scholarly journals Cardiac troponin T alterations in myocardium and serum of rats after stressful, prolonged intense exercise

2000 ◽  
Vol 88 (5) ◽  
pp. 1749-1755 ◽  
Author(s):  
Yingjie Chen ◽  
Robert C. Serfass ◽  
Shannon M. Mackey-Bojack ◽  
Karen L. Kelly ◽  
Jack L. Titus ◽  
...  

The goal of this study was to determine whether the stress of forced exercise would result in injury to the myocardium. Male rats with 8% of body weight attached to the tail were forced to swim 3.5 h (3.5S), forced to swim 5 h (5S), or pretrained for 8 days and then forced to swim 5 h (T5S). Rats were killed immediately after they swam (0 h PS) and at 3 h (3 h PS), 24 h (24 h PS), and 48 h after they swam (48 h PS). Tissue homogenates of the left ventricle were analyzed by Western blot analysis for cardiac troponin T (cTnT). Serum cTnT was quantified by immunoassay. Results indicated that, in the 3.5S, 5S, and T5S groups, serum cTnT was significantly ( P < 0.01) increased at 0 and 3 h PS. The 5S group demonstrated a greater increase in serum cTnT than the 3.5S group ( P < 0.01) and the T5S group ( P < 0.01) at 0 h PS. Western blot analysis indicated significant decreases ( P < 0.01) in myocardial cTnT in the 5S group only at 0 h PS ( P < 0.01) and 3 h PS ( P < 0.05). Histological evidence of localized myocyte damage demonstrated by interstitial inflammatory infiltrates consisting of neutrophils, lymphocytes, and histiocytes, as well as vesicular nuclei-enlarged chromatin patterns, was observed in left ventricle specimens from the 5S group at 24 and 48 h PS. Our findings demonstrate that stressful, forced exercise induces alterations in myocardial cTnT and that training before exercise attenuates the exercise-induced heart damage.

2013 ◽  
Vol 59 (7) ◽  
pp. 1083-1090 ◽  
Author(s):  
Eline PM Cardinaels ◽  
Alma MA Mingels ◽  
Tom van Rooij ◽  
Paul O Collinson ◽  
Frits W Prinzen ◽  
...  

BACKGROUNDCardiac troponin T (cTnT) is widely used for the diagnosis of acute myocardial infarction (AMI). However, it is still unclear whether degraded cTnT forms circulate in the patient's blood. We therefore aimed to elucidate which cTnT forms are detected by the clinical assay.METHODSSeparation of cTnT forms by gel filtration chromatography (GFC) was performed in sera from 13 AMI patients to examine cTnT degradation. The GFC eluates were subjected to Western blot analysis with the original antibodies from the Roche immunoassay used to mimic the clinical cTnT assay. To investigate the degradation pattern with time, standardized serum samples of 18 AMI patients collected 0–72 h after admission were analyzed by Western blot analysis.RESULTSGFC analysis of AMI patients' sera revealed 2 cTnT peaks with retention volumes of 5 and 21 mL. Western blot analysis identified these peaks as cTnT fragments of 29 and 14–18 kDa, respectively. Furthermore, the performance of direct Western blots on standardized serum samples demonstrated a time-dependent degradation pattern of cTnT, with fragments ranging between 14 and 40 kDa. Intact cTnT (40 kDa) was present in only 3 patients within the first 8 h after hospital admission.CONCLUSIONSThese results demonstrate that the Roche cTnT immunoassay detects intact as well as degraded cTnT forms in AMI patients' sera during the period of diagnostic testing. Moreover, following AMI, cTnT is degraded in a time-dependent pattern.


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

2015 ◽  
Vol 308 (8) ◽  
pp. H875-H883 ◽  
Author(s):  
Glenn M. Stewart ◽  
Akira Yamada ◽  
Luke J. Haseler ◽  
Justin J. Kavanagh ◽  
Gus Koerbin ◽  
...  

Transient reductions in myocardial strain coupled with cardiac-specific biomarker release have been reported after prolonged exercise (>180 min). However, it is unknown if 1) shorter-duration exercise (60 min) can perturb cardiac function or 2) if exercise-induced reductions in strain are masked by hemodynamic changes that are associated with passive recovery from exercise. Left ventricular (LV) and right ventricular global longitudinal strain (GLS), LV torsion, and high-sensitivity cardiac troponin T were measured in 15 competitive cyclists (age: 28 ± 3 yr, peak O2 uptake: 4.8 ± 0.6 l/min) before and after a 60-min high-intensity cycling race intervention (CRIT60). At both time points (pre- and post-CRIT60), strain and torsion were assessed at rest and during a standardized low-intensity exercise challenge (power output: 96 ± 8 W) in a semirecumbent position using echocardiography. During rest, hemodynamic conditions were different from pre- to post-CRIT60 (mean arterial pressure: 96 ± 1 vs. 86 ± 2 mmHg, P < 0.001), and there were no changes in strain or torsion. In contrast, during the standardized low-intensity exercise challenge, hemodynamic conditions were unchanged from pre- to post-CRIT60 (mean arterial pressure: 98 ± 1 vs. 97 ± 1 mmHg, not significant), but strain decreased (left ventricular GLS: −20.3 ± 0.5% vs. −18.5 ± 0.4%, P < 0.01; right ventricular GLS: −26.4 ± 1.6% vs. −22.4 ± 1.5%, P < 0.05), whereas LV torsion remained unchanged. Serum high-sensitivity cardiac troponin T increased by 345% after the CRIT60 (6.0 ± 0.6 vs. 20.7 ± 6.9 ng/l, P < 0.05). This study demonstrates that exercise-induced functional and biochemical cardiac perturbations are not confined to ultraendurance sporting events and transpire during exercise that is typical of day-to-day training undertaken by endurance athletes. The clinical significance of cumulative exposure to endurance exercise warrants further study.


2016 ◽  
Vol 49 (6) ◽  
pp. 421-432 ◽  
Author(s):  
Seoung Mann Sou ◽  
Christian Puelacher ◽  
Raphael Twerenbold ◽  
Max Wagener ◽  
Ursina Honegger ◽  
...  

2001 ◽  
Vol 47 (3) ◽  
pp. 451-458 ◽  
Author(s):  
Angelika Hammerer-Lercher ◽  
Petra Erlacher ◽  
Reginald Bittner ◽  
Rudolf Korinthenberg ◽  
Daniela Skladal ◽  
...  

Abstract Background: Because of controversial earlier studies, the purpose of this study was to provide novel experimental and additional clinical data regarding the possible reexpression of cardiac troponin T (cTnT) in regenerating skeletal muscle in Duchenne muscular dystrophy (DMD). Methods: Plasma from 14 patients (mean age, 7.5 years; range, 5.7–19.4 years) with DMD was investigated for creatine kinase (CK), the CK MB isoenzyme (CKMB), cTnT and cardiac troponin I (cTnI), and myoglobin. cTnT concentrations were measured by an ELISA (second-generation assay; Roche) using the ES 300 Analyzer. cTnI, myoglobin, and CKMB were measured by an ELISA using the ACCESS System (Beckman Diagnostics). Troponin isoform expression was studied by Western blot analysis in remnants of skeletal muscle biopsies of three patients with DMD and in an animal model of DMD (mdx mice; n = 6). Results: There was no relation of cTnT and cTnI to clinical evidence for cardiac failure. cTnI concentrations remained below the upper reference limit in all patients. cTnT was increased (median, 0.11 μg/L; range, 0.06–0.16 μg/L) in 50% of patients. The only significant correlation was found for CK (median, 3938 U/L; range, 2763–5030 U/L) with age (median, 7.5 years; range, 6.8–10.9 years; r = −0.762; P = 0.042). Western blot analysis of human or mouse homogenized muscle specimens showed no evidence for cardiac TnT and cTnI expression, despite strong signals for skeletal muscle troponin isoforms. Conclusions: We found no evidence for cTnT reexpression in human early-stage DMD and in mdx mouse skeletal muscle biopsies. Discrepancies of cTnT and cTnI in plasma samples of DMD patients were found, but neither cTnT nor cTnI plasma concentrations were related with other clinical evidence for cardiac involvement.


2021 ◽  
Vol 12 ◽  
Author(s):  
Feifei Li ◽  
Will G. Hopkins ◽  
Xuejing Wang ◽  
Julien S. Baker ◽  
Jinlei Nie ◽  
...  

Background: Kinetics, moderators and reference limits for exercise-induced cardiac troponin T (cTnT) elevations are still unclear.Methods: A systematic review of published literature was conducted adhering to the Preferred Reporting Items for Systematic Review and Meta-Analyses (PRISMA) guidelines. Studies reporting high-sensitivity cardiac troponin T (hs-cTnT) concentrations before and after a bout of exercise in athletes were included and analyzed. The final dataset consisted of 62 estimates from 16 bouts in 13 studies of 5–1,002 athletes (1,421 in total). Meta-analysis was performed using general linear mixed modeling and Bayesian inferences about effect magnitudes. Modifying fixed-effect moderators of gender, age, baseline level, exercise duration, intensity and modalities were investigated. Simulation was used to derive 99th percentile with 95% limits of upper reference ranges for hs-cTnT of athletic populations.Results: The mean and upper reference limits of hs-cTnT before exercise were 4.4 and 19 ng.L−1. Clear increases in hs-cTnT ranging from large to very large (factor changes of 2.1–7.5, 90% compatibility limits, ×/÷1.3) were evident from 0.7 through 25 h, peaking at 2.9 h after the midpoint of a 2.5-h bout of running, when the mean and upper reference limit for hs-cTnT were 33 and 390 ng L−1. A four-fold increase in exercise duration produced a large clear increase (2.4, ×/÷1.7) in post-exercise hs-cTnT. Rowing exercise demonstrated an extremely large clear reduction (0.1 ×/÷2.4).Conclusions: The kinetics of cTnT elevation following exercise, the positive effect of exercise duration, the impact of exercise modality and 99th upper reference limits for athletic populations were reasonably well defined by this meta-analysis.


2012 ◽  
Vol 158 (1) ◽  
pp. 129-131 ◽  
Author(s):  
Lieke J.J. Klinkenberg ◽  
Peter T. Res ◽  
Luc J.C. van Loon ◽  
Marja P. van Dieijen-Visser ◽  
Steven J.R. Meex

Author(s):  
Rafel Cirer-Sastre ◽  
Alejandro Legaz-Arrese ◽  
Francisco Corbi ◽  
Isaac López-Laval ◽  
Keith George ◽  
...  

2013 ◽  
Vol 23 (4) ◽  
pp. 240-247 ◽  
Author(s):  
Hakan Uçar ◽  
Mustafa Gür ◽  
Ali Kivrak ◽  
Nermin Yildiz Koyunsever ◽  
Taner Şeker ◽  
...  

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