Hu D, Huang X, Zheng C, Zhu Y, Chen L, Lin H, Liao Y
Department of Cardiology, State Key Laboratory of Organ Failure Research, Guangdong Provincial Key Laboratory of Shock and Microcirculation, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Nan Fang Yi Ke Da Xue Xue Bao. 2021 Apr 20;41(4):495-503. doi: 10.12122/j.issn.1673-4254.2021.04.03.
To investigate whether anti-hypertrophic memory exists after regression of exercise-induced physiological myocardial hypertrophy (PMH) and explore the contribution of sympathetic activation to hypertrophic memory formation.
Seventy-two mice were randomized equally into 6 groups, including sedentary sham-operated group, exercise hypertrophic preconditioning (EHP) + sham operation group, bisoprolol (an adrenergic β1 receptor blocker) + EHP + sham operation group (biso+Exe+Sham group), sedentary group with transverse aortic constriction (TAC) (Sed+TAC group), EHP+ TAC group (Exe+TAC group), and bisoprolol+EHP+TAC group (biso+Exe+TAC group). The mice in the EHP groups were subjected to 3 weeks of swimming training, and in the bisoprolol groups, bisoprolol was administered by gavage once daily from two days before till the end of the training. One week after the training, TAC or sham surgery was performed. Echocardiography and hemodynamic measurements were performed to evaluate cardiac function of the mice, and the myocardial tissues were examined histologically to detect cardiac remodeling.
Compared with the sedentary group, the mice receiving 3 weeks of swimming training had significantly increased heart weight to body weight ratio (HW/BW), HW to tibia length ratio (HW/TL), and the cross-sectional area of the cardiomyocytes ( < 0.05). One week after the training, exercise-induced PMH rapidly diminished and both HW/BW and HW/TL recovered the baseline levels. Treatment with bisoprolol obviously prevented the occurrence of PMH. Four weeks after TAC, the left ventricular posterior wall thickness, HW/BW, HW/TL, left ventricular end diastolic pressure and cross-sectional area of cardiomyocytes were all significantly lower ( < 0.05) while the left ejection fraction and maximal change rate of left ventricular pressure were significantly higher ( < 0.05) in Exe + TAC group than in Sed + TAC group. No significant difference was found in these parameters between biso + Exe + TAC group and Sed + TAC group.
Anti-hypertrophic memory exists even after the regression of exercise-induced PMH, which may be attributed to the activation of sympathetic nervous system during exercise.
研究运动诱导的生理性心肌肥厚（PMH）消退后是否存在抗肥厚记忆，并探讨交感神经激活对肥厚记忆形成的作用。
将72只小鼠平均随机分为6组，包括静息假手术组、运动性肥厚预处理（EHP）+假手术组、比索洛尔（一种肾上腺素能β1受体阻滞剂）+EHP+假手术组（比索+运动+假手术组）、静息主动脉缩窄（TAC）组（静息+TAC组）、EHP+TAC组（运动+TAC组）和比索洛尔+EHP+TAC组（比索+运动+TAC组）。EHP组小鼠进行3周游泳训练，比索洛尔组从训练前2天至训练结束每天经口灌胃给予比索洛尔。训练1周后，进行TAC或假手术。进行超声心动图和血流动力学测量以评估小鼠心脏功能，并对心肌组织进行组织学检查以检测心脏重塑。
与静息组相比，接受3周游泳训练的小鼠心脏重量与体重比（HW/BW）、心脏重量与胫骨长度比（HW/TL）以及心肌细胞横截面积显著增加（P<0.05）。训练1周后，运动诱导的PMH迅速消退，HW/BW和HW/TL均恢复至基线水平。比索洛尔治疗明显预防了PMH的发生。TAC后4周，运动+TAC组的左心室后壁厚度、HW/BW、HW/TL、左心室舒张末期压力和心肌细胞横截面积均显著低于（P<0.05）静息+TAC组，而左心室射血分数和左心室压力最大变化率显著高于（P<0.05）静息+TAC组。比索+运动+TAC组与静息+TAC组在这些参数上无显著差异。
即使运动诱导的PMH消退后仍存在抗肥厚记忆，这可能归因于运动过程中交感神经系统的激活。
