Key result
Aerobic exercise modestly improves EF in rats with supravalvar aortic stenosis independent of cardiomyocyte proliferation.
Why the study?
The mechanisms responsible for exercise training-induced improvement in cardiac function in supravalvar aortic stenosis remained incompletely understood.
Does aerobic exercise training improve cardiac function through cardiomyocyte proliferation and Ang-(1-7) levels in rats with supravalvar aortic stenosis?
Does aerobic exercise training improve cardiac function through cardiomyocyte proliferation and Ang-(1-7) levels in rats with supravalvar aortic stenosis?
Absolute Event Rate: 26.7% vs 24.8%
p-value: p=<0.05
Aerobic exercise training improves systolic function in pressure-overloaded rats by negatively modulating the ACE/Ang II axis rather than through cardiomyocyte proliferation or Ang-(1-7) pathways.
May support exercise in pressure overload via ACE/Ang II; leaves open human translation and mechanisms.
BACKGROUND/AIMS: The beneficial effect of aerobic exercise training (ET) on cardiac remodeling caused by supravalvar aortic stenosis (AS) has been demonstrated in experimental studies; however, the mechanisms responsible for improving cardiac function are not entirely understood. We evaluated whether ET-generated cardioprotection in pressure-overloaded rats is dependent on cardiomyocyte proliferation, increased angiotensin-(1-7) (Ang-1-7) levels, and its receptor in the myocardium. METHODS: Eighteen weeks after ascending AS surgery, Wistar rats were randomly assigned to four groups: sedentary control (C-Sed), exercised control (C-Ex), sedentary aortic stenosis (AS-Sed) and exercised aortic stenosis (AS-Ex) groups. The moderate treadmill exercise protocol was performed for ten weeks. The functional capacity was assessed by treadmill exercise testing. Cardiac structure and function were evaluated by echocardiogram. Cardiomyocyte proliferation was evaluated by flow cytometry. Expression of cell cycle regulatory genes as CCND2, AURKB, CDK1, and MEIS1 was verified by RT-qPCR. Cardiac and plasma angiotensin I (Ang I), angiotensin II (Ang II), and Ang-(1-7) levels were analyzed by high-performance liquid chromatography (HPLC). The angiotensin-converting enzyme (ACE) activity was assessed by the fluorometric method and protein expression of AT1 and Mas receptors by Western blot. RESULTS: The AS-Ex group showed reduced left ventricular wall relative thickness and improved ejection fraction; also, it showed decreased gene expression of myocyte cell cycle regulators, ACE, Ang I, Ang II and Ang II/Ang-(1-7) ratio levels compared to AS-Sed group. However, ET did not induce alterations in Ang-(1-7) and cardiac Mas receptor expression and myocyte proliferation. CONCLUSION: Aerobic exercise training improves systolic function regardless of myocyte proliferation and Ang-(1-7)/Mas receptor levels. However, the ET negatively modulates the vasoconstrictor/hypertrophic axis (ACE/Ang II) and decreases the expression of negative regulatory genes of the cell cycle in cardiomyocytes of rats with supravalvular aortic stenosis.
No takes yet. Share an insight, caveat, or question.
Mota et al. (2020) studied Supravalvar aortic stenosis (n=74). Aerobic exercise training vs. Sedentary control was evaluated on Ejection fraction at 28 weeks (%) (p=<0.05). Aerobic exercise training improved ejection fraction and systolic function in rats with supravalvar aortic stenosis, independent of cardiomyocyte proliferation or increased Ang-(1-7) levels.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: