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    • Cardiac troponin I cTnI is a well established sensitive and

    2019-05-17

    Cardiac troponin I (cTnI) is a well-established, sensitive, and specific marker of myocardial injury. However, evidence indicates that unrecognized myocardial injury may be occurring with certain conditions such as sepsis without acute coronary ischemic event, which demonstrate elevated cTnI levels. Like most prolonged endurance exercises, ultramarathon is known to cause elevation of cardiac markers, like cTnI. Previous studies revealed the association of several factors with such exercise-induced cTnI release, including age, exercise intensity, exercise duration and training levels, in the absence of clinical symptoms of myocardial infraction. However, those studies mainly focused on white populations. More than 240 million people globally are currently infected with buy congo red virus (HBV). At least 9.8% of the population are HBV chronic carriers in Asia-Pacific. Among Oriental endurance athletes, many are HBV carrier (HBVc) runners. Previous literature had demonstrated that subclinical myocardial injury occurs more commonly than has been recognized in acute liver failure. HBV has been associated with several extrahepatic manifestations. Here, we wondered whether HBVc runners had different degree of impairment of myocardiocytes in comparison with that for other athletes. In addition, we examined the potential independent factors known to be relevant to exercise-induced cTnI release in this exertional exercise model.
    Methods
    Results All 26 participants completed a 100-km ultramarathon. The training status of each participant and the completed 100-km running time were described in previous reports. The ultramarathon was held on a sunny day with temperatures between 24.9°C and 28.7°C, humidity between 66% and 87%, and wind speed ranging from 0 m/s to 6.5 m/s (information provided by Central Weather Bureau). None of these participants finished the race with any adverse medical event. All participants with age 46.9±9.0 years completed the ultramarathon in 670.0±85.3 minutes. The average distance after 4 hours’ running was 39.3±5.2 km. The average experience in all runners was 5.4±3.4 times, and the average best marathon time was 211.3±21.2 minutes. For the runners in this study, four had weekly training of <40 km, 15 had weekly training of 40 km to 100 km, and seven had weekly training of >100 km (Table 1). There were no missing and undetectable data. Similar to previous results, our data showed that cardiac biomarkers, including CK, CK-MB, and cTnI, had a statistically significant rise immediately after the race (Table 2). Specifically, CK levels showed a ∼25-fold increase immediately after the run, and the levels may have become a little higher even after 24 hours. For CK-MB, there was an approximately sevenfold increase in plasma activity immediately following the run, and this increase might persist for 24 hours. Between postrace and prerace values, there were statistically significant rises after the race in cTnI, a sensitive and specific marker of myocardial injury. Nineteen runners (73.1%) had postrace elevated cTnI levels. Eight participants (30.8%) had elevated cTnI values lasting more than 24 hours after the run. A multiple linear regression analysis was performed on the 26 participants to explore the association between cTnI levels and other potential factors, including HBV status, considering age, body mass index, performance record, training levels, and previous years of marathon running. We found that the HBV status was a factor related to the high level of cTnI after 24 hours of running (β=0.03, p=0.08) but it was not associated with the cTnI levels before and immediately after the ultramarathon. Other factors were not associated with cTnI levels at all three time points (p>0.1). The 26 participants were further divided into HBVc runners (n=8) and non-HBVc runners (n=18). The performances of the HBVc and non-HBVc runners in the race were largely similar (Table 1). For plasma cTnI, the levels before race showed no apparent difference between the two groups of runners. For non-HBVc runners, the cTnI levels increased from 0.02±0.03 ng/mL to 0.08±0.05 ng/mL immediately after the finish; 72% of these runners had elevated cTnI. By contrast, the cTnI levels in HBVc showed an increase from 0.01±0.01 ng/mL to 0.10±0.11 ng/mL after the race, and a similar percentage (75%) of these runners had elevated cTnI. Intriguingly, five (62.5%) of the HBVc runners had unusually high cTnI levels 24 hours after the run, in stark contrast to the low percentage (16.7%) for the non-HBVc runner group (Fig. 1). These data suggest that the recovery of plasma cTnI levels is delayed in ultramarathon runners with latent HBV infection. Multiple linear regression analysis was performed on a data set of HBVc and non-HBVc runners. We identified age (β=−0.01, p=0.03), previous running experience (β=−0.06, p=0.02), training (β=0.37, p=0.02), and 4-hour running distance (β=−0.04, p=0.04) as independent predictors of higher postrace cTnI levels in HBVc runners, whereas those parameters were not significant in non-HBVc runners. Our prediction model had an overall r2=0.8.