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Resistance training improves aortic structure in Wistar rats.

ABSTRACT: Little information is available on the effects of resistance training on the aortic wall.This study aimed to quantify the effects of a resistance-training program on blood pressure and aortic wall structural components.Rats (aged three months) were randomized into sedentary group (control group, CG; n=10) or trained group (TG; n=10). The TG rats performed resistance training by climbing a 1.1-m vertical ladder (80° incline) five times a week for 12 weeks, and the CG remained sedentary. The rats were sacrificed and 5mm of the ascending aorta was submitted to histological sections, which were stained with hematoxylin-eosin, Picrosirius red, and Verhoeff's elastin, and used for morphometric studies. Left ventricle (LV) hypertrophy was determined by measuring LV wall thickness and LV internal diameter.The rats had similar repetition maximum before the resistance training. At the end of the resistance training period, the repetition maximum of the TG was 3.04-fold greater than the body weight. In the twelfth month, the left ventricular weight was 15.3% larger in the TG than in the CG, and the left ventricular internal diameter was reduced by 10% in the TG. Rats exposed to resistance training had a significant increase in aortic wall thickness, in both elastic lamina and collagen fibers, and in the thickness of collagen fibrils.Resistance training induces the development of concentric cardiac hypertrophy and improves the aortic wall components by producing a morphological expression pattern distinct from aortic pathological adaptation.

SUBMITTER: Souza RR

PROVIDER: S-EPMC5537473 | biostudies-other | 2017 Jul - Aug

REPOSITORIES: biostudies-other

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Project description:BackgroundObesity has been associated with a variety of disease such as type II diabetes mellitus, arterial hypertension and atherosclerosis. Evidences have shown that exercise training promotes beneficial effects on these disorders, but the underlying mechanisms are not fully understood. The aim of this study was to investigate whether physical preconditioning prevents the deleterious effect of high caloric diet in vascular reactivity of rat aortic and mesenteric rings.MethodsMale Wistar rats were divided into sedentary (SD); trained (TR); sedentary diet (SDD) and trained diet (TRD) groups. Run training (RT) was performed in sessions of 60 min, 5 days/week for 12 weeks (70-80% VO2max). Triglycerides, glucose, insulin and nitrite/nitrate concentrations (NOx-) were measured. Concentration-response curves to acetylcholine (ACh) and sodium nitroprusside (SNP) were obtained. Expression of Cu/Zn superoxide dismutase (SOD-1) was assessed by Western blotting.ResultsHigh caloric diet increased triglycerides concentration (SDD: 216 +/- 25 mg/dl) and exercise training restored to the baseline value (TRD: 89 +/- 9 mg/dl). Physical preconditioning significantly reduced insulin levels in both groups (TR: 0.54 +/- 0.1 and TRD: 1.24 +/- 0.3 ng/ml) as compared to sedentary animals (SD: 0.87 +/- 0.1 and SDD: 2.57 +/- 0.3 ng/ml). On the other hand, glucose concentration was slightly increased by high caloric diet, and RT did not modify this parameter (SD: 126 +/- 6; TR: 140 +/- 8; SDD: 156 +/- 8 and TRD 153 +/- 9 mg/dl). Neither high caloric diet nor RT modified NOx- levels (SD: 27 +/- 4; TR: 28 +/- 6; SDD: 27 +/- 3 and TRD: 30 +/- 2 microM). Functional assays showed that high caloric diet impaired the relaxing response to ACh in mesenteric (about 13%), but not in aortic rings. RT improved the relaxing responses to ACh either in aortic (28%, for TR and 16%, to TRD groups) or mesenteric rings (10%, for TR and 17%, to TRD groups) that was accompanied by up-regulation of SOD-1 expression and reduction in triglycerides levels.ConclusionThe improvement in endothelial function by physical preconditioning in mesenteric and aortic arteries from high caloric fed-rats was directly related to an increase in NO bioavailability to the smooth muscle mostly due to SOD-1 up regulation.

Project description:This study investigated the effect of non-periodized training performed at 80, 100 and 120% of the anaerobic threshold intensity (AnT) and a linear periodized training model adapted for swimming rats on the gene expression of monocarboxylate transporters 1 and 4 (MCT1 and 4, in soleus and gastrocnemius muscles), protein contents, blood biomarkers, tissue glycogen, body mass, and aerobic and anaerobic capacities. Sixty Wistar rats were randomly divided into 6 groups (n = 10 per group): a baseline (BL; euthanized before training period), a control group (GC; not exercised during the training period), three groups exercised at intensities equivalent to 80, 100 and 120% of the AnT (G80, G100 and G120, respectively) at the equal workload and a linear periodized training group (GPE). Each training program lasted 12 weeks subdivided into three periods: basic mesocycle (6 weeks), specific mesocycle (5 weeks) and taper (1 week). Although G80, G100 and G120 groups were submitted to monotony workload (i.e. non-modulation at intensity or volume throughout the training program), rodents were evaluated during the same experimental timepoints as GPE to be able comparisons. Our main results showed that all training programs were capable to minimize the aerobic capacity decrease promoted by age, which were compared to control group. Rats trained in periodization model had reduced levels of lipid blood biomarkers and increased hepatic glycogen stores compared to all other trained groups. At the molecular level, only expressions of MCT1 in the muscle were modified by different training regimens, with MCT1 mRNA increasing in rats trained at lower intensities (G80), and MCT1 protein content showed higher values in non-periodized groups compared to pre-training and GPE. Here, training at different intensities but at same total workload promoted similar adaptations in rats. Nevertheless, our results suggested that periodized training seems to be optimize the physiological responses of rats.

Project description:BackgroundThe mechanism for cardiac hypertrophy process that would be a benefit for improvement of cardiovascular endurance needed to be investigated throughly. Specific intensity of training may play a role for homeostasis process in cardiac during training. In the present study, we examine the effect of different intensity of treadmill training on cardiac hypertrophy process and autophagy related gene expression in male wistar rats.MethodsThree different intensities of treadmill training were conducted on 15 male wistar rats (Low Intensity: 10 m/minute, Moderate Intensity: 20 m/minute, and High Intensity: 30 m/minute) compared to 5 sedentary rats as control. Training duration was 30 min per day, frequency was 5 days per week, during 8 weeks period. Heart weight and heart weight/body weight ratio were measured after the experiments. Left ventricle myocardium was taken for microscopic analysis with HE staining. mRNA was extracted from left ventricle myocardium for examining αMHC and autophagy related gene expression (PIK3CA, mTOR, LC3, p62) using semi quantitative PCR.ResultsWe observed that altered training intensity might stimulate cardiac hypertrophy process. MI and HI training increased heart weight and heart weight/body weight ratio. This finding is supported by microscopic result in which cardiac hypertrophy was found in MI and HI, with focal fibrosis in HI, and increased αMHC gene expression in MI (p < 0.05) and HI (p = 0.076). We also observed decreased PIK3CA (LI 0.8 fold, MI 0.9 fold), mTOR (LI 0.9 fold, MI 0.9 fold), LC3 (LI 0.9 fold, MI 0.8 fold, HI 0.8 fold), and p62 (LI 0.8 fold, MI 0.9 fold) compared to control. Interestingly, we found increased mTOR (HI 1.1 fold) and p62 (HI 1.1 fold) compared to control.ConclusionTraining with different intensity creates different cardiac hypertrophy process based on heart weight and heart weight/body weight ratio, microscopic examination and autophagy related gene expression.

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Resistance training improves aortic structure in Wistar rats.

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