To the Editor,

Although exercise can reduce the incidence of cardiovascular disease by between 33% and 50%,1, 2, 3 intense or prolonged exercise can increase cardiac troponin (cTn) levels in individuals with no coronary obstruction.4 Understanding the significance of elevated cTn could prevent unnecessary or invasive procedures in athletes. The objective of this study was to determine the behavior of cardiac troponin I (cTnI) in women participating in adventure races.

In the Women International Adventure Raid, participants cover a distance of 80 km with an elevation gain of 2600 m. The race includes sections of swimming, running, and cycling. Before the race, study participants completed an interview to collect data on age, weight, height, body mass index (BMI), toxic habits, medical history, medications, weekly training time, and nutrition. Blood tests were also performed.

Data collected after the event included the contestants’ race time and any symptoms appearing during it. A second blood test was performed and glucose, cholesterol, triglyceride, high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), creatine kinase (CK), and serum cTnI levels before and after the race were measured. An increase in cTnI was defined as ≥0.04 ng/mL.

Blood test results were compared using non-parametric tests. A logistic regression analysis was used to analyze the influence of different variables on elevated troponin levels.

Of the 50 riders who entered the race, 34 (68%) participated in the study. Median age was 32.5 [30-35.25] years; BMI was 21.44 [20.28-22.34]. Median weekly training and race times were 8.5 [5.37-12] h and 618 [610-629.25] min, respectively.

None of the racers reported symptoms of heart disease during the race.

At the end of the race, troponin I levels had increased significantly, by 0.03 [0.01-0.08] (P<.001); a moderate increase (≥0.04 ng/mL and ≤0.5 ng/mL) was observed in 14 runners (41.18%), and a >0.5 ng/mL (0.76 ng/mL) increase was observed in one case.

Significant increases were recorded in HDL-c (8.6 [5.15-11.53] mg/dL; P<.001), glucose (12 [7-31] mg/dL; P=.013), and CK (402 [227-668] mg/dL; P<.001). No increase was observed in any of the other variables (Table 1).

Table 1. Pre- and Post-Race Troponin, Creatine, Glucose, and Lipid Values

CK, creatine kinase; HDL-C, high density lipoproteins cholesterol; LDL-C, low density lipoproteins cholesterol.
Data are medians [interquartile range].

There was a statistically significant correlation between increased CK and race time (r=0.408; P=.017), but not between cTnI and CK, hours of training, or race time (Table 2). Finally, there was a negative correlation between LDL-C and increased cTn1.

Table 2. Spearman Correlations (P) Between Increased Cardiac Troponin I and Creatine Kinase, and Other Variables

BMI, body mass index; CK, creatine kinase; HDL-C, high density lipoproteins cholesterol; LDL-C, low density lipoproteins cholesterol.

The release of cTn secondary to myocardial injury can be due to ischemia from rupture of arterial plaque and coronary occlusion, ischemia without atherosclerosis, increased myocardial oxygen demand, and non-ischemic injury or direct damage (trauma, myocarditis or cardiotoxicity from drugs).5 These do not explain the release of cTn in healthy subjects after exercise.

Several studies have shown cTn elevations in sports in which cardiac output, heart rate, and blood pressure remain high for hours, such as marathons, ultra marathons, triathlons, and cycling.4, 5

This elevation could be due to damage to cardiomyocytes from the sustained increase in cardiac work rate combined with the physiological environment existing in situations of prolonged exercise (altered pH, increased core temperature, etc.).

A meta-analysis of 26 studies showed an increase in cTn in about half of the participants, a figure which was consistent with our study, in which increased troponin levels after racing was relatively common. Elevated cTn was related to the intensity and duration of exercise and the presence of cardiovascular disease,6 which is more frequent among sedentary people doing long walks, and marathon runners, than in ultramarathon runners.5

Except for myocardial fibrosis in veteran athletes or alterations in cardiovascular magnetic resonance imaging in marathon runners over 50 years of age,5 most non-invasive explorations find no association between increased cTn after exercise and the presence of permanent myocardial damage.4, 5 This difference in results may be due to the fact that cTn was determined.

Myocardial sarcolemmal hyperpermeability facilitates the release of cytosolic cTn into the extracelular space.5

Stimulation of integrins through stretching of the myocardium mediates transport of cTn or its degradation products to the exterior of the cardiomyocytes,4, 5 a process which differs from the release of cTn from necrotic myocardial tissue. Integrins are involved in cardiac remodeling after myocardial infarction or pressure overload.5

In rats, it has been shown that increased preload, without ischemia, leads to an increase in the degradation of cTnI, a finding which would indicate that myocardial stretching itself can degrade cTnI.5 Although periods of prolonged exercise produce persistent myocardial stretching, we have not found any studies into the products of cTnI degradation after exercise.

In conclusion, there is no evidence that elevation of cTn after exercise is due to myocardial necrosis, and endurance sports can cause mild elevations of cTn in the absence of cardiac ischemia.

The study of cTnI degradation products could help to determine whether the release of cTnI is due to myocardial stretching or ischemia and thereby help to clarify the mechanism underlying cTn elevation.

Corresponding author: esubirats@telefonica.net