Association with cardiovascular risk?
Regular exercise is widely accepted to have beneficial effects on cardiovascular health. Higher levels of physical activity over time are associated with a reduced age-related increase in circulating troponin levels (11). Combined with the absence of cardiovascular symptoms or pathological findings during physical exertion, this has been key to shaping our current understanding of exercise-induced troponin elevation as a benign physiological phenomenon. However, long-term follow-up with post-exercise troponin measurements in a sufficiently large cohort is needed to evaluate its relationship with cardiovascular risk. The first study to demonstrate an association between troponin concentrations and cardiovascular events included 725 middle-aged participants in a walking event with a median duration of eight hours (3). The association with increased risk was independent of baseline troponin I concentrations and conventional risk factors. One possible interpretation of these findings is that the walking event functioned as a stress test, and that a greater increase in troponin was associated with subclinical atherosclerotic disease, which in turn is associated with future events. It is important to emphasise that these results cannot be extrapolated to a younger population, for whom subclinical coronary artery disease is considerably less prevalent.
Elevated heart rate alone may impact on troponin levels
When troponin concentrations in individuals with chronic coronary artery disease are compared with the general population, baseline levels are found to be higher in those with confirmed coronary disease, and even values within the normal range are associated with a poorer prognosis (2, 12). It is therefore plausible that myocardial ischemia during physical exertion is linked to a greater increase in troponin levels. However, most studies have not found such a connection (13). In a study where participants' heart rates were raised to 160 beats per minute using a temporary pacemaker, patients with coronary artery disease and elevated lactate levels in the coronary sinus did not exhibit a significantly greater increase in troponin T concentration compared to healthy controls (12). This suggests that elevated heart rate alone may impact on troponin levels.
Physical activity can induce a troponin increase that meets the current biochemical criteria for acute myocardial infarction
Sudden cardiac death associated with prolonged and intense physical activity is rare and difficult to predict. The question of whether troponin measurements during physical activity can serve as a predictive test has therefore been raised (14). However, troponin concentrations measured during and up to two hours after exercise do not differ significantly between athletes with and without atherosclerotic disease (15). Neither has any correlation been observed between the severity of atherosclerosis and the troponin increase following physical activity (16). Conversely, troponin concentrations 24 hours after exercise have been shown to be significantly higher in athletes with atherosclerosis (17). The reason the troponin response appears to last longer in individuals with atherosclerotic disease is unclear, but prolonged release from the ischemic area may be a contributing factor.
Physical activity can induce a troponin increase that meets the current biochemical criteria for acute myocardial infarction. It is important to be aware that recent physical activity can significantly affect the troponin response in both healthy individuals and hospital in-patients. When evaluating patients with atypical infarction symptoms, additional information about their activity level during the preceding 24 hours will be relevant for assessing the clinical significance of the observed troponin elevation. In individuals with subclinical or confirmed coronary artery disease, a prolonged troponin increase following physical activity may indicate ischemic myocardial injury and be associated with an increased risk of cardiovascular events. More knowledge is needed about exercise-induced troponin elevation in order to help distinguish between physiological exercise-induced troponin elevation and troponin elevation secondary to more serious underlying pathology.