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Aerobic exercise training (ET) produces beneficial adaptations in skeletal muscles, including angiogenesis. The renin–angiotensin system (RAS) is highly involved in angiogenesis stimuli. However, the molecular mechanisms underlying capillary growth in skeletal muscle induced by aerobic ET are not completely understood. This study aimed to investigate the effects of volume-dependent aerobic ET on skeletal muscle angiogenesis involving the expression of miRNAs-27a and 27b on RAS and oxidant–antioxidant balance. Eight-week-old female Wistar rats were divided into three groups: sedentary control (SC), trained protocol 1 (P1), and trained protocol 2 (P2). P1 consisted of 60 min/day of swimming, 5×/week, for 10 weeks. P2 consisted of the same protocol as P1 until the 8th week, but in the 9th week, rats trained 2×/day, and in the 10th week, trained 3×/day. Angiogenesis and molecular analyses were performed in soleus muscle samples. Furthermore, to establish ET-induced angiogenesis through RAS, animals were treated with an AT1 receptor blocker (losartan). Aerobic ET promoted higher VO2 peak and exercise tolerance values. In contrast, miRNA-27a and -27b levels were reduced in both trained groups, compared with the SC group. This was in parallel with an increase in the ACE1/Ang II/VEGF axis, which led to a higher capillary-to-fiber ratio. Moreover, aerobic ET induced an antioxidant profile increasing skeletal muscle SOD2 and catalase gene expression, which was accompanied by high nitrite levels and reduced nitrotyrosine concentrations in the circulation. Additionally, losartan treatment partially re-established the miRNAs expression and the capillary-to-fiber ratio in the trained groups. In summary, aerobic ET promoted angiogenesis through the miRNA-27a/b–ACE1/Ang II/VEGF axis and improved the redox balance. Losartan treatment demonstrates the participation of RAS in ET-induced vascular growth. miRNAs and RAS components are promising potential targets to modulate angiogenesis for combating vascular diseases, as well as potential biomarkers to monitor training interventions and physical performance.

OBJECTIVES: Aerobic exercise training prevents cardiovascular risks. Regular exercise promotes functional and structural adaptations that are associated with several cardiovascular benefits. The aim of this study is to investigate the effects of swimming training on coronary blood flow, adenosine production and cardiac capillaries in normotensive rats. METHODS: Wistar rats were randomly divided into two groups: control (C) and trained (T). An exercise protocol was performed for 10 weeks and 60 min/day with a tail overload of 5% bodyweight. Coronary blood flow was quantified with a color microsphere technique, and cardiac capillaries were quantified using light microscopy. Adenine nucleotide hydrolysis was evaluated by enzymatic activity, and protein expression was evaluated by western blot. The results are presented as the means ± SEMs (p

Overweight and obesity (OBT) is a serious health condition worldwide, and one of the major risk factors for cardiovascular disease (CVD), the main reason for morbidity and mortality worldwide. OBT is the proportional increase of Adipose Tissue (AT) compared with other tissue and fluids, associated with pathological changes in metabolism, hemodynamic overload, cytokine secretion, systemic inflammatory profile, and cardiac metabolism. In turn, AT is heterogeneous in location, and displays secretory capacity, lipolytic activation, insulin sensitivity, and metabolic status, performing anatomic, metabolic, and endocrine functions. Evidence has emerged on the bidirectional crosstalk exerted by miRNAs as regulators between the heart and AT on metabolism and health conditions. Here, we discuss the bidirectional endocrine role of miRNAs between heart and AT, rescuing extracellular vesicles’ (EVs) role in cell-to-cell communication, and the most recent results that show the potential of common therapeutic targets through the elucidation of parallel and ⁄or common epigenetic mechanisms.

Os esteróides anabolizantes androgênicos (EAA) são sintéticos de testosterona desenvolvidos para fins terapêuticos. São também utilizados por populações fisicamente ativas, que normalmente excedem nas doses, o que potencializa danos à saúde. Para estudar alguns dos efeitos de EAA sobre o sistema cardiovascular, ratos "Wistar" foram divididos em quatro grupos: sedentário controle (SC), sedentário anabolizado (SA), treinado controle (TC) e treinado anabolizado (TA). Foram avaliados os efeitos da associação do uso de EAA (Decanoato de nandrolona - 5 mg/kg sc, 2x/sem) e do treinamento físico de natação (TFN - 60 min/dia, 5x/sem, durante 10 sem) sobre o débito cardíaco (DC) e fluxo sanguíneo basal (DCbasal, Qbasal) e após infusão do vasodilatador acetilcolina (DC Ach, Q Ach) para observar a vasodilatação endotélio dependente (QAch), razão capilar/fibra (rc/f) e expressão do fator de crescimento endotelial vascular (VEGF) em músculo sóleo (predominância de fibras oxidativas). A testosterona plasmática aumentou nos grupos com uso de EAA e foi observada bradicardia de repouso como efeito do TFN. O DC foi menor para o Grupo TA, tanto na condição basal quanto sob infusão de Ach. O Qbasal não foi diferente entre os grupos no músculo estudado. O QAch foi maior no grupo TC, entretanto, no grupo TA este efeito benéfico do TFN foi prejudicado pela associação com o EAA. Aumento da rc/f e VEGF foi observado somente no grupo TC. Estes resultados sugerem que a associação do EAA ao TFN atenua a angiogênese e arteriogênese observadas como efeito do treinamento físico aeróbio e causa prejuízo ao fluxo sanguíneo muscular, o que poderia predispor o praticante de esportes e atividades físicas e usuário destas substâncias a problemas vasculares.Androgenic anabolic steroids (EAA) are synthetic derivatives of testosterone, used in therapeutic dosages in medical practice and in high doses by physically active people that could be health damaging. To study the effects of EAA on the cardiovascular system, Wistar rats were randomized into Sedentary Control (SC), Sedentary Steroid (SA), Trained Control (TC) and Trained Steroid (TA) groups. We evaluated the effects of swimming training (60min/day, 5x/week during 10 week) and AAS (nandrolone decanoate - 5 mg/kg sc, 2x/week) on cardiac output, basal blood flow (Qb, DC basal) and after injection of a vasodilator to observe the endothelium dependent vasodilatation (acetylcholine - Q Ach)(Q Ach, DC Ach), capillary to fiber ratio (r c/f) and vascular-endothelial growth factor expression (VEGF) in soleus muscle (oxidative fibers). Serum testosterone increased in SA and TA. Exercise training significantly decreased resting heart rate. Qb was not different among groups, and QAch was higher in TC group, however in TA group this beneficial effect of swimming exercise training was lost by association with EAA. Rc/f and VEGF were higher only in TC group. These results suggest that swimming training associated with EAA inhibit angiogenesis and arteriogenesis observed as effects of aerobic training, and impairs the red skeletal muscle blood flow which predispose physically active AAS users to vascular diseases.

Hypertension is a complex disease that constitutes an important public health problem and demands many studies in order to understand the molecular mechanisms involving his pathophysiology. Therefore, an increasing number of studies have been conducted and new therapies are continually being discovered. In this context, exercise training has emerged as an important non-pharmacological therapy to treat hypertensive patients, minimizing the side effects of pharmacological therapies and frequently contributing to allow pharmacotherapy to be suspended. Several mechanisms have been associated with the pathogenesis of hypertension, such as hyperactivity of the sympathetic nervous system and renin-angiotensin aldosterone system, impaired endothelial nitric oxide production, increased oxygen-reactive species, vascular thickening and stiffening, cardiac hypertrophy, impaired angiogenesis, and sometimes genetic predisposition. With the advent of microRNAs (miRNAs), new insights have been added to the perspectives for the treatment of this disease, and exercise training has been shown to be able to modulate the miRNAs associated with it. Elucidation of the relationship between exercise training and miRNAs in the pathogenesis of hypertension is fundamental in order to understand how exercise modulates the cardiovascular system at genetic level. This can be promising even for the development of new drugs. This article is a review of how exercise training acts on hypertension by means of specific miRNAs in the heart, vascular system, and skeletal muscle.