Exercise-Induced Cardiac Troponin Elevations: From Underlying Mechanisms to Clinical Relevance

Abstract

Serological assessment of cardiac troponins (cTn) is the gold standard to assess myocardial injury in clinical practice. A greater magnitude of acutely or chronically elevated cTn concentrations is associated with lower event-free survival in patients and the general population. Exercise training is known to improve cardiovascular function and promote longevity, but exercise can produce an acute rise in cTn concentrations, which may exceed the upper reference limit in a substantial number of individuals. Whether exercise-induced cTn elevations are attributable to a physiological or pathological response and if they are clinically relevant has been debated for decades. Thus far, exercise-induced cTn elevations have been viewed as the only benign form of cTn elevations. However, recent studies report intriguing findings that shed new light on the underlying mechanisms and clinical relevance of exercise-induced cTn elevations. We will review the biochemical characteristics of cTn assays, key factors determining the magnitude of postexercise cTn concentrations, the release kinetics, underlying mechanisms causing and contributing to exercise-induced cTn release, and the clinical relevance of exercise-induced cTn elevations. We will also explain the association with cardiac function, correlates with (subclinical) cardiovascular diseases and exercise-induced cTn elevations predictive value for future cardiovascular events. Last, we will provide recommendations for interpretation of these findings and provide direction for future research in this field.

Exercise-induced cardiac troponin T release in veteran athletes recovered from COVID-19

“…The magnitude of exercise-induced cTn elevations, timing of peak concentrations and the prevalence of post-exercise hs-cTnT concentrations above the upper reference limit align with findings from previous publications. 2 , 5 These observations show that the intensity and duration of our exercise protocol sufficiently stressed the heart to cause significant increases in hs-cTnT concentrations.…”

“… 1 Stressing the heart with exercise potentially increases sensitivity of detecting myocardial injury, as evidenced by exercise-induced cTn elevations. 2 Hence, exercise might reveal myocardial vulnerability, which could remain unrecognized under resting conditions. Therefore, we assessed exercise-induced high-sensitivity cardiac troponin T (hs-cTnT) release in middle-aged athletes recovered from COVID-19 and compared their response to matched controls.…”

Metabolic Pathway of Cardiospecific Troponins: From Fundamental Aspects to Diagnostic Role (Comprehensive Review)

“…Thus, W. Cheng et al reported that apoptosis of CMC increases with stretching of the myocardial walls ( Cheng et al, 1995 ). This allows us to consider many physiological and pathological conditions that cause stretching of the myocardial walls as possible inducers of apoptosis and thus can, to some extent, explain the increased serum levels in patients after prolonged and intense physical exertion or having AH, PE, COPD and a number of other pathologies ( Cheng et al, 1995 ; Park et al, 2017 ; Gherasim, 2019 ; Aengevaeren et al, 2021 ).…”

Could Repeated Cardio-Renal Injury Trigger Late Cardiovascular Sequelae in Extreme Endurance Athletes?

“…The time course of elevated cTn levels after prolonged exercise (peak values between 2 and 6 h after exercise) is different to that caused by myocardial infarction (peak values between 10 and 12 h after an ST segment-elevation acute myocardial infarction) [21]. The early releasable cTn pool is considered the primary origin of release.…”

“…The early releasable cTn pool is considered the primary origin of release. Conversely, increased cTn levels caused by irreversible myocyte injury with apoptosis and/or necrosis stem from cTn complexes, which are structurally bound to the actin filament and represent the majority of cTn [21,22].…”