Exercise-Induced Cardiac Troponin Elevation: Evidence, Mechanisms, and Implications

Cardiac troponin may be released by ischemia alone, without necrosis

Purpose: Cardiac troponin T (cTnT) is a highly specific marker of myocardial damage and used clinically in the diagnosis of acute myocardial infarction (AMI). Release of cTnT has been demonstrated in several small studies after endurance exercise. The purpose of this study was to explore, using a meta-analytic approach, the incidence of postexercise cTnT release after endurance exercise.

Methods: Articles identified via Pubmed, SportDiscus, and Embase (1997-2006) searches using the key words cardiac troponin T, cTnT, cardiac biomarkers, and exercise; a search of bibliographies; and consultation with experts in the field were entered into a random-effects meta-analysis. We identified 26 relevant studies (1120 cases). Age, gender, and body mass of participants, as well as exercise mode and duration, were explored as possible moderator variables with meta-regressions.

Results: Postexercise cTnT levels exceeded the assay detection limit in 47% of participants (95% CI = 39-56%). The detection of postexercise cTnT after cycling events was approximately half that of running events (27 vs 52%, P = 0.042). The detection of postexercise cTnT decreased slightly as event duration increased (P = 0.022) and mean body mass decreased (P = 0.0033). Postexercise detection of cTnT was not affected by age (P= 0.309) and was only slightly higher for studies with more males in the sample (P = 0.028).

Conclusions: Exercise-induced cTnT release is apparent in almost half of the endurance athletes who have been studied to date. Relatively heavy individuals competing in shorter endurance events, primarily running marathons, are slightly more likely to demonstrate elevated cTnT postexercise than other athletes. These data are useful for clinicians evaluating athletes with cTnT elevations after competitive endurance exercise events.

Exercise-induced cardiac troponin T release: a meta-analysis

Exercise at the Extremes: The Amount of Exercise to Reduce Cardiovascular Events

Multiple epidemiological studies document that habitual physical activity reduces the risk of atherosclerotic cardiovascular disease (ASCVD), and most demonstrate progressively lower rates of ASCVD with progressively more physical activity. Few studies have included individuals performing high-intensity, lifelong endurance exercise, however, and recent reports suggest that prodigious amounts of exercise may increase markers for, and even the incidence of, cardiovascular disease. This review examines the evidence that extremes of endurance exercise may increase cardiovascular disease risk by reviewing the causes and incidence of exercise-related cardiac events, and the acute effects of exercise on cardiovascular function, the effect of exercise on cardiac biomarkers, including "myocardial" creatine kinase, cardiac troponins, and cardiac natriuretic peptides. This review also examines the effect of exercise on coronary atherosclerosis and calcification, the frequency of atrial fibrillation in aging athletes, and the possibility that exercise may be deleterious in individuals genetically predisposed to such cardiac abnormalities as long QT syndrome, right ventricular cardiomyopathy, and hypertrophic cardiomyopathy. This review is to our knowledge unique because it addresses all known potentially adverse cardiovascular effects of endurance exercise. The best evidence remains that physical activity and exercise training benefit the population, but it is possible that prolonged exercise and exercise training can adversely affect cardiac function in some individuals. This hypothesis warrants further examination.

Are There Deleterious Cardiac Effects of Acute and Chronic Endurance Exercise

Background: There is concern about whether cardiac damage occurs as a result of prolonged strenuous exercise. Objective: To investigate whether competing in a triathlon is associated with cardiac damage based on a sustained increase in cardiac troponin T (cTnT), and whether such an increase correlates with echocardiographic changes Methods: cTnT and echocardiographic measurements were made in 38 participants in the 2001 Australian ironman triathlon. cTnT was measured the day before, immediately after, and the day following the race. Echocardiography was done the day before, immediately after, and two to six weeks later for measurement of ejection fraction, stroke volume, cardiac output, wall motion analysis, and global left ventricular function (LVF). Results: No subject had detectable cTnT in the pre-race sample. Following the race, 32 subjects (86.5%) had detectable levels of cTnT (>0.01 ng/ml), with six (16.2%) having >0.10 ng/ml. The day after the race, nine subjects (23.7%) still had detectable cTnT, with two recording a level >0.10 ng/ml. Previously described echocardiographic changes of “cardiac fatigue” were observed in the whole cohort. There was a modest but significant correlation between change in ejection fraction and peak cTnT level (p = 0.02, r  = 0.39). Athletes with a post-race cTnT >0.10 ng/ml had a greater decrease in global LVF (p = 0.02) and a trend toward a greater fall in ejection fraction and stroke volume than athletes with cTnT levels 0.10 ng/ml (p>0.05). Conclusions: Participation in ironman triathlon often resulted in persistently raised cTnT levels, and the troponin rise was associated with echocardiographic evidence of abnormal left ventricular function. The clinical significance and long term sequelae of such damage remains to be determined.

/pdf/raised-troponin-t-and-echocardiographic-abnormalities-after-q3w5959h5q.pdf

Lynne Pressley

Papers

Raised troponin T and echocardiographic abnormalities after prolonged strenuous exercise—the Australian Ironman Triathlon