Cardiac effects of acute exhaustive exercise in a rat model

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Cardiac effects of acute exhaustive exercise in a rat model Attila Oláh, Balázs Tamás Németh, Csaba Mátyás, Eszter Mária Horváth, László Hidi, Ede Birtalan, Dalma Kellermayer, Mihály Ruppert, Gergő Merkely, Gábor Szabó, Béla Merkely, Tamás Radovits International Journal of Cardiology Volume 182, Pages 258-266 (March 2015) DOI: 10.1016/j.ijcard.2014.12.045 Copyright © 2014 The Authors Terms and Conditions

Fig. 1 Histological analysis of left ventricular (LV) myocardium. Panel A: Hematoxylin-eosin stained LV tissue sections showed sporadic fragmentation of myocardial fibers, interstitial edema, cytoplasmic eosinophilia (see star symbol) and leukocyte infiltration (see arrows) — signs of myocardial injury — in the LV myocardium of acute exercised rats compared to intact myocardium of control animals (magnification 400×, scale bar 60μm). Panel B: Myocardial dihydroethidium staining showed more intense red fluorescent signal (typically nuclear position) in LV myocardium after exhaustive exercise indicating increased superoxide formation (magnification 200×, scale bar 100μm). Panel C: Nitrotyrosine immunostaining revealed increased tyrosine nitration (dark gray color indicates nitrotyrosine positive area) in the myocardium of exercised group (magnification 200×, scale bar 100μm). Panel D: Acute exercised rats showed increased number of TUNEL-positive cardiomyocyte nuclei (see arrows) compared to control, suggesting enhanced myocardial apoptotic activation (magnification 400×, scale bar 60μm). International Journal of Cardiology 2015 182, 258-266DOI: (10.1016/j.ijcard.2014.12.045) Copyright © 2014 The Authors Terms and Conditions

Fig. 2 Myocardial gene expression analysis. Relative myocardial expression of genes related to oxidative stress (Panel A: glucose-6-phosphate dehydrogenase (G6PD), glutathione peroxidase 1 (GPX-1), glutathione reductase (GSR), thiordeoxin-1, catalase, superoxide dismutase-2 (SOD-2) and endothelial nitric oxide synthase (eNOS)), apoptotic signaling (Panel B: Bax, Bcl-2 and Bax/Bcl-2 ratio) and extracellular matrix turnover (Panel C: matrix metalloproteinase (MMP)-2, tissue inhibitor of metalloproteinase (TIMP)-2, MMP-2/TIMP-2 ratio, MMP-9, TIMP-1, MMP-9/TIMP-1 ratio) in control (Co) and acute exercised (AEx) rats. *: p<0.05 vs Co. International Journal of Cardiology 2015 182, 258-266DOI: (10.1016/j.ijcard.2014.12.045) Copyright © 2014 The Authors Terms and Conditions

Fig. 3 Steady-state left ventricular pressure-volume loops. Original recordings of steady-state pressure-volume (P-V) loops in representative rats from control (Co) and acute exercised (AEx) groups. The decreased width of P-V loops in exercised animals indicate reduced stroke volume as a result of unaltered end-diastolic volume and increased end-systolic volume, thus decreased ejection fraction. International Journal of Cardiology 2015 182, 258-266DOI: (10.1016/j.ijcard.2014.12.045) Copyright © 2014 The Authors Terms and Conditions

Fig. 4 Pressure-volume loop derived load independent left ventricular contractility parameters. The slope (Ees) of end-systolic pressure-volume relationship (ESPVR) (A); preload recruitable stroke work (PRSW), the slope of the relationship between stroke work (SW) and end-diastolic volume (EDV) (B); and maximal slope of the systolic pressure increment (dP/dtmax) — EDV relationship (dP/dtmax-EDV) (C) in representative rats from control (Co) and acute exercised (AEx) groups. As seen on the bar graphs, all of these contractility parameters are decreased in the AEx group, suggesting reduced systolic performance after exhaustive exercise. *: p<0.05 vs. Co. International Journal of Cardiology 2015 182, 258-266DOI: (10.1016/j.ijcard.2014.12.045) Copyright © 2014 The Authors Terms and Conditions

Fig. 5 Cardiac mechanoenergetics. Panel A: Decreased end-systolic elastance (Ees) and increased arterial elastance (Ea) resulted in deteriorated ventriculoarterial coupling (Ea/Ees) in acute exercised (AEx) rats compared with controls (Co). Panel B: Decreased stroke work (SW) along with unaltered pressure-volume area (P-V area) led to reduced mechanical efficiency (SW/P-V area) in the swimming group. All of these parameters suggest impaired LV mechanoenergetics after exhaustive exercise. *: p<0.05 vs. Co. International Journal of Cardiology 2015 182, 258-266DOI: (10.1016/j.ijcard.2014.12.045) Copyright © 2014 The Authors Terms and Conditions