Rat model of exercise-induced cardiac hypertrophy: hemodynamic characterization using left ventricular pressure-volume analysis

Abstract

Radovits T, Oláh A, Lux Á, Németh BT, Hidi L, Birtalan E, Kellermayer D, Mátyás C, Szabó G, Merkely B. Rat model of exercise-induced cardiac hypertrophy: hemodynamic characterization using left ventricular pressure-volume analysis. Am J Physiol Heart Circ Physiol 305: H124 -H134, 2013. First published May 3, 2013 doi:10.1152/ajpheart.00108.2013.-Long-term exercise training is associated with characteristic structural and functional changes of the myocardium, termed athlete's heart. Several research groups investigated exercise training-induced left ventricular (LV) hypertrophy in animal models; however, only sporadic data exist about detailed hemodynamics. We aimed to provide functional characterization of exercise-induced cardiac hypertrophy in a rat model using the in vivo method of LV pressure-volume (P-V) analysis. After inducing LV hypertrophy by swim training, we assessed LV morphometry by echocardiography and performed LV P-V analysis using a pressureconductance microcatheter to investigate in vivo cardiac function. Echocardiography showed LV hypertrophy (LV mass index: 2.41 Ϯ 0.09 vs. 2.03 Ϯ 0.08 g/kg, P Ͻ 0.01), which was confirmed by heart weight data and histomorphometry. Invasive hemodynamic measurements showed unaltered heart rate, arterial pressure, and LV enddiastolic volume along with decreased LV end-systolic volume, thus increased stroke volume and ejection fraction (73.7 Ϯ 0.8 vs. 64.1 Ϯ 1.5%, P Ͻ 0.01) in trained versus untrained control rats. The P-V loop-derived sensitive, load-independent contractility indexes, such as slope of end-systolic P-V relationship or preload recruitable stroke work (77.0 Ϯ 6.8 vs. 54.3 Ϯ 4.8 mmHg, P ϭ 0.01) were found to be significantly increased. The observed improvement of ventriculoarterial coupling (0.37 Ϯ 0.02 vs. 0.65 Ϯ 0.08, P Ͻ 0.01), along with increased LV stroke work and mechanical efficiency, reflects improved mechanoenergetics of exercise-induced cardiac hypertrophy. Despite the significant hypertrophy, we observed unaltered LV stiffness (slope of end-diastolic P-V relationship: 0.043 Ϯ 0.007 vs. 0.040 Ϯ 0.006 mmHg/l) and improved LV active relaxation (: 10.1 Ϯ 0.6 vs. 11.9 Ϯ 0.2 ms, P Ͻ 0.01). According to our knowledge, this is the first study that provides characterization of functional changes and hemodynamic relations in exercise-induced cardiac hypertrophy.exercise-induced cardiac hypertrophy; pressure-volume analysis; systolic function; diastolic function; cardiac mechanoenergetics ATHLETE'S HEART HAS BEEN DESCRIBED as the complex structural, functional, and electrical cardiac remodeling induced by longterm exercise training (40). Exercise training-induced cardiac hypertrophy is an important physiological adaption, which includes balanced increase of left ventricular (LV) and left atrial diameters, cardiac mass, and LV wall thicknesses effected by myocyte hypertrophy and neoangiogenesis (10,12,25,36,37).Cardiac enlargement in athletes has been reported since the late 1890s (6), and several aspects of athlete's heart have been intensively inv...

Strain and strain rate by speckle-tracking echocardiography correlate with pressure-volume loop-derived contractility indices in a rat model of athlete's heart

“…Accordingly, our baseline hemodynamic data obtained with the pressure-volume system showed an increase in systolic parameters (SV, EF, CO, and SW) in trained animals along with unaltered pressure values and heart rate as well as with decreased TPR (Table 2). These results are in good agreement with our previous hemodynamic data of exercise-induced hypertrophy using another anesthesia protocol (ketamine-xylazine) (23).…”

“…In agreement with previous results of the rat model of exercise-induced cardiac hypertrophy, an increase in postmortem-assessed cardiac mass was observed after swimming training protocol (23). The observed increase in cardiac mass was underpinned by increased wall thickness values and calculated LV mass data using echocardiography ( Table 1).…”

“…Exercise training was performed in a water tank divided into six lanes filled with tap water warmed to ϳ30 -32°C at the same time of day in all training sessions, as described previously (23). Exercised rats swam for a total period of 12 wk, 200-min long sessions/day and 5 days/wk.…”

“…In contrast to pathological hypertrophy, this adaptation leads to maintained or even enhanced cardiac function (2,14). Hemodynamic changes of exercise-induced hypertrophy were characterized by our research group in a rat model, focusing also on the improved LV inotropic state (23). Contractility is the intrinsic ability of the myocardium to generate force and to shorten independently of changes in preload or afterload with fixed heart rates.…”

Prevention of the development of heart failure with preserved ejection fraction by the phosphodiesterase‐5A inhibitor vardenafil in rats with type 2 diabetes

“…Echocardiography was performed as described previously 15. The LV anterior (AW) and posterior wall (PW) thicknesses and LV internal diameter (ID) in end‐diastole (d) and in end‐systole (s) were measured and relative wall thickness (RWT), LVmass, LVmass/tibia length (TL, cm), LVmass index (LVmass/BW) were calculated.…”