Physical inactivity, diabetes, hypertension, dyslipidemia, smoking and obesity were associated with imbalance in oxidative stress, leading to endothelial dysfunction. Such dysfunction is present in both cardiovascular disease (CVD) and erectile dysfunction (ED). ED is the persistent inability to achieve or sustain an erection sufficient for satisfactory sexual performance and is one of the first manifestations of endothelial damage in men with CVD risk factors. The purpose of this article is to review the results of studies involving physical activity, CVD, endothelial dysfunction and ED in order to verify its applicability for improving the health and quality of life of men with such disorders. There is consistent evidence that endothelial damage is intimately linked to ED, and this manifestation seems to be associated with the appearance CVDs. On the other hand, physical activity has been pointed out as an important clinical strategy in the prevention and treatment of CVDs and ED mainly associated with improvement of endothelial function. However, further experimental and clinical prospective investigations are needed to test the role of physical exercises in the modulation of endothelial function and their implications on erectile function and the appearance of CVDs.

Background: The estrogen deficiency, abnormal lipid profile, weight gain and a sedentary lifestyle are factors associated with the increased prevalence of cardiovascular disease in menopausal women. However, physical exercise practice reduces some of these risk factors. Moreover, it has been shown that exercise has an impact on inflammation, in sympathetic activity and improves endothelial function. Aims: The present study aims to evaluate the effects of moderate aerobic training on biochemical, morphological and physiological parameters in LDL Knockout mice with estrogen deprivation, evaluating the components of the ascending aortic wall. Methods: The animals were randomly divided into six groups (n=5): sedentary control (SC), sedentary control ovariectomized (SCO), trained control ovariectomized (TCO), LDL-Knockout sedentary (KS), LDL-Knockout sedentary ovariectomized (KOS) and LDL-Knockout trained ovariectomized (KOT). The trained groups underwent a protocol of moderate training for 4 weeks on a treadmill with speed and progressive load. After training, blood samples were collected for biochemical assessments and the aorta was removed for dissection and histological morphometry study. In addition, the expression of angiotensin-converting enzyme (ACE) and angiotensin II proteins were examined by immunohistochemistry in all groups of animals. Results: Changes of expressions of ACE and angiotensin II were found when the group was subjected to exercise. The concentrations of cholesterol and triglycerides were lower in the groups of animals with estrogen deprivation and dyslipidemia. In animals that performed exercises we found significant increase (p<0.05) in Vv[lam]; decrease in Vv[col] and CWT, and a tendency for decrease both in TS and IMT when compared to the SC groups. The histological morphometry findings showed consistency in the results of the aorta study when the ovariectomized group underwent the exercise protocol. Conclusion: We conclude that physical training contributed to reducing vessel rigidity and to improvements in vascular compliance, with the increase in volume density of elastic lamellae in the estrogen-deprived groups who had normal cholesterol levels.

Background: The increase in fructose consumption is paralleled by a higher incidence of metabolic syndrome, and consequently, cardiovascular disease mortality. We examined the effects of 8 weeks of low intensity exercise training (LET) on metabolic, hemodynamic, ventricular and vascular morphological changes induced by fructose drinking in male rats. Methods: Male Wistar rats were divided into (n = 8 each) control (C), sedentary fructose (F) and ET fructose (FT) groups. Fructose-drinking rats received D-fructose (100 g/l). FT rats were assigned to a treadmill training protocol at low intensity (30% of maximal running speed) during 1 h/day, 5 days/week for 8 weeks. Measurements of triglyceride concentrations, white adipose tissue (WAT) and glycemia were carried out together with insulin tolerance test to evaluate metabolic profile. Arterial pressure (AP) signals were directly recorded. Baroreflex sensitivity (BS) was evaluated by the tachycardic and bradycardic responses. Right atria, left ventricle (LV) and ascending aorta were prepared to morphoquantitative analysis. Results: LET reduced WAT (−37.7%), triglyceride levels (−33%), systolic AP (−6%), heart weight/body weight (−20.5%), LV (−36%) and aortic (−76%) collagen fibers, aortic intima-media thickness and circumferential wall tension in FT when compared to F rats. Additionally, FT group presented improve of BS, numerical density of atrial natriuretic peptide granules (+42%) and LV capillaries (+25%), as well as the number of elastic lamellae in aorta compared with F group. Conclusions: Our data suggest that LET, a widely recommended practice, seems to be particularly effective for preventing metabolic, hemodynamic and morphological disorders triggered by MS.

Introduction. Sarcopenia is a process characterized by reduction in protein mass and muscle strength with increasing age, especially in the postmenopausal period, resulting in functional limitations and with great impact on the physical autonomy of the elderly. Objective. To evaluate the effects of diets with vegetable proteins (VP) or animal proteins (AP) associated with resistance training (RT) on the structural and biochemical parameters of the medial gastrocnemius muscle in Wistar rats with sarcopenia. Methods. An experimental model with ovariectomized rats was used to induce sarcopenia and resistance training. The histochemical technique was used for the typing of muscle fibers, the cross‐sectional area of myocytes, and volume densities of myocytes and interstitium; the technique of Picrosirius stain was used to highlight the collagen fibers. Results. The VP diet was not able to minimize the effects of sarcopenia in the medial gastrocnemius of sedentary animals and when associated with RT, it promoted maintenance of the CSA, attenuating the atrophy of type IIB fibers in the medial gastrocnemius. The AP diet in sedentary animals protected the type I fibers. When combined with RT, the AP promoted muscle remodeling, with reduction in volume density of type I and IIA fibers, and increase of IIB fibers, together with an increase in collagen volume density. Conclusion. The data suggest a tendency to better results of hypertrophy in animal groups that consumed the AP diet, even the sedentary animals, although more evident in those trained.

Background: The present study was conducted to determine the location, the morphology and distribution of NADPH-diaphorase positive neurons in the cardiac nerve plexus of the atria of mice (ASn). This plexus lies over the muscular layer of the atria, dorsal to the muscle itself, in the connective tissue of the subepicardium. NADPH- diaphorase staining was performed on whole-mount preparations of the atria mice. For descriptive purposes, all data are presented as means ± SEM. Results: The majority of the NADPH-diaphorase positive neurons were observed in the ganglia of the plexus. A few single neurons were also observed. The number of NADPH-d positive neurons was 57 ± 4 (ranging from 39 to 79 neurons). The ganglion neurons were located in 3 distinct groups: (1) in the region situated cranial to the pulmonary veins, (2) caudally to the pulmonary veins, and (3) in the atrial groove. The largest group of neurons was located cranially to the pulmonary veins (66.7%). Three morphological types of NADPH-diaphorase neurons could be distinguished on the basis of their shape: unipolar cells, bipolar cells and cells with three processes (multipolar cells). The unipolar neurons predominated (78.9%), whereas the multipolar were encountered less frequently (5,3%). The sizes (area of maximal cell profile) of the neurons ranged from about 90 μm²to about 220 μm². Morphometrically, the three types of neurons were similar and there were no significant differences in their sizes. The total number of cardiac neurons (obtained by staining the neurons with NADH-diaphorase method) was 530 ± 23. Therefore, the NADPH-diaphorase positive neurons of the heart represent 10% of the number of cardiac neurons stained by NADH. Conclusion: The obtained data have shown that the NADPH-d positive neurons in the cardiac plexus of the atria of mice are morphologically different, and therefore, it is possible that the function of the neurons may also be different.