Changes in cardiac function parameters in 12-13-week-old, high-intensity exercised, healthy white experimental rats
Downloads
The aim of the study was to evaluate cardiac functional parameters after 11 weeks of dosed, high-intensity exercises on a treadmill in 12-13-week-old healthy rats. In general, physical activity is the cheapest and safest method to reduce cardiovascular disease risk factors (1,2,3). Within the scope of our study, we subjected 12-13-week-old healthy male rats to high-intensity exercise on a treadmill for 11 weeks and then studied cardiac function parameters by echocardiography to assess the effects of exercise on the healthy heart. The rats were divided into 2 groups: 1) control group, which did not receive any execrise (n=8); 2) The study group performed 10 full rotations on the treadmill per day, with 1-minute active breaks in between, 5 days a week (treadmill speed 19m/min, incline 300) – n=8.Cardiac function parameters were assessed through transthoracic echocardiography twice (at the start of the study and after 11 weeks). Compared to the control group, there were changes in the functional parameters in terms of improvement in the rats of the study group, in particular, the ejection fraction, stroke volume, left ventricular wall thickness, end-diastolic volume increased, and on the contrary, the end-systolic volume decreased, compared to the data of non-trained rats of the same sex and age.The present study can be considered as another step forward in the study of functional changes of healthy heart developed on the background of high-intensity physical activity.
Downloads
Metrics
Petit-Demouliere B, Chenu F, Bourin M. Forced swimming test in mice: a review of antidepressant activity. Psychopharmacology. (Berl) 2005;177:245–255.
David DJ, Renard CE, Jolliet P, Hascoet M, Bourin M. Antidepressant-like effects in various mice strains in the forced swimming test. Psychopharmacology (Berl) 2003;166:373–382.
Houser SR. When does spontaneous sarcoplasmic reticulum Ca2+ release cause a triggered arrhythmia? Cellular versus tissue requirements. Circ Res. 2000;87:725–7.
Mann DL, Bristow MR. Mechanisms and models in heart failure: The biomechanical model and beyond. Circulation. 2005;111:2837–49.
Pogwizd SM, Schlotthauer K, Li L, Yuan WL, Bers DM. Arrhythmogenesis and contractile dysfunction in heart failure - Roles of sodium-calcium exchange, inward rectifier potassium current, and residual beta-adrenergic responsiveness. Circ Res. 2001;88:1159–67.
Sipido KR, Volders PGA, Vos MA, Verdonck F. Altered Na/Ca exchange activity in cardiac hypertrophy and heart failure: a new target for therapy? Cardiovasc Res. 2002;53:782–805. https://animal.research.uiowa.edu/iacuc-guidelines-anesthesia
Bers DM. Cardiac excitation-contraction coupling. Nature. 2002;415:198–205.
Hilgemann DW. New insights into the molecular and cellular workings of the cardiac Na+/Ca2+ exchanger. Am J Physiol. 2004;287:C1167–C1172.
Reuter H, Pott C, Goldhaber JI, Henderson SA, Philipson KD, Schwinger RHG. Na+-Ca2+exchange in the regulation of cardiac excitation-contraction coupling. Cardiovasc Res. 2005;67:198–207.
Gaughan JP, Furukawa S, Jeevanandam V, Hefner CA, Kubo H, Margulies KB, et al. Sodium/calcium exchange contributes to contraction and relaxation in failed human ventricular myocytes. Amer J Physiol. 1999;277:H714–H724.
Houser SR, Piacentino V, Weisser J. Abnormalities of calcium cycling in the hypertrophied and failing heart. J Mol Cell Cardiol. 2000;32:1595–607.
Terracciano CMN, DeSouza AI, Philipson KD, MacLeod KT. Na+ - Ca2+ exchange and sarcoplasmic reticular Ca2+ regulation in ventricular myocytes overexpressing the Na+ - Ca2+ exchanger. J Physiol London. 1998;512:651–67.
Weisser-Thomas J, Piacentino V, Gaughan JP, Margulies K, Houser SR. Calcium entry via Na/Ca exchange during the action potential directly contributes to contraction of failing human ventricular myocytes. Cardiovasc Res. 2003;57:974–85.
Hampton TG, Wang JF, DeAngelis J, Amende I, Philipson KD, Morgan JP. Enhanced gene expression of Na+/Ca2+ exchanger attenuates ischemic and hypoxic contractile dysfunction. Amer J Physiol. 2000;279:H2846–H2854.
Hobai IA, ORourke B. Enhanced Ca2+-activated Na+-Ca2+ exchange activity in canine pacing-induced heart failure. Circ Res. 2000;87:690–8.
Kent RL, Rozich JD, McCollam PL, McDermott DE, Thacker UF, Menick DR, et al. Rapid expression of the Na+-Ca2+ exchanger in response to cardiac pressure overload - rapid communication. Am J Physiol. 1993;265:H1024–H1029.
Schillinger W, Fiolet JW, Schlotthauer K, Hasenfuss G. Relevance of Na+-Ca2+ exchange in heart failure. Cardiovasc Res. 2003;57:921–33.
Studer R, Reinecke H, Bilger J, Eschenhagen T, Bohm M, Hasenfuss G, et al. Gene expression of the cardiac Na+ - Ca2+ exchanger in end-stage human heart failure. Circ Res. 1994;75:443–53.
Wang ZY, Nolan B, Kutschke W, Hill JA. Na+-Ca2+ exchanger remodeling in pressure overload cardiac hypertrophy. J Biol Chem. 2001;276:17706–11.
Zhang XQ, Song JL, Rothblum LI, Lun MY, Wang XJ, Ding F, et al. Overexpression of Na+/Ca2+ exchanger alters contractility and SR Ca2+ content in adult rat myocytes. Amer J Physiol. 2001;281:H2079–H2088.
Gomez AM, Valdivia HH, Cheng H, Lederer MR, Santana LF, Cannell MB, et al. Defective excitation-contraction coupling in experimental cardiac hypertrophy and heart failure. Science. 1997;276:800–6.
Schultz JEJ, Glascock BJ, Witt SA, Nieman ML, Nattamai KJ, Liu LH, Lorenz JN, et al. Accelerated onset of heart failure in mice during pressure overload with chronically decreased SERCA2 calcium pump activity. Am J Physiol. 2004;286:H1146–H1153.
Recommendations for quantitation of the left ventricle by two-dimensional echocardiography. J Am Soc Echocardiogr. 1989; 2: 358-367
Monocyte chemoattractant protein-1 is upregulated in rats with volume-overload congestive heart failure. Circulation. 2000; 102: 1315-1322
This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.
