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1.
Arq Bras Cardiol ; 117(2): 309-316, 2021 08.
Artigo em Inglês, Português | MEDLINE | ID: mdl-34495225

RESUMO

BACKGROUND: Although maximal and submaximal walking are recommended for patients with peripheral artery disease (PAD), performing these exercises may induce different physiological responses. OBJECTIVES: To compare the acute effects of maximal and submaximal walking on post-exercise cardiovascular function, regulation, and associated pathophysiological processes in patients with symptomatic PAD. METHODS: Thirty male patients underwent 2 sessions: maximal walking (Gardner's protocol) and submaximal walking (15 bouts of 2 minutes of walking separated by 2 minutes of upright rest). In each session, blood pressure (BP), heart rate (HR), cardiac autonomic modulation (HR variability), forearm and calf blood flows (BF), vasodilatory capacity (reactive hyperemia), nitric oxide (NO), oxidative stress (lipid peroxidation), and inflammation (four markers) were measured pre- and post-walking. ANOVAs were employed, and p < 0.05 was considered significant. RESULTS: Systolic and mean BP decreased after the submaximal session, but they increased after the maximal session (interactions, p < 0.001 for both). Diastolic BP did not change after the submaximal session (p > 0.05), and it increased after maximal walking (interaction, p < 0.001). HR, sympathovagal balance, and BF increased similarly after both sessions (moment, p < 0.001, p = 0.04, and p < 0.001, respectively), while vasodilatory capacity, NO, and oxidative stress remained unchanged (p > 0.05). Vascular and intercellular adhesion molecules increased similarly after both maximal and submaximal walking sessions (moment, p = 0.001). CONCLUSIONS: In patients with symptomatic PAD, submaximal, but not maximal walking reduced post-exercise BP, while maximal walking maintained elevated cardiac overload during the recovery period. On the other hand, maximal and submaximal walking sessions similarly increased post-exercise HR, cardiac sympathovagal balance, and inflammation, while they did not change post-exercise NO bioavailability and oxidative stress.


Assuntos
Doença Arterial Periférica , Caminhada , Pressão Sanguínea , Teste de Esforço , Frequência Cardíaca , Humanos , Claudicação Intermitente , Masculino
2.
Eur J Vasc Endovasc Surg ; 61(6): 954-963, 2021 06.
Artigo em Inglês | MEDLINE | ID: mdl-33875324

RESUMO

OBJECTIVE: This study examined the impact of submaximal walking training (WT) on local and systemic nitric oxide (NO) bioavailability, inflammation, and oxidative stress in patients with intermittent claudication (IC). METHODS: The study employed a randomised, controlled, parallel group design and was performed in a single centre. Thirty-two men with IC were randomly allocated to two groups: WT (n = 16, two sessions/week, 15 cycles of two minutes walking at an intensity corresponding to the heart rate obtained at the pain threshold interspersed by two minutes of upright rest) and control (CO, n = 16, two sessions/week, 30 minutes of stretching). NO bioavailability (blood NO and muscle nitric oxide synthase [eNOS]), redox homeostasis (catalase [CAT], superoxide dismutase [SOD], lipid peroxidation [LPO] measured in blood and muscle), and inflammation (interleukin-6 [IL-6], C-reactive protein [CRP], tumour necrosis factor α [TNF-α], intercellular adhesion molecules [ICAM], vascular adhesion molecules [VCAM] measured in blood and muscle) were assessed at baseline and after 12 weeks. RESULTS: WT statistically significantly increased blood NO, muscle eNOS, blood SOD and CAT, and muscle SOD and abolished the increase in circulating and muscle LPO observed in the CO group. WT decreased blood CRP, ICAM, and VCAM and muscle IL-6 and CRP and eliminated the increase in blood TNF-α and muscle TNF-α, ICAM and VCAM observed in the CO group. CONCLUSION: WT at an intensity of pain threshold improved NO bioavailability and decreased systemic and local oxidative stress and inflammation in patients with IC. The proposed WT protocol provides physiological adaptations that may contribute to cardiovascular health in these patients.


Assuntos
Exercício Físico/fisiologia , Inflamação , Claudicação Intermitente , Músculo Esquelético/metabolismo , Estresse Oxidativo , Caminhada/fisiologia , Adaptação Fisiológica/fisiologia , Proteína C-Reativa/análise , Teste de Esforço/métodos , Fatores de Risco de Doenças Cardíacas , Humanos , Claudicação Intermitente/sangue , Claudicação Intermitente/fisiopatologia , Claudicação Intermitente/terapia , Masculino , Pessoa de Meia-Idade , Óxido Nítrico/análise , Avaliação de Resultados em Cuidados de Saúde , Superóxido Dismutase/análise , Molécula 1 de Adesão de Célula Vascular/análise
3.
J Am Heart Assoc ; 10(5): e018076, 2021 02.
Artigo em Inglês | MEDLINE | ID: mdl-33619982

RESUMO

Background Patients treated for breast cancer have a high incidence of cardiovascular complications. In this study, we evaluated the impact of breast cancer on cardiac function and cardiomyocyte Ca2+-handling protein expression. We also investigated whether exercise training (ET) would prevent these potential alterations. Methods and Results Transgenic mice with spontaneous breast cancer (mouse mammary tumor virus-polyomavirus middle T antigen [MMTV-PyMT+], n=15) and littermate mice with no cancer (MMTV-PyMT-, n=14) were studied. For the ET analysis, MMTV-PyMT+ were divided into sedentary (n=10) and exercise-trained (n=12) groups. Cardiac function was evaluated by echocardiography with speckle-tracking imaging. Exercise tolerance test was conducted on a treadmill. Both studies were performed when the tumor became palpable and when it reached 1 cm3. After euthanasia, Ca2+-handling protein expression (Western blot) was evaluated. Exercise capacity was reduced in MMTV-PyMT+ compared with MMTV-PyMT- (Pinteraction=0.031). Longitudinal strain (Pgroup <0.001) and strain rate (Pgroup=0.030) were impaired. Cardiomyocyte phospholamban was increased (P=0.011), whereas phospho-phospholamban and sodium/calcium exchanger were decreased (P=0.038 and P=0.017, respectively) in MMTV-PyMT+. No significant difference in sarcoplasmic or endoplasmic reticulum calcium 2 ATPase (SERCA2a) was found. SERCA2a/phospholamban ratio was reduced (P=0.007). ET was not associated with increased exercise capacity. ET decreased left ventricular end-systolic diameter (Pgroup=0.038) and end-diastolic volume (Pgroup=0.026). Other morphological and functional cardiac parameters were not improved by ET in MMTV-PyMT+. ET did not improve cardiomyocyte Ca2+-handling protein expression. Conclusions Breast cancer is associated with decreased exercise capacity and subclinical left ventricular dysfunction in MMTV-PyMT+, which is at least partly associated with dysregulation of cardiomyocyte Ca2+ handling. ET did not prevent or reverse these changes.


Assuntos
Neoplasias da Mama/complicações , Cálcio/metabolismo , Doenças Cardiovasculares/etiologia , Ventrículos do Coração/fisiopatologia , Miócitos Cardíacos/metabolismo , Condicionamento Físico Animal/métodos , Função Ventricular Esquerda/fisiologia , Animais , Neoplasias da Mama/metabolismo , Neoplasias da Mama/patologia , Doenças Cardiovasculares/diagnóstico , Doenças Cardiovasculares/metabolismo , Ecocardiografia Doppler , Feminino , Ventrículos do Coração/diagnóstico por imagem , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Transgênicos , Miócitos Cardíacos/patologia , Neoplasias Experimentais , ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático/metabolismo
4.
J Cell Physiol ; 236(2): 900-910, 2021 02.
Artigo em Inglês | MEDLINE | ID: mdl-32617979

RESUMO

This study investigated whether regulation of the renin-angiotensin system (RAS) by enalapril and/or aerobic exercise training (AET) causes browning of the subcutaneous white adipose tissue (sWAT). C57BL/6 mice were fed either a standard chow or a high-fat (HF) diet for 16 weeks. At Week 8, HF-fed animals were divided into sedentary (HF), enalapril (HF-E), AET (HF-T), and enalapril plus AET (HF-ET) groups. Subsequently, sWAT was extracted for morphometry, determination of RAS expression, and biomarkers of WAT browning. The HF group displayed adipocyte hypertrophy and induction of the classical RAS axis. Conversely, all interventions reduced adiposity and induced the counterregulatory RAS axis. However, only AET raised plasma irisin, increased peroxisome proliferator-activated receptor-γ coactivator-1α, and uncoupling protein-1 levels, and the expression of PR-domain containing 16 in sWAT. Therefore, we concluded that AET-induced sWAT browning was independent of the counterregulatory axis shifting of RAS in HF diet-induced obesity.


Assuntos
Tecido Adiposo Marrom/efeitos dos fármacos , Tecido Adiposo Marrom/fisiopatologia , Adiposidade/efeitos dos fármacos , Enalapril/farmacologia , Condicionamento Físico Animal/fisiologia , Corrida/fisiologia , Gordura Subcutânea/efeitos dos fármacos , Tecido Adiposo Marrom/metabolismo , Tecido Adiposo Branco/metabolismo , Tecido Adiposo Branco/fisiopatologia , Animais , Biomarcadores/metabolismo , Dieta Hiperlipídica/efeitos adversos , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Obesidade/metabolismo , Obesidade/fisiopatologia , Sistema Renina-Angiotensina/efeitos dos fármacos , Gordura Subcutânea/metabolismo , Gordura Subcutânea/fisiopatologia
5.
J Cardiovasc Nurs ; 2020 May 14.
Artigo em Inglês | MEDLINE | ID: mdl-32427794

RESUMO

OBJECTIVE: The aim of this study was to assess the effects of a single bout of maximal walking on blood and muscle nitric oxide (NO) bioavailability, oxidative stress, and inflammation in symptomatic peripheral artery disease (PAD) patients. METHODS: A total of 35 men with symptomatic PAD performed a graded maximal exercise test on a treadmill (3.2 km/h, 2% increase in grade every 2 minutes). Plasma samples and gastrocnemius muscle biopsies were collected preexercise and postexercise for assessment of NO bioavailability (plasma NO and muscle, endothelial NO synthase), oxidative stress and antioxidant function (lipid peroxidation [LPO], catalase [CAT], and superoxide dismutase), and inflammation (interleukin-6, C-reactive protein, tumor necrosis factor-α, intercellular adhesion molecules, and vascular adhesion molecules). The effects of the walking exercise were assessed using paired t tests or Wilcoxon tests. RESULTS: After maximal walking, plasma NO and LPO were unchanged (P > .05), plasma CAT decreased, and all blood inflammatory markers increased (all P ≤ .05). In the disease-affected skeletal muscle, endothelial NO synthase, CAT, LPO, and all inflammatory markers increased, whereas superoxide dismutase decreased (all P ≤ .05). CONCLUSION: In patients with symptomatic PAD, maximal exercise induces local and systemic impairments, which may play a key role in atherogenesis. Exercise strategies that avoid maximal effort may be important to reduce local and systemic damage and enhance clinical benefits.

6.
Med Sci Sports Exerc ; 52(10): 2117-2126, 2020 10.
Artigo em Inglês | MEDLINE | ID: mdl-32301852

RESUMO

PURPOSE: The beneficial effects of exercise training on the cardiovascular system are well known. Because our knowledge of exercise-induced vascular function is still limited, we aimed to uncover the molecular mechanisms conditioning the improved vascular relaxation in muscular arteries. METHODS: Male Wistar-Kyoto rats with the same ability to run on a treadmill after maximal exercise tests were allocated to the following two groups: trained (Tr) (treadmill, 50%-60% of maximal capacity, 5 d·wk) and untrained (UnTr). After 13 wk, the femoral arteries were harvested and used for functional, structural, and molecular analyses. RESULTS: Acetylcholine (ACh)-induced relaxation and nitric oxide (NO) production were enhanced in arteries from Tr rats compared with UnTr rats. Tr arteries exhibited reduced microRNA (miRNA)-124a expression (whose target is caveolin-1), increased the density of caveolae aligned along the sarcolemma and reduced ACh-induced relaxation in the presence of methyl-ß-cyclodextrin, which disrupts caveolae. Higher endothelial NO synthase (eNOS) expression with lower miRNA-155 expression and the posttranslational modification of eNOS (phosphorylation of stimulatory Ser1177 and dephosphorylation of inhibitory Thr495) by the PI3-kinase/Akt1/2/3 pathway also contributed to the higher NO production induced by exercise training. Furthermore, increased Cu/Zn- and extracellular-superoxide dismutase expression and enhanced effects of their pharmacological scavenger activity on the ACh-induced response were observed in Tr arteries. CONCLUSIONS: The results of the present study provide a molecular basis for exercise-induced NO bioavailability in healthy femoral arteries. Increased caveolae domain and eNOS expression/activity in Tr arteries are associated with downregulation of miRNA-124a and -155, as well as are involved with higher antioxidant defense, subsequently inducing a favorable endothelium-dependent milieu in Tr arteries.


Assuntos
Músculo Liso Vascular/fisiologia , Condicionamento Físico Animal/fisiologia , Vasodilatação/fisiologia , Animais , Disponibilidade Biológica , Proteínas de Transporte/metabolismo , Caveolina 1/metabolismo , Regulação para Baixo , Artéria Femoral/fisiologia , Masculino , MicroRNAs/metabolismo , Óxido Nítrico/metabolismo , Óxido Nítrico Sintase Tipo III/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Ratos Endogâmicos WKY
7.
Sleep Breath ; 24(4): 1463-1472, 2020 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31898194

RESUMO

PURPOSE: Obstructive sleep apnea (OSA) is associated with multiple comorbid conditions including cardiovascular diseases and cancer. There is a growing interest in exploring biomarkers to understand the related mechanisms and improve the risk stratification of OSA. Circulating microRNAs (miRNAs) are single noncoding strands of nearly 22 nucleotides that posttranscriptionally regulate target gene expression. Our aim was to identify miRNA profiles associated with OSA. METHODS: We studied 48 male subjects, mostly Caucasian (63%) and overweight, divided by polysomnography into the no OSA control group (n = 6), mild OSA group (n = 12), moderate OSA group (n = 15), and severe OSA group (n = 15). The study groups were matched for age, body mass index (BMI), and body fat composition. miRNA profiles were measured from peripheral whole blood using two steps: (1) microarray analysis comprising more than 2500 miRNAs in a subsample of 12 subjects (three from each group); and (2) validation phase using real-time quantitative polymerase chain reaction (RTqPCR). RESULTS: The microarray assessment identified 21 differentially expressed miRNAs among the groups. The RT-qPCR assessment showed that miR-1254 and miR-320e presented a gradual increase in expression parallel to OSA severity. Linear regression analysis showed that severe OSA was independently associated with miR-1254 (ß = 68.4; EP = 29.8; p = 0.02) and miR-320e (ß = 76.1; EP = 31.3; p = 0.02). CONCLUSION: Severe OSA is independently associated with miRNAs that are involved in heart failure (miR-1254), myocardial ischemia/reperfusion (miR-320e), and cell proliferation in some cancer types (miR-1254 and miR-320e). Future investigations addressing whether these miRs may provide prognostic information in OSA are needed.

8.
Nutr Metab Cardiovasc Dis ; 30(1): 60-70, 2020 01 03.
Artigo em Inglês | MEDLINE | ID: mdl-31753788

RESUMO

BACKGROUND AND AIMS: The purpose of this study was to investigate whether an intervention with physical activity (PA) would promote positive effects on the angiogenic factors, mobilization, and functionality of circulating endothelial progenitor cells (EPCs) in children with low birth weight (LBW). METHODS AND RESULTS: Thirty-five children participated in a 10-week PA program (intensity: 75-85% of heart rate reserve, frequency: four times/week, and duration: 45 min). Before and after the PA program, we evaluated anthropometric parameters, blood pressure levels, biochemical profile, number of EPCs, number of EPC colony forming units, and plasma levels of vascular endothelial growth factor-A (VEGF-A), nitric oxide (NO), and matrix metalloproteinases (MMPs) 2 and 9. We found a significant main effect of the PA program on waist circumference (ηp2 = 0.489), cardiorespiratory fitness (ηp2 = 0.463), and MMP-9 (ηp2 = 0.582). Birth weight or the PA program produced significant independent effects on systolic blood pressure (birth weight: ηp2 = 0.431; PA program: ηp2 = 0.615) and EPC colony forming units (birth weight: ηp2 = 0.541; PA program: ηp2 = 0.698) with no significant interactions. The combination of birth weight and the PA program produced a significant interaction effect on the number of circulating EPCs (ηp2 = 0.123), NO (ηp2 = 0.258), and VEGF-A (ηp2 = 0.175). The variation in the number of EPCs from baseline to 10 weeks of the PA program correlated positively with the change in NO (P = 0.002) and VEGF-A (P = 0.004). CONCLUSIONS: A 10-week PA program attenuates the adverse effect of LBW on the number and functionality of EPCs; this effect occurs through an improvement in circulating levels of NO and VEGF-A. CLINICAL TRIALS: https://www.clinicaltrials.gov. Unique Identifier: NCT02982967. Date: December/2016.


Assuntos
Proliferação de Células , Células Progenitoras Endoteliais/metabolismo , Terapia por Exercício , Recém-Nascido de Baixo Peso , Óxido Nítrico/sangue , Fator A de Crescimento do Endotélio Vascular/sangue , Adolescente , Desenvolvimento do Adolescente , Fatores Etários , Biomarcadores/sangue , Peso ao Nascer , Pressão Sanguínea , Brasil , Aptidão Cardiorrespiratória , Criança , Desenvolvimento Infantil , Feminino , Humanos , Recém-Nascido , Masculino , Metaloproteinase 2 da Matriz/sangue , Metaloproteinase 9 da Matriz/sangue , Fatores de Tempo , Resultado do Tratamento , Circunferência da Cintura
9.
J Cachexia Sarcopenia Muscle ; 11(1): 89-102, 2020 02.
Artigo em Inglês | MEDLINE | ID: mdl-31743617

RESUMO

BACKGROUND: The exercise intolerance in chronic heart failure with reduced ejection fraction (HFrEF) is mostly attributed to alterations in skeletal muscle. However, the mechanisms underlying the skeletal myopathy in patients with HFrEF are not completely understood. We hypothesized that (i) aerobic exercise training (AET) and inspiratory muscle training (IMT) would change skeletal muscle microRNA-1 expression and downstream-associated pathways in patients with HFrEF and (ii) AET and IMT would increase leg blood flow (LBF), functional capacity, and quality of life in these patients. METHODS: Patients age 35 to 70 years, left ventricular ejection fraction (LVEF) ≤40%, New York Heart Association functional classes II-III, were randomized into control, IMT, and AET groups. Skeletal muscle changes were examined by vastus lateralis biopsy. LBF was measured by venous occlusion plethysmography, functional capacity by cardiopulmonary exercise test, and quality of life by Minnesota Living with Heart Failure Questionnaire. All patients were evaluated at baseline and after 4 months. RESULTS: Thirty-three patients finished the study protocol: control (n = 10; LVEF = 25 ± 1%; six males), IMT (n = 11; LVEF = 31 ± 2%; three males), and AET (n = 12; LVEF = 26 ± 2%; seven males). AET, but not IMT, increased the expression of microRNA-1 (P = 0.02; percent changes = 53 ± 17%), decreased the expression of PTEN (P = 0.003; percent changes = -15 ± 0.03%), and tended to increase the p-AKTser473 /AKT ratio (P = 0.06). In addition, AET decreased HDAC4 expression (P = 0.03; percent changes = -40 ± 19%) and upregulated follistatin (P = 0.01; percent changes = 174 ± 58%), MEF2C (P = 0.05; percent changes = 34 ± 15%), and MyoD expression (P = 0.05; percent changes = 47 ± 18%). AET also increased muscle cross-sectional area (P = 0.01). AET and IMT increased LBF, functional capacity, and quality of life. Further analyses showed a significant correlation between percent changes in microRNA-1 and percent changes in follistatin mRNA (P = 0.001, rho = 0.58) and between percent changes in follistatin mRNA and percent changes in peak VO2 (P = 0.004, rho = 0.51). CONCLUSIONS: AET upregulates microRNA-1 levels and decreases the protein expression of PTEN, which reduces the inhibitory action on the PI3K-AKT pathway that regulates the skeletal muscle tropism. The increased levels of microRNA-1 also decreased HDAC4 and increased MEF2c, MyoD, and follistatin expression, improving skeletal muscle regeneration. These changes associated with the increase in muscle cross-sectional area and LBF contribute to the attenuation in skeletal myopathy, and the improvement in functional capacity and quality of life in patients with HFrEF. IMT caused no changes in microRNA-1 and in the downstream-associated pathway. The increased functional capacity provoked by IMT seems to be associated with amelioration in the respiratory function instead of changes in skeletal muscle. ClinicalTrials.gov (Identifier: NCT01747395).


Assuntos
Insuficiência Cardíaca/terapia , Inalação/fisiologia , MicroRNAs/metabolismo , Qualidade de Vida/psicologia , Volume Sistólico/fisiologia , Adulto , Idoso , Exercício Físico/fisiologia , Feminino , Insuficiência Cardíaca/genética , Humanos , Masculino , Pessoa de Meia-Idade
10.
Rev Port Cardiol (Engl Ed) ; 38(9): 649-656, 2019 Sep.
Artigo em Inglês, Português | MEDLINE | ID: mdl-31812373

RESUMO

INTRODUCTION AND OBJECTIVES: Stem cell therapy and aerobic exercise are non-pharmacological therapies following myocardial infarction. The aim of this study was to test whether aerobic exercise training enhances the benefits of mesenchymal stem cell (MSC) therapy on remodeling of the extracellular matrix and fetal gene expression in the left ventricle of infarcted rats. METHODS: Myocardial infarction was surgically induced in six-week old male Wistar rats. Animals were divided into four groups: sedentary control (SC) and sedentary and stem cell treated (SCMSC); exercised (EX) and exercised and stem cell treated (EXMSC). Bone marrow-derived MSCs were immediately transplanted via the tail vein (concentration: 1×106 cells). Exercise training (five days/week, 60 min/day; 60% of maximal running speed) started 24 hours after myocardial infarction and lasted for 12 weeks. RESULTS: Exercise capacity was higher in exercised than in sedentary groups. Animals in the SCMSC, EX and EXMSC groups exhibited better cardiac function than those in SC. Collagen content was lower in the SCMSC, EX and EXMSC groups than in SC and skeletal α-actin expression was lower in EX and EXMSC than in SC. The α/ß-MHC ratio was higher in EX and EXMSC than in SC. The combination of therapies further reduced collagen content in the remote region of the infarct (∼24%) and skeletal α-actin expression (∼30%). CONCLUSION: Aerobic exercise training appears to enhance the beneficial effects of stem cell therapy on remodeling of the extracellular matrix and fetal gene expression in the left ventricle of rats with moderate infarction.


Assuntos
Ventrículos do Coração , Transplante de Células-Tronco Mesenquimais , Infarto do Miocárdio/cirurgia , Condicionamento Físico Animal/fisiologia , Animais , Modelos Animais de Doenças , Ventrículos do Coração/metabolismo , Ventrículos do Coração/cirurgia , Masculino , Ratos , Ratos Wistar
11.
Cell Biol Int ; 43(8): 890-898, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-31062893

RESUMO

The present study aimed to test the hypothesis that increased sodium concentration affects the migratory phenotype of vascular smooth muscle cells (VSMCs) independently of the haemodynamic factors. Cell migration was evaluated by wound-healing assay under the following conditions: high sodium (HS, 160 mM) and control (CT, 140 mM). Cell viability was assessed by annexin V and propidium iodide labeling. Cyclooxygenase-2 (COX-2) gene expression was analysed by reverse transcription polymerase chain reaction. ERK1/2 phosphorylation was assessed by western blot. Exposure of VSMCs to HS reduced migration, and AT1R blockade prevented this response. HS increased COX-2 gene expression, and COX-2 blockade prevented the reduction in VSMC migration induced by HS. HS also increased ERK1/2 phosphorylation, and ERK1/2 inhibition recovered VSMC migration as well as blocked COX-2 gene expression. The TXA2 receptor blocker, but not the prostacyclin receptor blocker, prevented the HS-induced VSMCs migration decrease. HS reduces the migration of VSMCs by increasing COX-2 gene expression via AT1R-ERK1/2 phosphorylation. In addition, increased COX-2 by HS seems to modulate the reduction of VSMCs migration by the TXA2 receptor.


Assuntos
Movimento Celular/efeitos dos fármacos , Músculo Liso Vascular , Miócitos de Músculo Liso/metabolismo , Receptor Tipo 1 de Angiotensina/metabolismo , Sódio/farmacologia , Animais , Células Cultivadas , Ciclo-Oxigenase 2/metabolismo , Proteína Quinase 1 Ativada por Mitógeno/metabolismo , Proteína Quinase 3 Ativada por Mitógeno/metabolismo , Músculo Liso Vascular/citologia , Músculo Liso Vascular/metabolismo , Miócitos de Músculo Liso/citologia , Receptores de Tromboxano A2 e Prostaglandina H2/metabolismo , Sódio/química
12.
Lipids ; 54(6-7): 381-388, 2019 06.
Artigo em Inglês | MEDLINE | ID: mdl-31141200

RESUMO

Exercise training not only improves the plasma lipid profile but also reduces risk of developing coronary heart disease. We investigate whether plasma lipids and high density lipoprotein (HDL) metabolism are affected by aerobic training and whether the high-density lipoprotein cholesterol (HDL-C) levels at baseline influence exercise-induced changes in HDL. Seventy-one male sedentary volunteers were evaluated and allocated in two subgroups, according to the HLD-C levels (< or >40 mg/dL). Participants underwent an 18-week aerobic training period. Blood was sampled before and after training for biochemical analysis. Plasma lipids, apolipoproteins, HDL diameter, and VO2 peak were determined. Lipid transfers to HDL were determined in vitro by incubating plasma samples with a donor lipid artificial nanoemulsion. After the 18-week period of aerobic training, the VO2 peak increased, while the mean body mass index (BMI) decreased. HDL-C concentration was higher after the training period, but low-density lipoprotein cholesterol (LDL-C) and non-HDL-C did not change. The transfer of esterified cholesterol and phospholipids was greater after exercise training, but the triacylglycerol and unesterified cholesterol transfers were unchanged. The HDL particle diameter increased after aerobic training in all participants. When the participants were separated in low-HDL and normal-HDL groups, the postaerobic exercise increment in HDL-C was higher in the low-HDL group, while the transfer of esterified cholesterol was lower. In conclusion, aerobic exercise training increases the lipid transfers to HDL, as measured by an in vitro method, which possibly contributes to the classical elevation of the HDL-C associated with training.


Assuntos
Colesterol/metabolismo , Exercício Físico , Lipoproteínas HDL/química , Lipoproteínas HDL/metabolismo , Adulto , Colesterol/sangue , Humanos , Lipoproteínas HDL/sangue , Masculino , Tamanho da Partícula , Adulto Jovem
13.
J Strength Cond Res ; 33(4): 1119-1129, 2019 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-30908459

RESUMO

Montrezol, FT, Marinho, R, Mota, GdFAd, D'almeida, V, de Oliveira, EM, Gomes, RJ, and Medeiros, A. ACE gene plays a key role in reducing blood pressure in the hyperintensive elderly after resistance training. J Strength Cond Res 33(4): 1119-1129, 2019-Hypertension is a difficult disease to control and exercise training plays a key role in hypertension control. Some individuals are not responsive to exercise training; so, we highlight the polymorphism of I allele of angiotensin-converting enzyme (ACE) as a factor responsible for this lack of responsiveness. The aim of this study was to evaluate the influence of ACE insertion/deletion genotypes on effects of resistance training on blood pressure (BP) and chronic inflammation. Eighty-six hypertensive volunteers, aged between 60 and 80, were evaluated. They performed 16 weeks of resistance training at 50% of 1 maximal repetition. The greatest benefits were seen on homozygous of the Insertion allele, whom presented reduction of systolic blood pressure (SBP: 129.31 ± 13.34 vs. 122.56 ± 9.68 mm Hg, p < 0.001) and diastolic blood pressure (DBP: 79.18 ± 8.05 vs. 70.12 ± 7.71 mm Hg, p < 0.01) during daytime period, and in 24-hour period (SBP: 127.12 ± 13.65 vs. 121.06± 9.68 mm Hg, p < 0.001 and DBP: 71.87 ± 8.39 vs. 68.75 ± 8.72 mm Hg, p < 0.05) and also increased circulating adiponectin levels (4.04 ± 1.79 vs. 6.00 ± 2.81 ng·ml, p < 0.01). Other genotypes showed no changes in BP and biochemical parameters. Our results suggest a cardio protective factor of I allele because only those homozygous showed reductions in BP and increases in adiponectin.


Assuntos
Pressão Sanguínea/genética , Hipertensão/genética , Hipertensão/fisiopatologia , Peptidil Dipeptidase A/genética , Treinamento de Força , Adiponectina/sangue , Idoso , Idoso de 80 Anos ou mais , Alelos , Doença Crônica , Exercício Físico/fisiologia , Feminino , Homozigoto , Humanos , Hipertensão/sangue , Mutação INDEL , Inflamação/sangue , Inflamação/genética , Masculino , Pessoa de Meia-Idade , Polimorfismo Genético
15.
Clin Physiol Funct Imaging ; 38(2): 206-212, 2018 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-27925380

RESUMO

The renin-angiotensin aldosterone system (RAAS) is associated with diverse physiological responses and adaptations to exercise. The angiotensin converting enzyme (ACE) 2 has vasodilatory effects, which might be associated with the blood pressure (BP) responses to acute exercise. The aim of this study was to investigate the role of ACE2 polymorphisms in postexercise hypotension (PEH). Thirty-four medicated hypertensive (61·3 ± 1·7 years, 76·1 ± 2·7 kg, 160 ± 1·6 cm) men (n = 12) and women (n = 22), participated in a control and a moderate intensity exercise session in a randomized order. After both experimental sessions, they left the laboratory wearing an ambulatory BP device for 24-h monitoring. ACE2 polymorphisms (Int-1 and Int-3) were assessed by polymerase chain reaction. Over the course of 5-h monitoring, we observed a significant reduction in SBP and DBP following exercise in the AA/AG of the Int-1 polymorphism (p-interaction = 0·02 and 0·001, respectively), whereas this could not be found in the individuals homozygous G (p-interaction = 0·76 and 0·51, respectively). With regard to Int-3 polymorphism, individuals AA/AG showed a significant reduction in SBP following exercise (p-interaction <0·0001) but not for DBP (p-interaction = 0·06) whereas GG individuals showed only a significant reduction in DBP following exercise (p-interaction = 0·02). Our results suggest that ACE2 polymorphism could affect PEH; however, larger trials are needed to confirm our findings.


Assuntos
Anti-Hipertensivos/uso terapêutico , Pressão Sanguínea/efeitos dos fármacos , Pressão Sanguínea/genética , Exercício Físico , Hipertensão/tratamento farmacológico , Hipertensão/genética , Peptidil Dipeptidase A/genética , Polimorfismo Genético , Hipotensão Pós-Exercício/genética , Idoso , Enzima de Conversão de Angiotensina 2 , Monitorização Ambulatorial da Pressão Arterial , Feminino , Frequência do Gene , Predisposição Genética para Doença , Heterozigoto , Homozigoto , Humanos , Hipertensão/diagnóstico , Hipertensão/fisiopatologia , Masculino , Pessoa de Meia-Idade , Fenótipo , Hipotensão Pós-Exercício/diagnóstico , Hipotensão Pós-Exercício/fisiopatologia , Fatores de Tempo
16.
J Sports Sci ; 36(12): 1363-1370, 2018 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-28895489

RESUMO

Moderate physical exercise acts at molecular and behavioural levels, such as interfering in neuroplasticity, cell death, neurogenesis, cognition and motor functions. Therefore, the aim of this study is to analyse the cellular effects of moderate treadmill running upon substantia nigra during early neurodegeneration. Aged male Lewis rats (9-month-old) were exposed to rotenone 1mg/kg/day (8 weeks) and 6 weeks of moderate treadmill running, beginning 4 weeks after rotenone exposure. Substantia nigra was extracted and submitted to proteasome and antioxidant enzymes activities, hydrogen peroxide levels and Western blot to evaluate tyrosine hydroxylase (TH), alpha-synuclein, Tom-20, PINK1, TrkB, SLP1, CRMP-2, Rab-27b, LC3II and Beclin-1 level. It was demonstrated that moderate treadmill running, practiced during early neurodegeneration, prevented the increase of alpha-synuclein and maintained the levels of TH unaltered in substantia nigra of aged rats. Physical exercise also stimulated autophagy and prevented impairment of mitophagy, but decreased proteasome activity in rotenone-exposed aged rats. Physical activity also prevented H2O2 increase during early neurodegeneration, although the involved mechanism remains to be elucidated. TrkB levels and its anterograde trafficking seem not to be influenced by moderate treadmill running. In conclusion, moderate physical training could prevent early neurodegeneration in substantia nigra through the improvement of autophagy and mitophagy.


Assuntos
Doenças Neurodegenerativas/fisiopatologia , Condicionamento Físico Animal , Corrida , Substância Negra/patologia , Animais , Autofagia , Modelos Animais de Doenças , Peróxido de Hidrogênio/metabolismo , Masculino , Mitofagia , Complexo de Endopeptidases do Proteassoma/metabolismo , Ratos Endogâmicos Lew , Rotenona/toxicidade , Tirosina 3-Mono-Oxigenase/metabolismo , alfa-Sinucleína/metabolismo
17.
J. Sports Sci. ; 36(12): p. 1363-1370, 2018.
Artigo em Inglês | Sec. Est. Saúde SP, SESSP-IBPROD, Sec. Est. Saúde SP | ID: but-ib15003

RESUMO

Moderate physical exercise acts at molecular and behavioural levels, such as interfering in neuroplasticity, cell death, neurogenesis, cognition and motor functions. Therefore, the aim of this study is to analyse the cellular effects of moderate treadmill running upon substantia nigra during early neurodegeneration. Aged male Lewis rats (9-month-old) were exposed to rotenone 1mg/kg/day (8weeks) and 6weeks of moderate treadmill running, beginning 4weeks after rotenone exposure. Substantia nigra was extracted and submitted to proteasome and antioxidant enzymes activities, hydrogen peroxide levels and Western blot to evaluate tyrosine hydroxylase (TH), alpha-synuclein, Tom-20, PINK1, TrkB, SLP1, CRMP-2, Rab-27b, LC3II and Beclin-1 level. It was demonstrated that moderate treadmill running, practiced during early neurodegeneration, prevented the increase of alpha-synuclein and maintained the levels of TH unaltered in substantia nigra of aged rats. Physical exercise also stimulated autophagy and prevented impairment of mitophagy, but decreased proteasome activity in rotenone-exposed aged rats. Physical activity also prevented H2O2 increase during early neurodegeneration, although the involved mechanism remains to be elucidated. TrkB levels and its anterograde trafficking seem not to be influenced by moderate treadmill running. In conclusion, moderate physical training could prevent early neurodegeneration in substantia nigra through the improvement of autophagy and mitophagy.

18.
J Sports Sci, v. 36, n. 12, p. 1363-1370, 2018
Artigo em Inglês | Sec. Est. Saúde SP, SESSP-IBPROD, Sec. Est. Saúde SP | ID: bud-2449

RESUMO

Moderate physical exercise acts at molecular and behavioural levels, such as interfering in neuroplasticity, cell death, neurogenesis, cognition and motor functions. Therefore, the aim of this study is to analyse the cellular effects of moderate treadmill running upon substantia nigra during early neurodegeneration. Aged male Lewis rats (9-month-old) were exposed to rotenone 1mg/kg/day (8weeks) and 6weeks of moderate treadmill running, beginning 4weeks after rotenone exposure. Substantia nigra was extracted and submitted to proteasome and antioxidant enzymes activities, hydrogen peroxide levels and Western blot to evaluate tyrosine hydroxylase (TH), alpha-synuclein, Tom-20, PINK1, TrkB, SLP1, CRMP-2, Rab-27b, LC3II and Beclin-1 level. It was demonstrated that moderate treadmill running, practiced during early neurodegeneration, prevented the increase of alpha-synuclein and maintained the levels of TH unaltered in substantia nigra of aged rats. Physical exercise also stimulated autophagy and prevented impairment of mitophagy, but decreased proteasome activity in rotenone-exposed aged rats. Physical activity also prevented H2O2 increase during early neurodegeneration, although the involved mechanism remains to be elucidated. TrkB levels and its anterograde trafficking seem not to be influenced by moderate treadmill running. In conclusion, moderate physical training could prevent early neurodegeneration in substantia nigra through the improvement of autophagy and mitophagy.

19.
Adv Exp Med Biol ; 1000: 211-245, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-29098624

RESUMO

Nitric oxide (NO) is a small molecule implicated in multiple signal transduction pathways thus contributing to the regulation of many cellular functions. The identification of NO synthase (NOS) isoforms and the subsequent characterization of the mechanisms of cell activation of the enzymes permitted the partial understanding of both the physiological and pathological processes. NO bioavailability plays an important role in the pathophysiology of cardiovascular disease and its reduction in endothelial cells is strictly associated to endothelial dysfunction which, in turn, correlates with cardiovascular mortality. Indeed, endothelial NO synthase (eNOS) has a key role in limiting cardiac dysfunction and remodeling in heart diseases, in part by decreasing myocyte hypertrophy. Conversely, exercise training is recommended to prevent and treat cardiovascular diseases-associated disorders at least by enhanced NO synthase activity and expression, and increased production of antioxidants, which prevents premature breakdown of NO. Exercise training may cause an improvement in endothelial function for both experimental animals and humans; Studies in both healthy subjects and patients with impaired NO-related vasorelaxation remarked exercise training ability to improve vascular structure and function and endothelial homeostasis. This chapter will briefly consider the importance of NO signaling in the maintenance of cardiovascular physiology, and discuss recent insights into the effect of exercise training on the signaling pathways that modulate NO synthesis and degradation in health and cardiovascular disease. In addition, we will highlight the molecular mechanisms via which microRNAs (miRs) target NO signaling in the cardiovascular system, and NO as a candidate molecule for development of new therapies.


Assuntos
Fenômenos Fisiológicos Cardiovasculares , Sistema Cardiovascular/metabolismo , Exercício Físico/fisiologia , Óxido Nítrico/metabolismo , Transdução de Sinais/fisiologia , Animais , Doenças Cardiovasculares/genética , Doenças Cardiovasculares/metabolismo , Doenças Cardiovasculares/fisiopatologia , Endotélio Vascular/metabolismo , Endotélio Vascular/fisiopatologia , Regulação da Expressão Gênica , Humanos , MicroRNAs/genética , Óxido Nítrico Sintase/metabolismo , Transdução de Sinais/genética
20.
Oxid Med Cell Longev ; 2017: 1549014, 2017.
Artigo em Inglês | MEDLINE | ID: mdl-29138674

RESUMO

We previously reported that aerobic exercise training (AET) consisted of 10 weeks of 60-min swimming sessions, and 5 days/week AET counteracts CH in obesity. Here, we evaluated the role of microRNAs and their target genes that are involved in heart collagen deposition and calcium signaling, as well as the cardiac remodeling induced by AET in obese Zucker rats. Among the four experimental Zucker groups: control lean rats (LZR), control obese rats (OZR), trained lean rats (LZR + TR), and trained obese rats (OZR + TR), heart weight was greater in the OZR than in the LZR group due to increased cardiac intramuscular fat and collagen. AET seems to exert a protective role in normalizing the heart weight in the OZR + TR group. Cardiac microRNA-29c expression was decreased in OZR compared with the LZR group, paralleled by an increase in the collagen volumetric fraction (CVF). MicroRNA-1 expression was upregulated while the expression of its target gene NCX1 was decreased in OZR compared with the LZR group. Interestingly, AET restored cardiac microRNA-1 to nonpathological levels in the OZR-TR group. Our findings suggest that AET could be used as a nonpharmacological therapy for the reversal of pathological cardiac remodeling and cardiac dysfunction in obesity.


Assuntos
Coração/fisiopatologia , MicroRNAs/metabolismo , Obesidade/genética , Obesidade/terapia , Condicionamento Físico Animal/fisiologia , Animais , Masculino , Obesidade/patologia , Obesidade/fisiopatologia , Ratos , Ratos Zucker
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