Cardiac effects of acute exhaustive exercise in a rat model

Oláh, Attila; Németh, Balázs Tamás; Mátyás, Csaba; Horváth, Eszter; Hidi, László; Birtalan, Ede; Kellermayer, Dalma; Ruppert, Mihály; Merkely, Gergő; Szabó, Gábor; Merkely, Béla; Radovits, Tamás

doi:10.1016/j.ijcard.2014.12.045

Cited by 60 publications

(57 citation statements)

References 38 publications

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“…The authors showed elevated plasma levels of cardiac troponin T and creatinine kinase after exhaustive exercise, compared to controls, along with elevated nitro-oxidative stress, myocardium enhanced apoptotic signaling and dysregulation of the matrix metalloproteinase system [1]. In this line, Legaz-Arrese et al have investigated the influence of a mild endurance training program (14 weeks running, 3-4 days/week, 120-240 min/week, 65-85% of maximum heart rate) on exercise-induced increase of high-sensitivity cardiac troponin T (hs-cTnT) in humans, showing that both baseline and post-exercise hs-cTnT values after training were higher compared with pre-training and the response of the control group (P = 0.008) [2].…”

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confidence: 96%

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Olah et al have recently shown adverse effects of exhaustive exercise on the heart in a murine model [1]. The authors showed elevated plasma levels of cardiac troponin T and creatinine kinase after exhaustive exercise, compared to controls, along with elevated nitro-oxidative stress, myocardium enhanced apoptotic signaling and dysregulation of the matrix metalloproteinase system [1].

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confidence: 99%

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Hs-cTnT levels in professional soccer players throughout a season: No evidence of sustained cardiac damage

Sanchís-Gomar

Alis

Rampinini³

et al. 2015

International Journal of Cardiology

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confidence: 96%

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confidence: 99%

Hs-cTnT levels in professional soccer players throughout a season: No evidence of sustained cardiac damage

Sanchís-Gomar

Alis

Rampinini³

et al. 2015

International Journal of Cardiology

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“…The control group was given treatment proportional which swam for 20 minutes per day, five times a week, for six weeks. While overtraining group swam for one and half hour, twice a day, every day, for six weeks [26,27,28]. Last day of treatment, the rats in both groups, were sacrificed and the heart to be examined.…”

Section: Methodsmentioning

confidence: 99%

Myocardial Pathological Changes in Overtraining Exercise

Giri

Doewes

Jatmika

et al. 2017

IOP Conf. Ser.: Mater. Sci. Eng.

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Abstract. Excessive training practices without sufficient recovery period (overtraining) may be influential to promote myocardial injury. The aim of this study was to tested the hypothesis that overtraining exercise caused myocardial changes within histopathobiological analysis in rats. In this study, male wistar rats (n= 16) underwent ten weeks of overtraining weeks. Rats were divided into 2 groups: 1) controls (swam 15 minute/day, 5 days/week) and 2) overstrained rats that in 6 week swam twice a day for 1 hour. After sacrificing, the hearts excised for pathological preparation slides.There was significant difference in morphologic histopathological slides between groups. Compared to controlled groups, there was histopathological analysis showed increased chromatin activity fragmentation of myocardial structure in the overstrained group. Hypertrophic of left ventricle also higher in overstrained groups than control. Necrotic bodies spread in left ventricles myocardium of overstrained groups and there were not found in controlled group. The results of study gives an add it ion of evidence about negative effects of overtraining for myocardium. Furthermore, this study shows that avoiding overtraining should be an important rules in order to protect that myocardial injury and needed for an extended investigations.

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“…The most typical mechanism is ischemia, which can be modified by many factors, such as pre-conditioning 8 , post-conditioning 9,10 , length of ischemic insult, and rate of coronary obturation. Ischemia triggers the apoptotic cascade 11 , leading to the presence of detectable troponin fragments in apoptotic bodies 12 . Ischemia also initiates the release of troponin fragments from so-called "myocardial blebs" (ref.…”

Section: Methodsmentioning

confidence: 99%

Factors underlying elevated troponin I levels following pacemaker primo-implantation

Hnátek¹,

Táborský²,

Malý³

et al. 2016

BIOMED PAP

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Background. Cardiac troponins are routinely used as markers of myocardial damage. Originally, they were only intended for use in diagnosing acute coronary syndromes; however, we now know that raised serum troponin levels are not always caused by ischemia. There are many other clinical conditions that cause damage to cardiomyocytes, leading to raised levels of troponin. However, the specificity of cardiac troponins towards the myocardium is absolute. Our work focuses on mechanical damage to the myocardium and on monitoring the factors that raise the levels of cardiospecific markers after primo-implantation of a pacemaker with an actively fixed electrode. Aims. (i) To determine whether the use of a primo-implanted pacemaker with an electrode system with active fixation will raise troponin levels over baseline. (ii) To assess whether troponin I elevation is dependent on procedure complexity. Methods. We enrolled 219 consecutive patients indicated for pacemaker primo-implantation; cardiospecific marker values (troponin I, CKMB, myoglobin) were determined before the implantation procedure and again at 6-and 18-h intervals after the procedure. We monitored duration of cardiac skiascopy, number of attempts to place the electrode (active penetration into the tissue) and intervention range (single-chamber versus dual-chamber pacing), and we assessed the clinical data. Results. The average age of the enrolled patients was 78.2 ± 8.0 years (median age, 80 years); women constituted 45% of the group. We implanted 128 dual-chamber and 91 single-chamber devices with an average skiascopic time of 38.6 ± 22.0 s (median, 33.5 s). Troponin I serum levels increased from an initial 0.03 ± 0.07 μg/L (median, 0.01) to 0.18 ± 0.17 μg/L (median, 0.13) and 0.09 ± 0.18 μg/L (median, 0.04) at 6 and 18 h, respectively. The differences were statistically significant (P < 0.001 or P < 0.001). We confirmed a correlation between troponin increase and duration of skiascopy (P < 0.001). We also demonstrated a correlation between increased troponin I and number of attempts to place a pacemaker electrode (penetration into the tissue) at 6 h (P < 0.001) post-implantation. Conclusion. We detected slightly elevated troponin I levels in patients with primo-implanted pacemakers using electrodes with active fixation. We demonstrated a direct correlation between myocardial damage (number of electrode penetrations into the myocardium) and troponin I elevation, as well as between complexity (severity) of the implantation procedure (indicated by prolonged skiascopy) and raised troponin I. The described phenomenon demonstrates the loss of the diagnostic role of troponin I early after pacemaker primo-implantation in patients with concomitant chest pain.

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Cardiac effects of acute exhaustive exercise in a rat model

Abstract: Excessive physical activity has an adverse effect on the heart. The observed functional impairment is associated with increased nitro-oxidative stress, enhanced apoptotic signaling and dysregulation of the matrix metalloproteinase system after exhaustive exercise.

Cited by 60 publications

References 38 publications

Hs-cTnT levels in professional soccer players throughout a season: No evidence of sustained cardiac damage

Hs-cTnT levels in professional soccer players throughout a season: No evidence of sustained cardiac damage

Myocardial Pathological Changes in Overtraining Exercise

Factors underlying elevated troponin I levels following pacemaker primo-implantation

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