
insufficient residual blood for analysis, and one athlete had two tests
1 h apart. There thus were 64 samples from 63 athletes analyzed
for CK, cTnI, and cTnT. The plasma CK activities were increased,
consistent with skeletal muscle damage. The median CK was 1515 U/L
(range, 328–23 500 U/L; reference interval, 30–300 U/L). The
scattergram for cTnT (reference interval, 0–0.10 µg/L) and cTnI
(reference interval, 0–2.0 µg/L) is shown in Fig. 1
. Regression analysis confirmed significant correlation between
cTnI and cTnT (r = 0.870; P <0.01).
Reanalysis with the results above the reference interval excluded still
showed strong correlation (r = 0.822; P
<0.01). Both cTnI and cTnT were above the reference interval in four
athletes, and cTnI but not cTnT was above the reference interval in
one. Of these five athletes, three were available for follow-up 3–6
days after the race. Clinical review was conducted, and assays for CK,
cTnI, and cTnT were repeated. The review gave no cause to suspect
myocardial damage or disease.
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Although there are reports on cTnI and cTnT after a marathon (3)(4)(5), we have no prior experience of, and could find no published accounts of their assay after physiological stress of the magnitude induced in the Ironman race. Since conducting this study, we have noted similar results published from the Hawaii Ironman competition (6), where mildly increased cTnI and cTnT in some athletes were associated with echocardiographic evidence of cardiac wall hypokinesia.
It is apparent that all of the athletes that we tested had suffered skeletal muscle damage, as evidenced by their increased plasma CK activities. The plasma cTnI and cTnT concentrations were within the reference intervals in most athletes, consistent with the belief that these markers are relatively unaffected by skeletal muscle injury. In five athletes, however, cTnT and/or cTnI were above the reference interval, suggestive of myocardial injury. These increases were relatively minor, to at most 2.5 times the upper limit of the reference interval; in our experience, larger increases are common in myocardial infarction with increased CKMB. In athletes who were available for follow-up at 3–6 days, the increases were not sustained, as is usual with myocardial infarction (7).
It remains undetermined whether the increases in troponin concentrations were indicative of significant acute myocardial damage in these five athletes. However, the overall correlation of plasma cTnI and cTnT concentrations leads us to hypothesize that the extreme exertion had produced some minor transient myocardial injury or "stunning", as described previously (3)(6), in many of the athletes and that this injury was sufficient to increase the troponin concentrations above the reference intervals in a small group.
Acknowledgments
We thank Abbott Laboratories New Zealand Ltd and Boehringer Mannheim New Zealand Ltd for donating reagents for these assays. We also thank the athletes and their volunteer medical attendants for allowing us to conduct the study, and the staff of Middlemore Hospital Laboratory and Diagnostic Laboratory for their help in sample preparation and analysis.
References
The following articles in journals at HighWire Press have cited this article:
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  M. Herrmann, J. Scharhag, M. Miclea, A. Urhausen, W. Herrmann, and W. Kindermann Post-Race Kinetics of Cardiac Troponin T and I and N-Terminal Pro-Brain Natriuretic Peptide in Marathon Runners Clin. Chem., May 1, 2003; 49(5): 831 - 834. [Full Text] [PDF]
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