Abstract：Objective To observe the effects of regular exercise training on cardiac hypertrophy in spontaneously hypertensive rats (SHR) and to explore the possible mechanism of exercise-induced cardioprotective effect.Methods Thirty SHRs were randomly divided into hypertension exercise group (SHR-Ex) and hypertension control group (SHR-C), and fifteen healthy Wistar rats were used as normotensive control group (NC). Rats of SHR-Ex group performed swimming training for 8 weeks (60 min per day, 5 days per week), while those of SHR-C and NC groups were kept quiet in a cage. After the experiment, the caudal artery blood pressure was measured by intelligent non-invasive blood pressure tester, the cardiac structure and function were monitored by echocardiography, the left ventricle was separated and weighed, the cross sectional area (CSA) and collagen volume fraction (CVF) of myocardial cells were obtained by HE and Masson staining respectively, and embryo genes and cardiac hypertrophy signal pathway protein expression were determined by Western Blot.Results During the experiment, a total of 7 rats were excluded due to refusal to run, death or other reasons, and finally 38 rats were included, including 15 rats in the NC group, 12 rats in the SHR-C group and 11 rats in the SHR-Ex group. Compared with NC group, SHR-C group rats showed concentric cardiac hypertrophy, myocardial fibrosis (CVF increased, P<0.05), and up-regulated expression of atrial natriuretic factor (ANF), myosin light chain-2(MLC-2), Calcineurin Aβ subunit (CNAβ), PI3 kinase p110 α subunit [PI3-K (p110α)] and phosphorylated Akt (p-Akt) . Compared with SHR-C group, SHR-Ex group showed eccentric cardiac hypertrophy, reduced myocardial fibrosis (CVF decreased, P<0.05) and enhanced cardiac function (P<0.05), the expression levels of ANF, MLC-2 and CNAβ protein expression were down-regulated (P<0.05), and PI3-K(p110α) and p-Akt had no significant change.Conclusions Long-term exercise training can promote the change from pathological cardiac hypertrophy to physiological cardiac hypertrophy in SHR, which may be related with the decline of calcineurin signal pathway activity.
彭朋, 何瑞波, 马刚, 王大宁, 薄海, 秦永生. 运动训练诱导自发性高血压大鼠生理性心脏肥大[J]. 武警医学, 2022, 33(9): 759-763.
PENG Peng, HE Ruibo, MA Gang, WANG Daning, BO Hai, QIN Yongsheng. Effects of exercise training on physiologic cardiac hypertrophy in spontaneously hypertensive rats. Med. J. Chin. Peop. Armed Poli. Forc., 2022, 33(9): 759-763.
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