Preventive aerobic training exerts a cardioprotective effect on rats treated with monocrotaline

Abstract

Pulmonary arterial hypertension (PAH) is a chronic disease which causes overload to the right ventricle. The effect of preventive training on cardiac remodelling in this condition is still unknown. This study aimed to evaluate the influence of preventive training on hypertrophy, heart function and gene expression of calcium transport proteins in rats with monocrotaline-induced PAH. Thirty-two male Wistar rats were randomly divided into four groups: S, sedentary control; T, trained control; SM, sedentary monocrotaline; and TM, trained monocrotaline. The preventive training protocol was performed on a treadmill for 13 weeks, five times/week. The first two weeks were adopted for adaptation to training with gradual increases in speed/time. The speed of the physical training from the third to tenth weeks was gradually increased from 0.9 to 1.1 km/h for 60 min. Next, monocrotaline was applied (60 mg/kg) to induce PAH and lactate threshold analysis performed to determine the training speeds. The training speed of the TM group in the following two weeks was 0.8 km/h for 60 min and the T = 0.9 km/h for 60 min; in the final two weeks, both groups trained at the same speed and duration 0.9 km/h, 60 min. Cardiac function was assessed through echocardiography, ventricular hypertrophy through histomorphometric analysis and gene expression through RT-qPCR. Right cardiac function assessed through the peak flow velocity was SM = 75.5 cm/s vs. TM = 92.0 cm/s (P = 0.001), and ventricular hypertrophy was SM = 106.4 μm² vs. TM = 77.7 μm² (P = 0.004). There was a decrease in the gene expression of ryanodine S = 1.12 au vs. SM = 0.60 au (P = 0.02) without alterations due to training. Thus, we conclude that prior physical training exerts a cardioprotective effect on the right ventricle in the monocrotaline rat model.

Keywords: exercise; monocrotaline; ventricular dysfunction.

Figure 1

Scheme of the aerobic training and experimental design. S, sedentary control; SM, sedentary monocrotaline; T, trained control; TM, trained monocrotaline; MCT, monocrotaline.

Figure 2

Echocardiogram. Values are expressed as mean and standard deviation. (a) Peak flow velocity (PFV). (b) Pulmonary velocity acceleration time (PVAT) and pulmonary ejection time (PET). S, sedentary control; SM, sedentary monocrotaline; T, trained control; TM, trained monocrotaline; cm/s, centimetres per second; ms, millisecond. *P < 0.05.

Figure 3

Box plot corresponding to the evaluation of anatomical parameters. (a) Atria; (b) RV (right ventricle); and (c) LV (left ventricle). S, sedentary control; SM, sedentary monocrotaline; T, trained control; TM, trained monocrotaline. *P < 0.05.

Figure 4

Histomorphometric analysis. Values are expressed as mean and standard deviation. S, sedentary control; SM, sedentary monocrotaline; T, trained control; TM, trained monocrotaline; *P < 0.05.

Figure 5

Gene expression of cardiac calcium proteins. Data are expressed as mean ± standard deviation. RyR, PLB and Serca2a. All analyses of the genes were normalized by β‐actin. S, sedentary control; SM, sedentary monocrotaline; T, trained control; TM, trained monocrotaline; RyR, ryanodine; PLB, phospholamban, SERCA, Serca2a. P < 0.05, *S vs. M.