Exercise-Induced Cardiac Troponin Release: Real-Life Clinical Confusion

2011 ◽  
Vol 18 (23) ◽  
pp. 3457-3461 ◽  
Author(s):  
T. M.H. Eijsvogels ◽  
R. Shave ◽  
A. van Dijk ◽  
M. T.E. Hopman ◽  
D. H.J. Thijssen
PLoS ONE ◽  
2013 ◽  
Vol 8 (11) ◽  
pp. e79280 ◽  
Author(s):  
Lieke J. J. Klinkenberg ◽  
Peter T. Res ◽  
Guido R. Haenen ◽  
Aalt Bast ◽  
Luc J. C. van Loon ◽  
...  

2011 ◽  
Vol 43 (Suppl 1) ◽  
pp. 435
Author(s):  
Glyn Howatson ◽  
Jessica A. Hill ◽  
Malachy P. McHugh ◽  
David Gaze ◽  
Rob Shave

2020 ◽  
Vol 6 (7) ◽  
pp. 107-117
Author(s):  
A. Chaulin ◽  
Ju. Grigoryeva ◽  
G. Suvorova

It is well known that regular physical activity has a beneficial effect on the cardiovascular system and reduces the risk of heart disease; however, numerous studies have shown an increase in heart troponin levels after exercise, which indicates damage to the myocardium in apparently healthy people. The prevalence of these results in various exercise conditions and population groups, as well as the potential underlying mechanisms and clinical significance of exercise-induced cardiac troponin release, has not yet been fully determined. This review discusses the effect of exercise on cardiac troponin levels and possible mechanisms for increasing these biomarkers.


2011 ◽  
Vol 152 (1) ◽  
pp. 101-102 ◽  
Author(s):  
G. Howatson ◽  
S. Goodall ◽  
J. Hill ◽  
J. Brouner ◽  
D. Gaze ◽  
...  

Author(s):  
Rafel Cirer-Sastre ◽  
Francisco Corbi ◽  
Isaac López-Laval ◽  
Luis Enrique Carranza-García ◽  
Joaquín Reverter-Masià

To examine the exercise-induced release of cardiac troponin T (cTnT) in adolescent and adult swimmers. Thirty-two trained male (18 adolescents, 14 adults) swam at maximal pace in a 45 min distance trial, and blood samples were drawn before, immediately and 3 h after exercise for subsequent cTnT analysis and comparison. Having comparable training experience and baseline values of cTnT (p = 0.78 and p = 0.13), adults exercised at lower absolute and relative intensity (p < 0.001 and p < 0.001, respectively), but presented higher immediate cTnT after exercise than adolescents (p < 0.001). Despite that, peak concentrations were observed at 3 h post exercise and peak elevations were comparable between groups (p = 0.074). Fourteen (44%) apparently healthy subjects exceeded the cutoff value for myocardial infarction (MI). Adolescents presented a delayed elevation of cTnT compared with adults, but achieved similar peak values.


2007 ◽  
Vol 39 (12) ◽  
pp. 2099-2106 ◽  
Author(s):  
ROBERT SHAVE ◽  
KEITH P. GEORGE ◽  
GREG ATKINSON ◽  
EMMA HART ◽  
NATALIE MIDDLETON ◽  
...  

Circulation ◽  
2020 ◽  
Vol 141 (1) ◽  
pp. 83-85 ◽  
Author(s):  
Lucy Marshall ◽  
Kuan Ken Lee ◽  
Stacey D. Stewart ◽  
Adam Wild ◽  
Takeshi Fujisawa ◽  
...  

Circulation ◽  
2019 ◽  
Vol 140 (10) ◽  
pp. 804-814 ◽  
Author(s):  
Vincent L. Aengevaeren ◽  
Maria T.E. Hopman ◽  
Paul D. Thompson ◽  
Esmée A. Bakker ◽  
Keith P. George ◽  
...  

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
T Paana ◽  
S Jaakkola ◽  
E Tuunainen ◽  
S Wittfooth ◽  
K Bamberg ◽  
...  

Abstract Background Cardiac troponins (cTn) are highly sensitive and specific markers for cardiac injury and a key element in the diagnosis of acute coronary syndrome. Strenuous exercise is known to induce increases in cTn, but the causative factors remain ambiguous. It is also equivocal whether exercise induced skeletal muscle injury is associated with cTn elevation. Purpose The aim of this study was to identify independent predictors for the rise in cardiac troponin T (cTnT) and I (cTnI) concentration and to focus on the relationship between skeletal muscle injury measured by skeletal troponin I (skTnI) and cTn elevations after a marathon race in a large group of male recreational runners. Methods A total of 40 recreational runners participating in the marathon in our city were recruited. The study included baseline visit (prerace) and immediate post-race sampling. Results The post-marathon cTnT concentration rose above the reference limit in 38 (95%) participants and the detection limit for cTnI was exceeded in 34 (85%) participants. Similarly, a 10-fold increase in skTnI concentration was observed and elevated post-race values were seen in all participants. There was no significant correlation between the post-race cTnT or cTnT change and post-race skTnI (Spearman's rho = 0.249, p=0.122, rho = 0.285, p=0.074). However, post-race cTnI and change in cTnI were associated with post-race skTnI (rho = 0.404, p=0.01, rho = 0.460, p=0.003) and creatine kinase (r=0.368, p=0.019) concentration. Subjective exertion or self-reported muscle symptoms did not correlate with post-race cTnT, cTnI or skTnI levels. Post-Race cTnT <40 Post-Race cTnT ≥40 p-value n=18 n=22 Age, years 53.3±12.2 44.0±11.9 0.002 Active training, years 12.0 (9.3) 17.0 (15.8) 0.190 Muscle symptoms 7 (38.9) 11 (52.4) 0.523 Creatinine kinase, ug/l 406 (137) 399 (319) 0.163 N-terminal proBNP ng/l 137±168 158±277 0.783 Skeletal Troponin I, ng/ml 28.6 (41) 56.7 (143) 0.199 Figure 1 Conclusions Cardiac troponin became abnormal in almost all runners after marathon race. The exercise-induced rise in cardiac troponin I is related to simultaneous release of skeletal troponin I. The mechanism of this association remains uncertain, but clinicians should be cautious when interpreting post-exercise troponin levels without clinical symptoms and signs of myocardial ischemia.


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