Cardiac hypertrophy in mice submitted to a swimming protocol: influence of training volume and intensity on myocardial renin-angiotensin system

Abstract

Exercise promotes physiological cardiac hypertrophy and activates the renin-angiotensin system (RAS), which plays an important role in cardiac physiology, both through the classical axis [angiotensin II type 1 receptor (AT1R) activated by angiotensin II (ANG II)] and the alternative axis [proto-oncogene Mas receptor (MASR) activated by angiotensin-(1–7)]. However, very intense exercise could have deleterious effects on the cardiovascular system. We aimed to analyze the cardiac hypertrophy phenotype and the classical and alternative RAS axes in the myocardium of mice submitted to swimming exercises of varying volume and intensity for the development of cardiac hypertrophy. Male Balb/c mice were divided into three groups, sedentary, swimming twice a day without overload (T2), and swimming three times a day with a 2% body weight overload (T3), totaling 6 wk of training. Both training groups developed similar cardiac hypertrophy, but only T3 mice improved their oxidative capacity. We observed that T2 had increased levels of MASR, which was followed by the activation of its main downstream protein AKT; meanwhile, AT1R and its main downstream protein ERK remained unchanged. Furthermore, no change was observed regarding the levels of angiotensin peptides, in either group. In addition, we observed no change in the ratio of expression of the myosin heavy chain β-isoform to that of the α-isoform. Fibrosis was not observed in any of the groups. In conclusion, our results suggest that increasing exercise volume and intensity did not induce a pathological hypertrophy phenotype, but instead improved the oxidative capacity, and this process might have the participation of the RAS alternative axis.

Two protocols of aerobic exercise modulate the counter-regulatory axis of the renin-angiotensin system

“…Confirming these findings, ACE2 deficiency was related to impaired physical performance and cardiac and skeletal muscle adaptations to exercise in mice (Motta-Santos et al, 2016). Another recent study showed that swimming training improves the oxidative capacity in mice, and the RAS counter-regulatory axis may exert a role in this process (Soares et al, 2019).…”

The Anti-Inflammatory Effect of Taurine on Cardiovascular Disease

“…A regulator of the cardiovascular system is the renin-angiotensin system (RAS), a system exhibited on various tissues and cells, which has been established as a key regulator of the body’s hormonal and fluid balance system. The RAS is usually pharmacologically targeted for the management of heart failure [ 34 , 35 , 36 , 37 ], diabetes [ 38 , 39 ], and hypertension/blood pressure control [ 40 , 41 , 42 ]. The main effector of RAS is angiotensin II (AngII), which is produced by angiotensin-converting enzyme (ACE) within the circulation or in ACE-expressed cells [ 43 , 44 , 45 ].…”

A Probable Relationship between Physical Exercise and COVID-19 Mediated by the Renin-Angiotensin-Aldosterone System

“…Previous studies, especially experimental studies, have shown that physical exercise can reduce the activation of the classic RAS pathway and increase the activation of the components of the counter-regulatory pathway (ACE2/Angio-1-7/MAS) (Figure 2). [7][8][9][10][11][12][13] However, the literature is still scarce about the effects of physical exercise on the ACE2/Angio-1-7/ MAS pathway, mainly on ACE2 (the primary receptor site of SARS-CoV-2). In short, it was shown in rodents that physical exercise increased the expression of MAS receptors in aortas, thereby improving the vasodilatory effect of Angio-1-7.…”