The main finding of the present study lies in the fact that LET was able to prevent metabolic disorders, increase of arterial pressure values and variability, as well as baroreflex sensitivity impairment and peripheral sympathetic modulation in a MS model induced by high-fructose drinking. In addition, LET prevented cardiac and arterial structural changes, thus reducing collagen deposition, increasing the capillarity and the number of elastic lamellae, and increasing the number of atrial natriuretic peptide granules in the trained group.
It has been shown that fructose-fed rats present moderate hypertension and glucose intolerance, associated with high levels of plasma insulin, cholesterol and triglycerides [11, 22–24]. In the present investigation, chronic fructose consumption induced an increase in triglyceride levels and arterial pressure, together with a decrease in insulin sensitivity, thus corroborating previous findings of our group [9, 11].
Candidates underlying mechanisms for increments in the arterial pressure values and insulin resistance has been associated with increased sympathetic activity , and endothelial dysfunction due to reduction of endothelial nitric oxide synthase, and impairment of insulin receptor substrate 1 signaling pathways in muscle, liver, heart, kidney, and aorta [26, 27]. Furthermore, uric acid production, hypertriglyceridemia, aldehyde formation, altered vascular reactivity, oxidative stress, augmented activity of renin angiotensin system, increased sodium reabsorption, and reduced baroreflex sensitivity have also been implicated [9, 11, 12, 23, 28, 29]. In the present investigation, we observed a decrease in baroreflex sensitivity, as well as an increase of peripheral sympathetic modulation in the F group when compared to the C group. Thus, it is possible that the increase of arterial pressure has been influenced by autonomic derangements in the fructose rats.
ET was designed to reduce total cholesterol, triglycerides, systolic blood pressure, overweight/obesity, and diabetes mellitus, and has had a profound favorable impact on decreasing the incidence of initial and recurrent cardiovascular events [30, 31]. In the present study, LET prevented the increase of circulating triglycerides and insulin resistance, reinforcing the role of physical training on lipid control and storage, as well as on the insulin sensitivity. It should be noted that the reduced adipose tissue observed in FT rats may be associated with these triglyceride and insulin resistance improvements. In this aspect, previous studies using ET as a therapeutic approach have described improvements on triglyceride and insulin profiles in fructose overload rats [9, 11, 32, 33], reduction of inflammatory and oxidant status in type II diabetes [34–36], and Obese Zucker rats .
Regarding arterial pressure, although the FT group presented a slight but significant decrease in systolic blood pressure, the values were still higher when compared to C rats, revealing that LET was not able to totally prevent changes in this parameter. These findings corroborate a previous study carried out by our group , achieving lower blood pressure may be intensity-training dependent. In fact, Tjønna et al.  have demonstrated that high intensity aerobic interval training was more effective in promoting metabolic, physical capacity, and blood pressure improvements than continuous moderate exercise in MS individuals. The blood pressure improvements by high intensity ET observed by the authors were associated with greater benefit in the endothelial function of MS patients. They hypothesize that the low-and high-intensity ET programs differently affect shear stress on the walls of blood vessels during ET, and this yields that differences in molecular responses .
In the present study, the slight decrease of systolic arterial pressure after ET may be associated with the normalization of baroreflex sensitivity, reduction of systolic arterial pressure variability and peripheral sympathetic modulation in FT rats when compared to F rats. In this sense, our group has previously demonstrated that ET leads to changes in blood pressure mediated by baroreflex improvements in hypertensive , diabetic , dyslipidemic , and MS  animals. Thus, although we observed important autonomic benefits by low intensity ET, it is possible that endothelial function has not been fully restored, since it appears to be intensity training dependent , justifying the non-normalization of blood pressure in this study.
Our results demonstrated that, in addition to the metabolic and hemodynamic alterations promoted by high fructose drinking, the animals of F group displayed an increase in heart weight / body weight ratio, area, volumetric and numerical density of myocite, volumetric density of collagen fibers, together with a decrease in the numerical density of capillaries and ANP granules. Regarding ANP, previous evidence has shown that LV hypertrophy is favored by low levels of ANP, independently from blood pressure in hypertension . More recently, Rubattu et al.  demonstrates that levels of N-terminal-proatrial natriuretic peptide are significantly reduced in hypertensive patients affected by MS, and they are significantly inversely related to the increased LV hypertrophy observed in these patients.
Similarly, arterial remodeling was also observed in F rats, since that these animals presented an increase in area, diameter, intima media thickness and circumferential wall tension, along with a reduction in the number of elastic lamellae. We may hypothesize that the increase in systolic arterial pressure together with increased aorta circumferential wall tension would account, at least in part, for arterial remodeling.
In addition, the loss of distensibility of the aorta and carotid arteries has been associated with changes in baroreflex sensitivity [44, 45], since the mechanical stress of the arteries wall would not be able to adequately trigger the mechanoreceptors. Thus, the increase in volumetric density of collagen in the aorta of the F rats, as well as the correlations observed between the numbers of elastic lamellae with baroreflex sensitivity, seem to lend support to our contention that structural changes are associated with reduced autonomic function observed in the MS rats. Furthermore, we observed positive correlations between white adipose tissue and heart weight/body weight ratio, as well as with LV volumetric density of collagen fibers, suggesting that fat mass increments, and putative increased metabolic activity, may be associated with cardiac remodeling.
Few data exist with respect to how ET superimposed on hypertension impacts on LV and aorta remodeling. In the present study, LET was able to prevent the ventricular and aortic remodeling, normalizing heart weigh / body weight ratio, numerical density of capillaries, volumetric density of myocytes and collagen fibers in the LV, as well as improving intima-media thickness, volumetric density of collagen fibers, and circumferential wall tension in the aorta. Thus, it is possible that the changes induced by ET, as decrease of arterial pressure levels and arterial pressure variability, improvement of baroreflex sensitivity, as well as reduction of peripheral sympathetic modulation, have prevented ventricular and arterial pathological remodeling in trained animals. Furthermore, we cannot rule out the hypothesis that the normalization of numerical density of ANP granules may suggest peptide levels normalization, a fact that could also be associated with improved ventricular remodeling  in the trained group. However, future studies are necessary to better understand the possible mechanisms associated with this structural improvement.
This study has its limitations and opens opportunities for future research. First, although in this study comparative data with trained control group are not presented, we provided a range of in vivo and histological evidences about the effects of low intensity ET in a MS model. Moreover, the main focus of this study was to evaluate the effects of low intensity ET on the MS cardiovascular complications. Analysis of ANP activity, insulin concentration and receptors expression, as well as possible molecular mechanisms associated with the prevention of hemodynamic, autonomic and structural impairment by ET, were not performed in this study. Further studies are needed that address such issues.