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Made available in DSpace on 2021-06-25T11:02:57Z (GMT). No. of bitstreams: 0 Previous issue date: 2020-12-01 Dexamethasone (DEX) has important anti-inflammatory activities; however, it induces hypertension and skeletal muscle microcirculation rarefaction. Nevertheless, nothing is known about DEX outcomes on cardiac microcirculation. By contrast, exercise training prevents skeletal and cardiac microvessel loss because of microRNA expression and a better balance between their related angiogenic and apoptotic proteins in spontaneously hypertensive rats. The purpose of this study was to investigate whether DEX and/or exercise training could induce microRNA alterations leading to cardiac angiogenesis or microvascular rarefaction. Animals performed 8 weeks of exercise training and were treated with DEX (50 μg/kg per day, subcutaneously) for 14 days. Cardiovascular parameters were measured, and the left ventricle muscle was collected for analyses. DEX treatment increased arterial pressure and did not cause cardiac microcirculation rarefaction. Treadmill training prevented the DEX-induced increase in arterial pressure. In addition, training, regardless of DEX treatment, increased microRNA-126 expression, phospho-protein kinase B/protein kinase B, and endothelial nitric oxide synthase levels associated with cardiac angiogenesis. In conclusion, this study suggests, for the first time, that treadmill training induces myocardial angiogenesis because of angiogenic pathway improvement associated with an increase in microRNA-126. Furthermore, DEX, per se, did not cause capillary density alterations and did not attenuate cardiac angiogenesis induced by training. Joint Graduate Program in Physiological Sciences PIPGCF UFSCar/UNESP Department of Biological Sciences Bauru School of Dentistry University of São Paulo Department of Physical Education School of Sciences São Paulo State University (UNESP) Joint Graduate Program in Physiological Sciences PIPGCF UFSCar/UNESP Department of Physical Education School of Sciences São Paulo State University (UNESP)

Made available in DSpace on 2022-04-28T17:21:56Z (GMT). No. of bitstreams: 0 Previous issue date: 2021-04-01 Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) Sympathetic activity, arteriolar structure, and angiogenesis are important mechanisms modulating hypertension and this study aimed to analyze the effects of perindopril treatment, associated or not with exercise training, on the mechanisms that control blood pressure (BP) in hypertensive rats. Spontaneously hypertensive rats (SHR) were allocated into 4 groups: 1/sedentary (S); 2/perindopril (P, 3.0 mg/kg/d); 3/trained (T); and 4/trained + perindopril (TP). Wistar rats were used as normotensive sedentary control group. SHR were assigned to undergo a treadmill training (T) or were kept sedentary. Heart rate, BP, sympathetic activity to the vessels (LF-SBP), and skeletal muscle and myocardial morphometric analyses were performed. BP was significantly lower after all 3 strategies, compared with S and was accompanied by lower LF-SBP (-76%, -53%, and -44%, for P, T, and TP, respectively). Arteriolar vessel wall cross-sectional area was lower after treatments (-56%, -52%, and -56%, for P, T, and TP, respectively), and only TP presented higher arteriolar lumen area. Capillary rarefaction was present in soleus muscle and myocardium in S group and both trained groups presented higher vessel density, although perindopril attenuated this increase in soleus muscle. Although myocyte diameter was not different between groups, myocardial collagen deposition area, higher in S group, was lower after 3 strategies. In conclusion, we may suggest that perindopril could be an option for the hypertensive people who practice exercise and need a specific pharmacological treatment to reach a better BP control, mainly because training-induced angiogenesis is an important response to facilitate blood flow perfusion and oxygen uptake and perindopril did not attenuate this response. PIPGCF UFSCar UNESP, Joint Grad Program Physiol Sci, Sao Carlos, SP, Brazil Inst Biosci Humanities & Exact Sci UNESP, Sch Sci, Dept Biol, Sao Jose Do Rio Preto, SP, Brazil UNESP, Sch Sci, Dept Biol Sci, Bauru, SP, Brazil UNESP, Sch Sci, Dept Phys Educ, Bauru, SP, Brazil PIPGCF UFSCar UNESP, Joint Grad Program Physiol Sci, Sao Carlos, SP, Brazil Inst Biosci Humanities & Exact Sci UNESP, Sch Sci, Dept Biol, Sao Jose Do Rio Preto, SP, Brazil UNESP, Sch Sci, Dept Biol Sci, Bauru, SP, Brazil UNESP, Sch Sci, Dept Phys Educ, Bauru, SP, Brazil FAPESP: 2017/00509-1 CAPES: 001 CAPES: 1692103 CAPES: 88882.426908/2019-01 FAPESP: 2017/14405-3

Made available in DSpace on 2021-06-25T10:53:51Z (GMT). No. of bitstreams: 0 Previous issue date: 2021-01-01 Dexamethasone (DEX)-induced hypertension is observed in normotensive rats, but little is known about the effects of DEX on spontaneously hypertensive animals (SHR). This study aimed to evaluate the effects of DEX on hemodynamics, cardiac hypertrophy and arterial stiffness in normotensive and hypertensive rats. Wistar rats and SHR were treated with DEX (50 μg/kg s.c., 14 d) or saline. Pulse wave velocity (PWV), echocardiographic parameters, blood pressure (BP), autonomic modulation and histological analyses of heart and thoracic aorta were performed. SHR had higher BP compared with Wistar, associated with autonomic unbalance to the heart. Echocardiographic changes in SHR (vs. Wistar) were suggestive of cardiac remodeling: higher relative wall thickness (RWT, +28%) and left ventricle mass index (LVMI, +26%) and lower left ventricle systolic diameter (LVSD, −19%) and LV diastolic diameter (LVDD, −10%), with slightly systolic dysfunction and preserved diastolic dysfunction. Also, SHR had lower myocardial capillary density and similar collagen deposition area. PWV was higher in SHR due to higher aortic collagen deposition. DEX-treated Wistar rats presented higher BP (~23%) and autonomic unbalance. DEX did not change cardiac structure in Wistar, but PWV (+21%) and aortic collagen deposition area (+21%) were higher compared with control. On the other side, DEX did not change BP or autonomic balance to the heart in SHR, but reduced RWT and LV collagen deposition area (−12% vs. SHRCT). In conclusion, the results suggest a differential effect of dexamethasone on arterial stiffness, myocardial remodeling and blood pressure between normotensive and spontaneously hypertensive rats. Joint Graduate Program in Physiological Sciences PIPGCF UFSCar/UNESP Department of Biology School of Sciences São Paulo State University (UNESP) Department of Medical Clinic Botucatu Medical School São Paulo State University (UNESP) Department of Physical Education School of Sciences São Paulo State University (UNESP) Joint Graduate Program in Physiological Sciences PIPGCF UFSCar/UNESP Department of Biology School of Sciences São Paulo State University (UNESP) Department of Medical Clinic Botucatu Medical School São Paulo State University (UNESP) Department of Physical Education School of Sciences São Paulo State University (UNESP)

Made available in DSpace on 2021-06-25T11:03:35Z (GMT). No. of bitstreams: 0 Previous issue date: 2021-03-01. Added 1 bitstream(s) on 2021-07-15T14:36:02Z : No. of bitstreams: 1 S0066-782X2021000400516.pdf: 3972880 bytes, checksum: b9bdbad26f21c4bcb57e0ea9683f5e70 (MD5) Universidade Federal de Goiás Liga de Hipertensão Arterial Pontifícia Universidade Católica de São Paulo Faculdade de Ciências Médicas e da Saúde Instituto do Coração (InCor) Centro Universitário CESMAC, AL - Brasil Universidade Federal de Pernambuco Pronto Socorro Cardiológico de Pernambuco (PROCAPE) Pontifícia Universidade Católica do Rio Grande do Sul Universidade Federal de São Paulo (UNIFESP) Hospital das Clínicas da Faculdade de Medicina da USP Serviço Hipertensão e Cardiometabolismo da Santa Casa de Porto Alegre Hospital das Clínicas da Faculdade de Medicina de Ribeirão Preto da Universidade de São Paulo Hospital São Francisco Universidade Federal da Bahia (UFBA) BA - Brasil Faculdade Estadual de Medicina de São José do Rio Preto Faculdade de Medicina da Universidade Federal do Rio Grande do Sul (UFRGS) Universidade Federal do Paraná (UFPR) Hospital Agamenom Magalhães Hospital Alemão Oswaldo Cruz Universidade de São Paulo (USP) Universidade Estadual de Campinas (UNICAMP) Cardiocentro Universidade Federal do Rio de Janeiro (UFRJ) Universidade Estadual de Santa Cruz BA - Brasil Instituto de Cardiologia Fundação Universitária de Cardiologia (IC/FUC) Centro Universitário da Serra Gaúcha (FSG) Universidade Federal do Pará (UFPA) Ministério da Saúde Departamento de Cardiogeriatria da Sociedade Brazileira de Cardiologia Hospital Nossa Senhora da Conceição (HNSC) SC - Brasil Universidade Estácio de Sá (UNESA) Hospital de Clínicas da Universidade Federal do Paraná (HC/UFPR) Universidade Iguaçu (UNIG) Faculdade de Ciências Farmacêuticas de Ribeirão Preto da Universidade de São Paulo Associação Ribeirãopretana de Ensino Pesquisa e Assistência ao Hipertenso (AREPAH) Faculdade de Medicina de Ribeirão Preto da Universidade de São Paulo MT - Brasil Programa de Pós-Graduação em Medicina da Universidade Nove de Julho (UNINOVE) Instituto Dante Pazzanese de Cardiologia Hospital de Clínicas de Porto Alegre Escola Bahiana de Medicina e Saúde Pública BA - Brasil Universidade Santo Amaro (UNISA) SC - Brasil, Universidade Federal de Santa Catarina (UFSC) Hospital Israelita Albert Einstein Centro de Ciências da Saúde Universidade Federal do Espírito Santo Faculdade Ciências Médicas de Minas Gerais MG - Brasil Hospital Felício Rocho MG - Brasil Hospital do Coração (HCor) Instituto Estadual de Cardiologia Aloysio de Castro Centro Universitário de Tecnologia e Ciência (UniFTC) BA - Brasil Universidade Estadual Paulista (UNESP) Faculdade de Medicina da Universidade Federal de Mato Grosso MT - Brasil Sociedade Brazileira de Nefrologia Pontifícia Universidade Católica do Paraná Pontifícia Universidade Católica de Goiás Cardios Vita Centro de Medicina Cardiológica Hospital Pró-Cradíaco MG - Brasil, Universidade Federal de Juiz de Fora Avancor Cardiologia Universidade Estadual de Maringá Faculdade de Ciências Médicas da Santa Casa de São Paulo Universidade Federal de Uberlândia MG - Brasil Hospital Getúlio Vargas Universidade Estadual Paulista (UNESP)

Made available in DSpace on 2020-12-10T20:10:32Z (GMT). No. of bitstreams: 0 Previous issue date: 2020-08-28 Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) Introduction: Dexamethasone (DEX)-induced hypertension and cardiac remodeling are still unclear, especially in spontaneously hypertensive rats (SHR). On the other side, exercise training is a good strategy to control hypertension. Therefore, this study investigated the effects of DEX treatment and physical training on arterial pressure and cardiac remodeling in SHR. Material and Methods: SHR underwent treadmill training (5 days/week, 1h/session, at 50-60% of maximal capacity, 0% degree, 75 days) and received low-dose of DEX (50 mu g/kg,s.c.) during the last 15 days. Sedentary Wistar rats (W) were used as control. Echocardiography and artery catheterization were performed for cardiac remodeling and function, arterial pressure and autonomic nervous system analyses. In addition, left ventricle (LV) capillary density, myocyte diameter and collagen deposition area were analyzed using specific histological staining. Results: Low-dose of DEX treatment did not exacerbate arterial pressure of SHR and trained groups had lower values, regardless of DEX. DEX and training decreased relative left ventricle wall thickness (RWT) and determined LV angiogenesis (+19%) and lower collagen deposition area (-22%). In addition, it determined increased left ventricular diastolic diameter. These changes were followed by improvements on systolic and diastolic function, since it was observed increased posterior wall shortening velocity (PWSV) and reduced isovolumetric relaxation time (IVRT). Conclusion: In conclusion, this study is unique to indicate that low-dose of DEX treatment does not exacerbate arterial pressure in SHR and, when associated with training, it improves LV systolic and diastolic function, which may be due to LV angiogenesis and reduction of wall collagen deposition area. UNESP, PIPGCF UFSCar, Joint Grad Program Physiol Sci, Sao Carlos, SP, Brazil Sao Paulo State Univ Unesp, Sch Sci, Dept Biol Sci, Bauru, SP, Brazil Sao Paulo State Univ Unesp, Botucatu Med Sch, Dept Internal Med, Botucatu, SP, Brazil Univ Sao Paulo, Bauru Sch Dent, Dept Biol Sci, Bauru, SP, Brazil Sao Paulo State Univ Unesp, Sch Sci, Dept Phys Educ, Bauru, SP, Brazil UNESP, PIPGCF UFSCar, Joint Grad Program Physiol Sci, Sao Carlos, SP, Brazil Sao Paulo State Univ Unesp, Sch Sci, Dept Biol Sci, Bauru, SP, Brazil Sao Paulo State Univ Unesp, Botucatu Med Sch, Dept Internal Med, Botucatu, SP, Brazil Sao Paulo State Univ Unesp, Sch Sci, Dept Phys Educ, Bauru, SP, Brazil FAPESP: 2017/00509-1 FAPESP: 2015/03965-2 FAPESP: 2018/00567-4 FAPESP: 2017/14405-3 CAPES: 88882.426908/2019-01 FAPESP: 2016-12532-5 CAPES: 88882.426901/2019-01

Made available in DSpace on 2020-12-12T01:12:35Z (GMT). No. of bitstreams: 0 Previous issue date: 2020-05-20 Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) National Institutes of Health Glucocorticoids have important anti-inflammatory and immunomodulatory activities. Dexamethasone (Dex), a synthetic glucocorticoid, induces insulin resistance, hyperglycemia, and hypertension. The hypertensive mechanisms of Dex are not well understood. Previously, we showed that exercise training prior to Dex treatment significantly decreases blood vessel loss and hypertension in rats. In this study, we examined whether the salutary effects of exercise are associated with an enhanced metabolic profile. Analysis of the NAD and ATP content in the tibialis anterior muscle of trained and non-trained animals indicated that exercise increases both NAD and ATP; however, Dex treatment had no effect on any of the experimental groups. Likewise, Dex did not change NAD and ATP in cultured endothelial cells following 24 h and 48 h of incubation with high concentrations. Reduced VEGF-stimulated NO production, however, was verified in endothelial cultured cells. Reduced NO was not associated with changes in survival or the BH4 to BH2 ratio. Moreover, Dex had no effect on bradykinin- or shear-stress-stimulated NO production, indicating that VEGF-stimulated eNOS phosphorylation is a target of Dex's effects. The PTP1B inhibitor increased NO in Dex-treated cells in a dose-dependent fashion, an effect that was replicated by the glucocorticoid receptor inhibitor, RU486. In combination, these results indicate that Dex-induced endothelial dysfunction is mediated by glucocorticoid receptor and PTP1B activation. Moreover, since exercise reduces the expression of PTP1B and normalized insulin resistance in aging rats, our findings indicate that exercise training by reducing PTP1B activity counteracts Dex-induced hypertension in vivo. Joint Graduate Program in Physiological Sciences PIPGCF UFSCar/UNESP, Rodovia Washington Luiz, São Carlos/SP Department of Physical Education São Paulo State University School of Sciences, Av. Eng. Luiz Edmundo Carrijo Coube Department of Biophysics Redox Biology Program Medical College of Wisconsin Joint Graduate Program in Physiological Sciences PIPGCF UFSCar/UNESP, Rodovia Washington Luiz, São Carlos/SP Department of Physical Education São Paulo State University School of Sciences, Av. Eng. Luiz Edmundo Carrijo Coube FAPESP: #2017/00509-1 FAPESP: 2016/12532-5 FAPESP: 2017/14405-3 FAPESP: 2018/06998-7 National Institutes of Health: R01 NS081936

Made available in DSpace on 2020-12-12T02:24:06Z (GMT). No. of bitstreams: 0 Previous issue date: 2020-04-05 Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) Microcirculation maintenance is associated with microRNAs. Nevertheless, the role of microRNAs induced by training in preventing dexamethasone (DEX)-induced microvascular rarefaction remains unknown. The study aim was to investigate if training-induced microRNAs are able to improve microcirculation proteins and prevent DEX-induced microvascular rarefaction. Rats underwent training for 8 weeks and then were treated with DEX (50 μg/kg per day, s.c.) for 14 days. Arterial pressure was measured and tibialis anterior (TA) muscle was collected for analyses. DEX induced hypertension concomitantly with capillary density loss (CD, −23.9%) and decrease of VEGF (−43.0%), p-AKT/AKT (−39.6%) and Bcl-2 (−23.0%) and an increase in caspase-3-cleaved protein level (+34.0%) in TA muscle. Training upregulated microRNA-126 expression (+13.1%), prevented VEGF (+61.4%), p-AKT/AKT (+37.7%), Bcl-2 (+7.7%) decrease and caspase-3-cleaved (−23.1%) increase associated with CD (+54.7%) reduction and hypertension prevention. MiRNA-126 upregulation, induced by training, plays a role in controlling microcirculation, which may be a potential target against DEX-induced microvascular rarefaction. Joint Graduate Program in Physiological Sciences PIPGCF UFSCar/UNESP, Rodovia Washington Luiz, km 235 Monjolinho 676 Department of Biological Sciences Bauru School of Dentistry University of São Paulo, Alameda Octávio Pinheiro Brisolla 9-75 Department of Physical Education - São Paulo State University (UNESP) School of Sciences, Av. Eng. Luiz Edmundo Carrijo Coube, 14-01, Vargem Limpa Joint Graduate Program in Physiological Sciences PIPGCF UFSCar/UNESP, Rodovia Washington Luiz, km 235 Monjolinho 676 Department of Physical Education - São Paulo State University (UNESP) School of Sciences, Av. Eng. Luiz Edmundo Carrijo Coube, 14-01, Vargem Limpa FAPESP: 2015/03965-2 FAPESP: 2016/12532-5 FAPESP: 2017/00509-1 FAPESP: 2017/14405-3 FAPESP: 2018/06998-7 CAPES: 88882.426901/2019-01 CAPES: 88882.426908/2019-01

Dexamethasone (DEX) causes rarefaction. In contrast, training (T) prevents rarefaction and stimulates angiogenesis. This study investigated the mechanisms responsible for the preventive role of T in DEX-induced rarefaction. Rats underwent T or were kept sedentary (8 weeks) and were treated with DEX or saline during the following 14 days. Tibialis anterior muscle was used for measurements of capillary density (CD), capillary-to-fiber ratio (C:F ratio), superoxide dismutase CuZn (SOD-1), superoxide dismutase MnSOD (SOD-2), catalase (CAT) mRNA as well as SOD-1, SOD-2, CAT, vascular endothelial growth factor (VEGF), vascular endothelial growth factor receptor-2 (VEGF-R2), cyclooxygenase-2 (COX-2), B-cell lymphoma 2 (Bcl-2), Bd-2-like protein 4 (Bax), p-Bax, and caspase-3 cleaved protein levels. DEX decreased CD (-38.1%), C:F ratio (-30.0%), VEGF (-19.0%), VEGFR-2 (-20.1%), COX-2 (-22.8%), Bcl-2 (-20.5%), Bcl-2/Bax ratio (-13.7%), p-Bax/Bax (-20.0%) and increased SOD-2 (+41.6%) and caspase-3 cleaved (+24.1%). Conversely, T prevented reductions in CD (+54.2%), C:F ratio (+32.9%), VEGF (+25.3%), VEGFR-2 (+22.2%), COX-2 (+31.5%), Bcl-2 (+35.5%), Bcl-2/Bax ratio (+19.9%), p-Bax/Bax (+32.1%), and caspase-3 cleaved increase (-7.8%). T increased CAT mRNA (+21.5%) in the DEX-treated group. In conclusion, T prevented the DEX-induced rarefaction by increasing antioxidant enzymes resulting in a better balance between apoptotic and anti-apoptotic protein levels.

The purpose of this study was to analyze the effect of aging and the estimated training status (TS) on the blood pressure (BP) and antihypertensive medicine consumption (AMC) which are supposed to be high in older people compared with adults. Participants (n=396) performed the following tests: Functional fitness battery test proposed by AAHPERD, blood pressure measurement and a questionnaire about habits of physical exercise and medicine consumptions. In summary, older group present high level of blood pressure and medicine consumptions compared with adults groups (BP - 125±5/77±9 vs 119±12/78±9 mmHg and AMC - 1.8±0.1 vs 1.4±0.1 respectively). However, when participants were divided according to TS, good level of TS was associated with low level of blood pressure. These results were not observed in adults group. Thus, the current study contributes to establish the good level of TS as a marker of good level of blood pressure, especially in older group.

Made available in DSpace on 2020-12-12T02:23:59Z (GMT). No. of bitstreams: 0 Previous issue date: 2020-04-01 Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) This work investigated the mechanisms induced by exercise training that may contribute to attenuate dexamethasone (DEX)-induced microvascular rarefaction and hypertension. Wistar rats underwent training protocol or were kept sedentary for 8 weeks. Dexamethasone was administered during the following 14-days and hemodynamic parameters were recorded at the end. Capillary density (CD) and capillary-to-fiber ratio (C:F ratio) were obtained in soleus muscle (SOL). Also, vascular endothelial growth factor (VEGF), vascular endothelial growth factor receptor-2 (VEGFR-2), endothelial nitric oxide synthase (eNOS), B-cell lymphoma 2 (Bcl-2), Bcl-2-like protein 4 (Bax), p-BAX and caspase-3 cleaved protein levels were analyzed. DEX treatment significantly increased blood pressure (+14%), which was associated with reduced C:F ratio (−41.0%) and CD (−43.1%). Reduction of vessel density was associated with decreased VEGF (−15.6%), VEGFR-2 (−14.6%), Bcl-2 (−18.4%), Bcl-2/Bax ratio (−29.0%) and p-Bax/Bax (−25.4%), and also with increased caspase-3 cleaved protein level (25%). Training, on the other hand, prevented microvessels loss by mitigating all proteins changes induced by DEX. In addition, angiogenic and apoptotic proteins were significantly correlated with CD, which, in turn, was associated with blood pressure. Therefore, we may point out that exercise training is a good strategy to attenuate DEX-induced microvascular rarefaction in soleus muscle and this response involves a better balance between apoptotic and angiogenic proteins, which may contribute for the attenuation of hypertension. Department of Physical Education – São Paulo State University (UNESP) Science Faculty, Av. Eng. Luiz Edmundo Carrijo Coube, 14-01 – Vargem Limpa Joint Graduate Program in Physiological Sciences PIPGCF UFSCar/UNESP, Rodovia Washington Luiz, km 235 Monjolinho, 676 Department of Biological Sciences Bauru School of Dentistry University of São Paulo, Alameda Octávio Pinheiro Brisolla, 9-75 Department of Physical Education – São Paulo State University (UNESP) Science Faculty, Av. Eng. Luiz Edmundo Carrijo Coube, 14-01 – Vargem Limpa Joint Graduate Program in Physiological Sciences PIPGCF UFSCar/UNESP, Rodovia Washington Luiz, km 235 Monjolinho, 676

Introduction In this study we investigated the effects of high-intensity resistance training (RT) on dexamethasone (DEX)-induced muscle atrophy in flexor hallucis longus (FHL), tibialis anterior (TA), and soleus (SOL) muscles. Methods Rats underwent either high-intensity RT or were kept sedentary. In the last 10 days they received either DEX (0.5 mg/kg/day, intraperitoneally) or saline. Results DEX reduced body weight (-21%), food intake (-28%), FHL and TA muscle mass (-20% and -18%, respectively), and increased muscle-specific ring finger 1 (MuRF-1) protein level (+37% and +45.5%). RT attenuated FHL muscle atrophy through a combination of low increase in MuRF-1 protein level (-3.5%) and significant increases in mammalian target of rapamycin (mTOR) (+63%) and p70S6K (+46% and +49% for control and DEX, respectively) protein levels. Conclusion RT attenuated DEX-induced muscle atrophy through a combination of increases in mTOR and p70S6K protein levels and a low increase in MuRF-1 protein level.

Made available in DSpace on 2018-12-11T17:24:14Z (GMT). No. of bitstreams: 0 Previous issue date: 2018-08-01 Hypertension is one of the chronic side effects of dexamethasone (DEX) treatment; however, almost nothing is known about its acute effects. Therefore, the aim of this study was to investigate the possible mechanisms involved in blood pressure control after acute or short-term DEX treatment in adult animals. Eighty Wistar rats were divided into four groups: C1 and C5, for rats treated with saline for 1 or 5 days, respectively; D1 and D5, for rats treated with DEX for 1 or 5 days, respectively (decadron, 1 mg/kg, i.p.). Heart rate was increased in DEX treatment, but arterial pressure and cardiac muscle mass were not altered. Only few and isolated changes on gene expression and protein level of renin-angiotensin system components were observed. Five days of DEX treatment, but not one day, determined an increase in sympathetic component of spectral analysis (+75.93%, P

Made available in DSpace on 2018-12-11T17:24:19Z (GMT). No. of bitstreams: 0 Previous issue date: 2018-06-01 Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Objective: Polymorphisms of the renin angiotensin system (RAS) are associated with increases in blood pressure (BP). Physical exercise has been considered the main strategy to prevent this increase. This study aimed to investigate the relationship between estimated training status (TS), BP and angiotensin-converting enzyme (ACE) activity in elderly people classified as low or high risk to develop hypertension according to genetic profile. Methods: A total of 155 elderly participants performed the following assessments: general functional fitness index (GFFI), systolic BP (SBP) and diastolic BP (DBP), blood collection for ACE activity and analyses of the RAS polymorphisms. Results: Uncontrolled hypertensive (UHT) participants presented higher values of SBP and DBP compared with normotensive (NT) and controlled hypertensive (CHT) participants. No differences were found in ACE activity and GFFI between groups. In the high risk group, UHT presented higher values of SBP and DBP compared with other groups. CHT presented higher values of SBP compared with NT. Furthermore, UHT presented higher values of ACE activity compared with CHT and lower values of GFFI compared with NT. Conclusion: MDA, TIA and TIC genetic combinations were associated with high risk of developing hypertension while the maintenance of good levels of TS was associated with lower BP values and ACE activity. Department of Physical Education São Paulo State University (UNESP) School of Science School of Nursing of Ribeirão Preto USP - University of São Paulo Faculty of Medicine of Ribeirão Preto USP - University of São Paulo Bauru School of D entistry University of São Paulo Department of Physical Education São Paulo State University (UNESP) School of Science FAPESP: Grants no 2015/24847-8 to ASZ.

Made available in DSpace on 2018-11-26T17:48:14Z (GMT). No. of bitstreams: 0 Previous issue date: 2018-02-16 Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Teesside University Newcastle University The present study investigated the effect of chronic exercise on fluoride (F) metabolism in fluorosis-susceptible mice exposed to high-F and explored the relationship between F concentrations in bone and plasma. Thirty male mice were randomised into three groups: Group I (No-F, No-Exercise), Group II (50 ppmF, No-Exercise), Group III (50 ppmF, Exercise). Body weight and physical performance of all mice were measured at baseline and end of experiment. F concentrations of plasma and bone were measured at the end of experiment. Mean plasma F concentration was significantly higher (p < 0.001) in Groups II and III compared with Group I. Mean bone F concentration was also significantly higher (p < 0.01) in Groups II and III compared with Group I. There was a significant correlation (p = 0.01, r = 0.54) between F concentration of plasma and bone. Mean body weight of Group I mice was significantly higher than Group II (p < 0.001) and Group III (p = 0.001) mice at the end of the experiment. This study, which provides the first data on the effect of chronic exercise on F metabolism in fluorosis-susceptible mice, suggests no effect of chronic exercise on F in plasma and bone. However, exposure to high-F resulted in lower body weight and exercise capacity in mice. Sao Paulo State Univ, Sci Fac, Dept Phys Educ, BR-17033360 Bauru, SP, Brazil Teesside Univ, Sch Hlth & Social Care, Middlesbrough TS1 3BA, Cleveland, England Univ Sao Paulo, Bauru Sch Dent, BR-17012901 Bauru, SP, Brazil Newcastle Univ, Sch Dent Sci, Ctr Oral Hlth Res, Newcastle Upon Tyne NE2 4BW, Tyne & Wear, England Sao Paulo State Univ, Sci Fac, Dept Phys Educ, BR-17033360 Bauru, SP, Brazil

O objetivo desse estudo foi descrever e analisar o condicionamento físico de alunos de graduação do curso de Educação Física. A amostra foi composta por 110 mulheres e 115 homens. Foram avaliados peso, altura, índice de massa corpórea, porcentagem de gordura (GC), frequência cardíaca, pressão arterial sistólica (PAS) e diastólica, flexibilidade, força e resistência muscular localizada (RML). Como principais resultados observamos maior porcentagem de mulheres com gordura corporal e RML acima dos valores ideais para a idade quando comparados aos homens (GC: 37% vs 4%, p= 0,001; RML: 32% vs 13%, p= 0,001), enquanto houveram mais homens com alteração na PAS quando confrontado com mulheres (22% vs 6%, p= 0,001). Em conclusão, estudantes do sexo masculino apresentaram maiores níveis de aptidão física em relação às mulheres, e parcela expressiva de alunos de Educação Física apresentam alterações nos valores de referência à normalidade para variáveis antropométricas, hemodinâmicas e de desempenho motor.

Made available in DSpace on 2018-12-11T16:47:37Z (GMT). No. of bitstreams: 0 Previous issue date: 2017-01-01 Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) This study investigated whether ACTN3 R577X, AMPD1 C34T, I/D ACE, and M235T AGT polymorphisms can affect performance tests such as jumping, sprinting, and endurance in 220 young male athletes from professional minor league soccer team from São Paulo Futebol Clube, Brazil. I/D ACE and M235T AGT polymorphisms were also analyzed according to cardiac and hemodynamic parameters. Athletes were grouped or not by age. DNA from saliva and Taqman assays were used for genotyping 220 athletes and the results were associated with performance tests. Ventricle mass, ventricle end-diastolic diameter, enddiastolic volume, and ejection fraction were assessed by echocardiogram. Arterial pressure, heart rate, and oximetry were assessed by a cardioscope. The main results of this study were that athletes who carried RR/RX (ACTN3) and DD (ACE) genotypes presented better performance during jump and sprint tests. On the other hand, athletes with ID/II genotype presented better results during endurance test, while AGT genotypes did not seem to favor the athletes during the evaluated physical tests. CC genotype (AMPD1) only favored the athletes during 10-m sprint test. Although there are environmental interactions influencing performance, the present results suggest that RR/RX ACTN3 and ACE DD genotypes may benefit athletes in activities that require strength and speed, while II ACE genotype may benefit athletes in endurance activities. This information could help coaches to plan the training session to improve the athletes’ performance. Joint Graduate Program in Physiological Sciences PIPGCF UFSCar/UNESP Bauru School of Dentistry University of São Paulo State University of Campinas Institute of Bioscience University of São Paulo State (UNESP) Physiological Sciences PIPGCF UFSCar/UNESP Joint Graduate Program in Physiological Sciences PIPGCF UFSCar/UNESP Institute of Bioscience University of São Paulo State (UNESP) Physiological Sciences PIPGCF UFSCar/UNESP CNPq: 140206/2011-6 FAPESP: 2011/21586-8

Made available in DSpace on 2018-12-11T17:23:40Z (GMT). No. of bitstreams: 0 Previous issue date: 2017-12-01 Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Dexamethasone-induced hypertension may be caused by baroreflex alterations or renin-angiotensin system (RAS) exacerbation. Aerobic training has been recommended for hypertension treatment, but the mechanisms responsible for reduction of arterial pressure (AP) in dexamethasone (DEX) treated rats are still inconclusive.This study evaluated whether mechanisms responsible for training-induced attenuation of hypertension involve changes in autonomic nervous system and in RAS components. Rats underwent aerobic training protocol on treadmill or were kept sedentary for 8 weeks. Additionally, animals were treated with DEX during the last 10 days of exercise. Body weight (BW), AP and baroreflex activity were analyzed. Tibialis anterior (TA), soleus (SOL) and left ventricle (LV) were collected for evaluation of RAS components gene expression and protein levels. Dexamethasone decreased BW (20%), caused TA atrophy (16%) and increased systolic AP (SAP, 16%) as well as decreased baroreflex activity. Training attenuated SAP increase and improved baroreflex activity, although it did not prevent DEX-induced BW reduction and muscle atrophy. Neither DEX nor training caused expressive changes in RAS components. In conclusion, exercise training was effective in attenuating hypertension induced by DEX and this response may be mediated by a better autonomic balance through an improvement of baroreflex activity rather than changes in RAS components. Joint Graduate Program in Physiological Sciences PIPGCF UFSCar/UNESP, Rodovia Washington Luiz, km 235, Monjolinho, 676 Department of Physical Education Science Faculty São Paulo State University (UNESP), Av. Eng. Luiz Edmundo Carrijo Coube, 14-01, Vargem Limpa Department of Biological Sciences Bauru School of Dentistry University of São Paulo, Alameda Octávio Pinheiro Brisolla, 9-75 Laboratory of Pharmacology School of Pharmaceutical Sciences São Paulo State University (UNESP), Rodovia Araraquara Jaú, km 01 – s/n, Campos Ville Joint Graduate Program in Physiological Sciences PIPGCF UFSCar/UNESP, Rodovia Washington Luiz, km 235, Monjolinho, 676 Department of Physical Education Science Faculty São Paulo State University (UNESP), Av. Eng. Luiz Edmundo Carrijo Coube, 14-01, Vargem Limpa Laboratory of Pharmacology School of Pharmaceutical Sciences São Paulo State University (UNESP), Rodovia Araraquara Jaú, km 01 – s/n, Campos Ville CNPq: 140206/2011-6 FAPESP: 2011/21522-0 FAPESP: 2012/03816-9 FAPESP: 2012/14376-0 FAPESP: 2012/19722-3 FAPESP: 2014/18177-7 FAPESP: 2014/23050-6

The purpose of this study was to evaluate the relationship between 3 eNOS gene polymorphisms and training status (TS) in affecting plasma nitrite concentration (NO2) in normotensive adults over 50 years old. Resting blood pressure (BP) was measured in all participants (n = 101). Plasma was taken to analyze: lipid profile, nitrite concentration (NO2) and lipid peroxide levels (T-BARS). Also, genomic DNA was extracted from plasma for genotyping NOS3 polymorphisms (-786T>C; 894G>T; and VNTR in intron 4). TS was determined by one-mile walk test and Functional Fitness Test Battery from AAHPERD (TS1—regular TS; TS2—good TS; and TS3—very good TS). BP was not influenced by TS, but NO2 was 15 % higher in TS3 (123 ± 27 nM) compared to TS-2 (106 ± 22 nM). No differences were found in plasma NO2 in the haplotype analyses. However, the presence of the C allele (T-786C) and ASP allele (Glu298Asp) was found to enhance the correlation between TS and NO2 levels (r = 0.492 in C/4b/ASP haplotype and r = 0.855 in C/4a/ASP haplotype). This study thus identifies NOS3 polymorphism-dependent sensitivity to the effects of physical training on plasma NO2. Maintenance of good levels of training status, in carriers of C allele for T-786C polymorphism, combined with ASP allele for Glu298Asp polymorphism, may result in an increase in the NO2 plasma concentrations, which may reflect improved NO bioavailability in older adult normotensive individuals.

Made available in DSpace on 2018-12-11T17:23:24Z (GMT). No. of bitstreams: 0 Previous issue date: 2015-01-01 The purpose of this study was to evaluate the influence of functional fitness and oxidative capacity on the nitric oxide concentration associated with hemodynamic control in older adult women. The sample consisted of 134 women (65.73 ± 6.14 years old). All subjects underwent a physical examination to assess body mass index, waist-hip ratio, body fat measurement by dual energy X-ray absorptiometry, and blood pressure (BP). Training status (TS) was evaluated by indirect determination of maximal oxygen uptake by a treadmill test using Balke protocol modified for older adults. Functional fitness was also evaluated through a Functional Fitness Battery Test to determine the general fitness functional index (GFFI). All participants were separated according to the functional fitness (TS1, very weak and weak; TS2, regular; TS3, good and very good). Plasma blood samples were used to evaluate prooxidant and antioxidant activity and nitrite and nitrate concentrations. The general results of this study showed that good levels of TS were related to lower levels of lipoperoxidation and protein damage, higher levels of antioxidant, and higher concentration of nitrite and nitrate. This combination may be responsible for the lower levels of BP in subjects with better TS. Ribeirao Preto Medical School, University of Sao Paulo (USP), Avenida Bandeirantes 3900, 14049-900 Ribeirao Preto, SP, Brazil Translational Physiology Laboratory, Universidade Nove de Julho (UNINOVE), Rua Vergueiro 235/249, Liberdade, 01504-001 Sao Paulo, SP, Brazil School of Nursing of Ribeirao Preto, University of Sao Paulo (USP), Avenida Bandeirantes 3900, 14040-902 Ribeirao Preto, SP, Brazil Department of Physical Education, Universidade Estadual Paulista (UNESP), Avenida Engenheiro Luiz Edmundo Carrijo Coube, 14-01, Bairro Vargem Limpa, 17033-360 Bauru, SP, Brazil

Objective Although aerobic exercise training has been recommended as nonpharmacological treatment of high blood pressure, the mechanisms of training-induced blood pressure lowering effects in dexamethasone (DEX)-induced hypertension remain unclear. Therefore, the aim of this study was to investigate the preventive role of exercise training in counteracting DEX-induced hypertension. Methods Rats were submitted to aerobic exercise training for 8 weeks or kept sedentary and then treated with DEX (50 μg/kg/day, s.c.) or saline injections for 14 days. Thereafter, all rats underwent carotid artery catheterization, and cardiovascular autonomic modulation was evaluated by spectral analysis. In addition, soleus muscle was collected for morphometric and protein level analysis. Results DEX treatment increased arterial pressure concomitantly with an increase in low-frequency spectral power of systolic arterial pressure and low frequency in pulse interval (94.11 and 58.58%, respectively), and a decrease in high-frequency spectral power of pulse interval (-12.05%). Capillary density (-25.87%), capillary-to-fibers ratio (-21.22%), vascular endothelial growth factor level (-15.10%), B-cell lymphoma 2 (Bcl-2) level (-16.40%) and Bcl-2/Bcl-2 associated X protein ratio (-27.14%) were all decreased after DEX treatment. Exercise training attenuated DEX-induced increase in arterial pressure accompanied by an attenuation of low-frequency spectral power of systolic arterial pressure, low frequency in pulse interval increases and high-frequency spectral power of pulse interval decrease. Training also prevented the decrease in capillary density (+44.43%), capillary-to-fibers ratio (+36.97%), vascular endothelial growth factor (+16.46%), Bcl-2 (+15.21%) protein level and Bcl-2/Bcl-2-associated X protein ratio (+30.93%). Conclusion These results demonstrate that exercise training improves cardiovascular autonomic balance to the heart associated with an improvement in sympathetic modulation of vascular tone and microcirculatory function in the skeletal muscle of DEX-induced hypertensive rats.

To evaluate the effect of low-intensity chronic exercise training (ExT) on blood pressure (BP), as well as the cardiac alterations associated with hypertension in aging hypertensive rats.Male spontaneously hypertensive rats (SHR; 21 months old) and their normotensive control Wistar-Kyoto (WKY) rats were submitted to low-intensity training protocol for 13 weeks. BP, cardiac morphological and morphometric analysis, as well as gene expression of fibrotic and inflammatory factors were analyzed at the end of the training period.ExT reduced BP and heart rate in aged SHR. Left ventricle hypertrophy, collagen volume fraction and wall-to-lumen ratio of myocardium arterioles were also decreased in trained SHR. However, ExT was unable to reverse the either reduced capillary density or the cardiac myocyte hypertrophy observed in SHR as compared with WKY rats. Trained SHR showed higher metalloproteinase-2/tissue inhibitor metalloproteinase-2 (MMP-2/TIMP-2) ratio and lower levels of α-smooth muscle actin, but similar levels of connective tissue growth factor, transforming growth factor beta or IL-1 beta to that of nontrained SHR.Low to moderate-intensity chronic ExT reverses the cardiac alterations associated with hypertension: myocardial arteriole, left ventricle hypertrophy, collagen content and tachycardia. These changes could be consequence or cause of the reduction in BP observed in trained SHR. In addition, ExT does not worsen the underlying inflammatory burden associated with hypertension. Therefore, the data support a beneficial effect of ExT in aging SHR similar to that reported in young or middle-aged individuals, confirming that exercise is a healthy habit that induces cardiac improvements independently of age.

Stellate ganglion (SG) represents the main sympathetic input to the heart. This study aimed at investigating physical exercise-related changes in the quantitative aspects of SG neurons in treadmill-exercised Wistar rats. By applying state-of-the-art design-based stereology, the SG volume, total number of SG neurons, mean perikaryal volume of SG neurons, and the total volume of neurons in the whole SG have been examined. Arterial pressure and heart rate were also measured at the end of the exercise period. The present study showed that a low-intensity exercise training program caused a 12% decrease in the heart rate of trained rats. In contrast, there were no effects on systolic pressure, diastolic pressure, or mean arterial pressure. As to quantitative changes related to physical exercise, the main findings were a 21% increase in the fractional volume occupied by neurons in the SG, and an 83% increase in the mean perikaryal volume of SG neurons in treadmill-trained rats, which shows a remarkable neuron hypertrophy. It seems reasonable to infer that neuron hypertrophy may have been the result of a functional overload imposed on the SG neurons by initial posttraining sympathetic activation. From the novel stereological data we provide, further investigations are needed to shed light on the mechanistic aspect of neuron hypertrophy: what role does neuron hypertrophy play? Could neuron hypertrophy be assigned to the functional overload induced by physical exercise?

Made available in DSpace on 2013-08-12T19:22:58Z (GMT). No. of bitstreams: 0 Previous issue date: 2008-09-01 Made available in DSpace on 2013-09-30T19:21:53Z (GMT). No. of bitstreams: 0 Previous issue date: 2008-09-01 Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-20T15:33:38Z No. of bitstreams: 0 Made available in DSpace on 2014-05-20T15:33:38Z (GMT). No. of bitstreams: 0 Previous issue date: 2008-09-01 Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) Evidence of mild hypertension in women and female rats and our preliminary observation showing that training is not effective to reduce pressure in female as it does in male spontaneously hypertensive rats (SHR) prompt us to investigate the effects of gender on hemodynamic pattern and microcirculatory changes induced by exercise training. Female SHR and normotensive controls (Wistar- Kyoto rats) were submitted to training (55% VO2 peak; 3 months) or kept sedentary and instrumented for pressure and hindlimb flow measurements at rest and during exercise. Heart, kidney, and skeletal muscles (locomotor/ nonlocomotor) were processed for morphometric analysis of arterioles, capillaries, and venules. High pressure in female SHR was accompanied by an increased arteriolar wall: lumen ratio in the kidney (+30%; P < 0.01) but an unchanged ratio in the skeletal muscles and myocardium. Female SHR submitted to training did not exhibit further changes on the arteriolar wall: lumen ratio and pressure, showing additionally increased hindlimb resistance at rest (+29%; P < 0.05). on the other hand, female SHR submitted to training exhibited increased capillary and venular densities in locomotor muscles (+50% and 2.3- fold versus sedentary SHR, respectively) and normalized hindlimb flow during exercise hyperemia. Left ventricle pressure and weight were higher in SHR versus WKY rats, but heart performance (positive dP/dt(max) and negative dP/dt(max)) was not changed by hypertension or training, suggesting a compensated heart function in female SHR. In conclusion, the absence of training- induced structural changes on skeletal muscle and myocardium arterioles differed from changes observed previously in male SHR, suggesting a gender effect. This effect might contribute to the lack of pressure fall in trained female SHRs. Univ São Paulo, Inst Biomed Sci, Dept Physiol & Biophys, ICB, BR-05508900 São Paulo, Brazil São Paulo State Univ, UNESP, Fac Sci, Dept Phys Educ, São Paulo, Brazil São Paulo State Univ, UNESP, Fac Sci, Dept Phys Educ, São Paulo, Brazil

Background: Vascular endothelial growth factor (VEGF) is a macromolecule of importance in inflammation that has been implicated in periodontitis. The aims of this study were to investigate VEGF expression during the progression of periodontal disease and to evaluate the effect of a preferential cyclooxygenase (COX)-2 inhibitor meloxicam on VEGF expression and alveolar bone loss in experimentally induced periodontitis. Methods: A total of 120 Wistar rats were randomly separated into groups 1 (control) and 2 (meloxicam, 3mg/kg/day,intraperitoneally,for3,7,14,or30days).Silkligatureswereplacedatthegingivalmarginlevel of the lower right first molar of all rats. VEGF expression was assessed by reverse transcription-polymerase chain reaction (RT-PCR), Western blot (WB), and immunohistochemical (IHC) analyses. The hemiarcades wereprocessedforhistopathologicanalysis.RT-PCRandWBresultsweresubmittedtoanalysisofvariance, the Tukey test, and Pearson correlation analysis (P

Previous studies have indicated the importance of angiotensin II (ANG II) in skeletal muscle angiogenesis. The present study explored the effect of regulation of the renin gene on angiogenesis induced by electrical stimulation with the use of physiological, pharmacological, and genetic manipulations of the renin-angiotensin system (RAS). Transfer of the entire chromosome 13, containing the physiologically regulated renin gene, from the normotensive inbred Brown Norway (BN) rat into the background of an inbred substrain of the Dahl salt-sensitive (SS/Mcwi) rat restored renin levels and the angiogenic response after electrical stimulation. This restored response was significantly attenuated when SS-13BN/Mcwi consomic rats were treated with lisinopril or high-salt diet. The role of ANG II on this effect was confirmed by the complete restoration of skeletal muscle angiogenesis in SS/Mcwi rats infused with subpressor doses of ANG II. Congenic strains derived from the SS-13BN/Mcwi consomic were used to further verify the role of the renin gene in this response. Microvessel density was markedly increased after stimulation in congenic strains that contained the renin gene from the BN rat (congenic lines A and D). This angiogenic response was suppressed in control strains that carried regions of the BN genome just above (congenic line C) or just below (congenic line B) the renin gene. The present study emphasizes the importance of maintaining normal renin regulation as well as ANG II levels during the angiogenesis process with a combination of physiological, genetic, and pharmacological manipulation of the RAS.

Made available in DSpace on 2018-12-11T17:23:03Z (GMT). No. of bitstreams: 0 Previous issue date: 2016-03-01 Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) This study was designed to describe the time-course changes of catabolic proteins following muscle atrophy induced by 10 days of dexamethasone (DEX). Rats underwent DEX treatment for 1, 3, 5, 7 and 10 days. Body weight (BW) and lean mass were obtained using a dual energy X-ray absorptiometry (DEXA) scan. Muscle ringer finger1 (MuRF-1), atrogin-1 and myostatin protein levels were analyzed in the tibialis anterior (TA), flexor hallucis longus (FHL) and soleus muscles. DEX treatment reduced lean mass since day-3 and reduced BW since day-5. Specific muscle weight reductions were observed after day-10 in TA (-23%) and after day-5 in FHL (-16%, -17% and -29%, for days 5, 7 and 10, respectively). In TA, myostatin protein level was 36% higher on day-5 and its values were normalized in comparison with controls on day-10. MuRF-1 protein level was increased in TA muscle from day-7 and in FHL muscle only on day-10. This study suggests that DEX-induced muscle atrophy is a dynamic process which involves important signaling factors over time. As demonstrated by DEXA scan, lean mass declines earlier than BW and this response may involve other catabolic proteins than myostatin and MuRF-1. Specifically for TA and FHL, it seems that myostatin may trigger the catabolic process, and MuRF-1 may contribute to maintain muscle atrophy. This information may support any intervention in order to attenuate the muscle atrophy during long period of treatment. Joint Graduate Program in Physiological Sciences PIPGCF UFSCar UNESP Department of Physiological Sciences Federal University of São Carlos - UFSCAR Department of Physical Education Universidade Estadual Paulista - UNESP Department of Kinesiology Faculty of Applied Health Sciences University of Waterloo Department of Biological Sciences Bauru School of Dentistry University of São Paulo USP Joint Graduate Program in Physiological Sciences PIPGCF UFSCar UNESP Department of Physiological Sciences Federal University of São Carlos - UFSCAR Department of Physical Education Universidade Estadual Paulista - UNESP CNPq: 130232/2011-4 FAPESP: 2012/03816-9 FAPESP: 2012/21820-3

Made available in DSpace on 2018-11-26T17:55:38Z (GMT). No. of bitstreams: 0 Previous issue date: 2015-08-05 Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) University of Sao Paulo [USP] The initiation or progression of periodontitis might involve a local renin-angiotensin system (RAS) in periodontal tissue. The aim of this study was to further characterize the local RAS in human and rat periodontal tissues between healthy and periodontally-affected tissue. Components of the RAS were investigated using in vitro, ex vivo and in vivo experiments involving both human and Wistar rat periodontium. Although not upregulated when challenged with P. gingivalis-lipopolysaccharide, human gingival and periodontal ligament fibroblasts expressed RAS components. Likewise, healthy and inflamed human gingiva expressed RAS components, some of which were shown to be functional, yet no differences in expression were found between healthy and diseased gingiva. However, in inflamed tissue the immunoreactivity was greater for the AT(1)R compared to AT(2)R in fibroblasts. When compared to healthy tissue, ACE activity was increased in human gingiva from volunteers with gingivitis. Human-gingiva homogenates generated Ang II, Ang 1-9 and Ang 1-7 when incubated with precursors. In gingiva homogenates, Ang II formation from Ang I was nearly abolished only when captopril and chymostatin were combined. Ang 1-7 formation was significantly greater when human gingiva homogenates were incubated with chymostatin alone compared to incubation without any inhibitor, only captopril, or captopril and chymostatin. In rat gingiva, RAS components were also found; their expression was not different between healthy and experimentally induced periodontitis (EP) groups. However, renin inhibition (aliskiren) and an AT(1)R antagonist (losartan) significantly blocked EP-alveolar-bone loss in rats. Collectively, these data are consistent with the hypothesis that a local RAS system is not only present but is also functional in both human and rat periodontal tissue. Furthermore, blocking AT(1)R and renin can significantly prevent periodontal bone loss induced by EP in rats. Univ Sao Paulo, Dept Biol Sci, Bauru Sch Dent, Sao Paulo, Brazil Univ Sao Paulo, Sch Dent, Dept Restorat Dent, Sao Paulo, Brazil Sao Paulo State Univ, Fac Sci, Dept Phys Educ, Sao Paulo, Brazil Univ Sao Paulo, Sch Med Ribeirao Preto, Sao Paulo, Brazil Med Coll Wisconsin, Dept Physiol, Milwaukee, WI 53226 USA Sao Paulo State Univ, Fac Sci, Dept Phys Educ, Sao Paulo, Brazil FAPESP: 2004/13479-3 FAPESP: 2005/60167-0 FAPESP: 2009/53848-1 FAPESP: 2009/15372-5 FAPESP: 2010/01230-1 FAPESP: 2013/16113-9 CNPq: 473856/2010-7 CNPq: 558171/2010-9 CNPq: 303494/2013-1 CNPq: 506802/2013-2 CNPq: 480160/2013-9 CAPES: 2435/09-9 University of Sao Paulo [USP]: 08.1.2066.25.3

Made available in DSpace on 2015-08-06T16:14:39Z (GMT). No. of bitstreams: 0 Previous issue date: 2015-04-01. Added 1 bitstream(s) on 2015-08-06T16:44:32Z : No. of bitstreams: 1 S0066-782X2015000400009-pt.pdf: 293433 bytes, checksum: 2e2e465b814fb503717fa96783f0b6d5 (MD5). Added 1 bitstream(s) on 2015-08-06T16:44:32Z : No. of bitstreams: 2 S0066-782X2015000400009-pt.pdf: 293433 bytes, checksum: 2e2e465b814fb503717fa96783f0b6d5 (MD5) S0066-782X2015000400009-en.pdf: 271141 bytes, checksum: f9fda24fbd4507ad1746ece81c771070 (MD5) Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) A associação do tratamento medicamentoso por estatinas com a prática de exercícios físicos pode reduzir substancialmente o risco de mortalidade cardiovascular de indivíduos dislipidêmicos, porém sua realização vem sendo associada à exacerbação de quadros miopáticos. O presente trabalho teve como objetivo apresentar os resultados mais recentes da literatura específica sobre os efeitos da associação de estatinas ao exercício físico na musculatura esquelética. Para tanto, realizou-se levantamento da literatura nas bases de dados PubMed e SciELO, utilizando a combinação dos unitermos: “estatina/estatinas” AND “exercício” AND “músculo” (“statin” AND “exercise” AND “muscle”), sendo selecionados apenas artigos originais publicados entre janeiro de 1990 e novembro de 2013. Foram analisados 16 artigos que avaliaram o efeito da associação das estatinas com exercício agudo ou crônico na musculatura esquelética. Os resultados dos estudos apontaram que atletas podem experimentar efeitos deletérios na musculatura esquelética quando do uso de estatinas, visto que os quadros de exacerbação da lesão muscular pelo exercício foram mais frequentes com treinamento intenso ou exercícios agudos excêntricos e extenuantes. O treinamento físico moderado, por sua vez, quando associado às estatinas, não aumenta os relatos de dor nem os níveis de creatina quinase, além de acarretar ganhos nas funções musculares e metabólicas advindas do treinamento. Sugere-se, portanto, que pacientes dislipidêmicos em tratamento com estatinas sejam expostos ao treinamento físico aeróbio combinado a exercícios resistidos, de intensidade moderada, em três sessões semanais, sendo que a oferta do treinamento físico previamente à administração do tratamento medicamentoso, quando possível, faz-se desejável. Statin treatment in association with physical exercise practice can substantially reduce cardiovascular mortality risk of dyslipidemic individuals, but this practice is associated with myopathic event exacerbation. This study aimed to present the most recent results of specific literature about the effects of statins and its association with physical exercise on skeletal musculature. Thus, a literature review was performed using PubMed and SciELO databases, through the combination of the keywords “statin” AND “exercise” AND “muscle”, restricting the selection to original studies published between January 1990 and November 2013. Sixteen studies evaluating the effects of statins in association with acute or chronic exercises on skeletal muscle were analyzed. Study results indicate that athletes using statins can experience deleterious effects on skeletal muscle, as the exacerbation of skeletal muscle injuries are more frequent with intense training or acute eccentric and strenuous exercises. Moderate physical training, in turn, when associated to statins does not increase creatine kinase levels or pain reports, but improves muscle and metabolic functions as a consequence of training. Therefore, it is suggested that dyslipidemic patients undergoing statin treatment should be exposed to moderate aerobic training in combination to resistance exercises three times a week, and the provision of physical training prior to drug administration is desirable, whenever possible. Universidade Estadual Paulista Instituto de Biociências Programa de Pós-Graduação em Ciências da Motricidade Universidade Federal de São Paulo Escola Paulista de Medicina Setor de Doenças Neuromusculares Universidade Estadual Paulista Faculdade de Ciências Departamento de Educação Física Universidade Estadual Paulista Instituto de Biociências Programa de Pós-Graduação em Ciências da Motricidade Universidade Estadual Paulista Faculdade de Ciências Departamento de Educação Física

This study investigated how proteins of the insulin signaling cascade could modulate insulin resistance after dexamethasone (Dexa) treatment and aerobic training. Rats were distributed into 4 groups: sedentary control (SC), sedentary+Dexa (SD), trained control (TC), and trained+Dexa (TD), and underwent aerobic training for 70 days or remained sedentary. Dexa was administered during the last 10 days (1 mg · kg −1 per day i. p.). After 70 days, an intraperitoneal glucose tolerance test (ipGTT) was performed. Protein levels of IRS-1, AKT, and PKC-α in the tibialis anterior (TA) muscle were identified using Western blots. Dexa treatment increased blood glucose and the area under the curve (AUC) of ipGTT. Training attenuated the hyperglycemia and the AUC induced by Dexa. Dexa reduced IRS-1 (− 16%) and AKT (− 43%) protein level with no changes in PKC-α levels. Moreover, these effects on IRS-1 and AKT protein level were prevented in trained animals. These results show for the first time that aerobic exercise prevented reductions of IRS-1 and AKT level induced by Dexa in the TA muscle, suggesting that aerobic exercise is a good strategy to prevent Dexa-induced peripheral insulin resistance.

Results from our laboratory have suggested a pathway involving angiotensin II type 1 (AT1) receptors and vascular endothelial growth factor (VEGF) in angiogenesis induced by electrical stimulation. The present study investigated if similar mechanisms underlie the angiogenesis induced by short-term exercise training. Seven days before training and throughout the training period, male Sprague-Dawley rats received either captopril or losartan in their drinking water. Rats underwent a 3-day treadmill training protocol. The tibialis anterior and gastrocnemius muscles were harvested under anesthesia and lightly fixed in formalin (vessel density) or frozen in liquid nitrogen (VEGF expression). In controls, treadmill training resulted in a significant increase in vessel density in all muscles studied. However, the angiogenesis induced by exercise was completely blocked by either losartan or captopril. Western blot analysis showed that VEGF expression was increased in the exercised control group, and both losartan and captopril blocked this increase. The role of VEGF was directly confirmed using a VEGF-neutralizing antibody. These results confirm the role of angiotensin II and VEGF in angiogenesis induced by exercise.

Objective To investigate whether training changes skeletal muscle venular profile and hemodynamic responses to exercise we studied spontanesouly hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats submitted to training programme (T = 50-60% of VO 2 max). Design Training (T) was performed on a treadmill over a period of 13 weeks. Age-matched control groups were kept sedentary (S). T and S rats were chronically instrumented for hindlimb flow (HLF) and arterial pressure (AP) measurements at rest, during dynamic exercise and recovery in two different situations: control and after extensive intravenous blockade (hexamethonium + losartan + N ω -nitro-L-arginine methyl ester + hydralazine). For morphometric analysis, skeletal muscle samples (gracilis) were obtained after transcardiac perfusion with fixative. Results T caused a significant reduction of resting mean arterial pressure (MAP) (-11%) only in the SHR group without changing basal HLF. In the sedentary SHR (SHR S ), basal relative hindlimb resistance was increased by 45%, but was significantly reduced after T (P < 0.05). During dynamic exercise, MAP increased similarly (10-20 mmHg) in all groups. HLF increases were similar for the four groups up to 0.8 km/h; at higher workloads, HLF was higher in trained SHR (SHR T ) versus trained WKY (WKY T ) (3.9- versus 2.9-fold increase over basal HLF, respectively). After blockade (and pressure correction with IV phenylephrine infusion), steady-state exercise was performed with similar hindlimb vasodilation in all groups and was accompanied by MAP reduction (-17 ± 8 mmH only in SHR T group. Skeletal muscle venular profile (density, diameter and lumen cross-sectional area) was similar in WKY T . WKY S and SHRs, but significantly increased in SHR T . In this group the two-fold increase in venule density was correlated with both the reduction in baseline MAP and the increase in HLF during dynamic exercise. Conclusions The results suggest that increased venule density is a specific adaptation of SHR skeletal muscle t training. Venular growth may contribute to both the pressure-lowering effect and the large HLF at high exercise intensities observed in the trained SHR.

Objective:Physiological angiogenesis in skeletal muscle is an adaptive response to physical training and electrical stimulation. This study investigated the role of angiotensin II (Ang II) in regulating both angiogenesis and vascular endothelial growth factor (VEGF) protein expression induced by electrical stimulation. Methods:The right tibialis anterior (TA) and extensor digitorum longus (EDL) muscles of Sprague-Dawley rats were stimulated for 8 hours per day for 7 days. The contralateral muscles served as controls. Two days before the surgery and throughout the stimulation protocol, the rats received either lisinopril or losartan in their drinking water. Rats without any drug treatment were used as control. Immunohistochemistry and Western blot analysis were performed to identify the source and quantify the VEGF protein expression in these muscles. The relationship between angiogenesis and VEGF expression was explored using a VEGF-neutralizing antibody. Results:Chronic electrical stimulation of the skel...

This study investigated the potential protective effect of low-intensity resistance training (RT) against dexamethasone (DEX) treatment induced muscle atrophy. Rats underwent either an 8 week period of ladder climbing RT or remained sedentary. During the last 10 days of the exercise protocol, animals were submitted to a DEX treatment or a control saline injection. Muscle weights were assessed and levels of AKT, mTOR, FOXO3a, Atrogin-1 and MuRF-1 proteins were analyzed in flexor hallucis longus (FHL), tibialis anterior (TA), and soleus muscles. DEX induced blood glucose increase (+46%), body weight reduction (-19%) and atrophy in FHL (-28%) and TA (-21%) muscles, which was associated with a decrease in AKT and an increase in MuRF-1 proteins levels. Low-intensity RT prevented the blood glucose increase, attenuated the FHL atrophy effects of DEX, and was associated with increased mTOR and reductions in Atrogin-1 and MuRF-1 in FHL. In contrast, TA muscle atrophy and signaling proteins were not affected by RT. These are the first data to demonstrate that low-intensity ladder-climbing RT specifically mitigates the FHL atrophy, which is the main muscle recruited during the training activity, while not preventing atrophy in other limb muscle not as heavily recruited. The recruitment-dependent prevention of atrophy by low intensity RT likely occurs by a combination of attenuated muscle protein degradation signals and enhanced muscle protein synthesis signals including mTOR, Atrogin-1 and MuRF-1.

OBJETIVO: Comparar os limites inferiores (L.inf.) e superiores (L.sup.) da prescrição de treinamento físico aeróbio determinada pelo teste ergométrico convencional (60-70% do VO2máx estimado ou 70-85% da FCmáx atingida), com a prescrição obtida pelo teste ergoespirométrico [limiar anaeróbio (LA) e ponto de compensação respiratória (PCR)]. MÉTODOS: Realizaram teste ergoespirométrico progressivo até a exaustão 47 homens (30±5 anos), divididos em subgrupos, de acordo com a velocidade da esteira durante o teste (4 ou 5mph) e a capacidade física medida [baixa (BCF) e moderada (MCF)]. RESULTADOS: Os L.inf. de prescrição indireta apresentaram valores de VO2 e FC significantemente maiores que os valores de VO2 e FC no LA (4mph= 34,4±4,5 vs 19,6±4,6 e 5mph= 28,9±2 vs 18,9±5,4, e BCF= 32,0±4,1 vs 17,2±2,8 e MCF= 31,6±4,9 vs 21,1±5,7(mlO2.kg-1.min-1) e (4mph = 128,9±7,8 vs 113,1± 15,6 e 5mph= 130,3±5,2 vs 114,1± 18,9, e BCF= 127,6±7,2 vs 109,3±13,2 e MCF= 131,2± 5,7 vs 117,4± 19,2bpm). Os L.sup. de prescrição indireta no grupo de 4mph e BCF apresentaram valores de VO2 significantemente maiores que os valores medidos no PCR (40,1±5,3 vs 32,2±4,3 e 37,4±4,8 vs 30,6±2,5 mlO2.kg-1.min-1, respectivamente), e valores de FC semelhantes aos medidos no PCR. CONCLUSÃO: Os L.inf. da prescrição indireta de treinamento físico superestimam o LA, enquanto os L.sup. parecem adequados somente para indivíduos ativos com MCF. PURPOSE: To compare the lower (LL) and upper limits (UL) of exercise intensity prescription based on standard exercise test (60-70% of estimated VO2max or 70-85% of HRmax measured) with exercise intensity prescription based on cardiopulmonary exercise test [anaerobic threshold (AT) and respiratory compensation point (RCP)]. METHODS: Fourty seven men (30±5 years) who were submitted to a progressive cardiopulmonary exercise test until exhaustion were divided in subgroups according to treadmill speed during exercise test (4 or 5mph) and the physical capacity [lower (LPC) and moderate physical capacity (MPC)]. RESULTS: The LL of the indirect exercise intensity prescription showed VO2 and HR values significantly higher than VO2 and HR values measured at AT (4mph= 34.4±4.5 vs 19.6±4.6 and 5mph= 28.9±2 vs 18.9±5.4, and LPC= 32.0±4.1 vs 17.2±2.8 and MPC= 31.6±4.9 vs 21.1± 5.7mlO2.kg-1.min-1 ) and (4mph= 128.9±7.8 vs 113.1±15.6 and 5mph= 130.3±5.2 vs 114.1±18.9, and LPC= 127.6±7.2 vs 109.3±13.2 and MPC= 131.2±5.7 vs 117.4±19.2bpm) The UL of the indirect exercise intensity prescription in 4mph and LPC group showed VO2 values significantly higher than those measured at RCP (40.1±5.3 vs 32.2±4.3 and 37.4±4.8 vs 30.6±2.5mlO2.kg-1.min-1, respectively), but similar HR values to those obtained at RCP. CONCLUSION: The LL of prescription based on standard exercise test overestimate the AT, whereas the UL seem adequate only for subjects with moderate physical capacity.

Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-27T11:29:46Z No. of bitstreams: 0Bitstream added on 2014-05-27T14:37:39Z : No. of bitstreams: 1 2-s2.0-84879113536.pdf: 325437 bytes, checksum: 8f57170c44aaf8513ced2f6f150153c4 (MD5) Made available in DSpace on 2014-05-27T11:29:46Z (GMT). No. of bitstreams: 0 Previous issue date: 2013-06-21 Background: Hypertension can be generated by a great number of mechanisms including elevated uric acid (UA) that contribute to the anion superoxide production. However, physical exercise is recommended to prevent and/or control high blood pressure (BP). The purpose of this study was to investigate the relationship between BP and UA and whether this relationship may be mediated by the functional fitness index.Methods: All participants (n = 123) performed the following tests: indirect maximal oxygen uptake (VO2max), AAHPERD Functional Fitness Battery Test to determine the general fitness functional index (GFFI), systolic and diastolic blood pressure (SBP and DBP), body mass index (BMI) and blood sample collection to evaluate the total-cholesterol (CHOL), LDL-cholesterol (LDL-c), HDL-cholesterol (HDL-c), triglycerides (TG), uric acid (UA), nitrite (NO2) and thiobarbituric acid reactive substances (T-BARS). After the physical, hemodynamic and metabolic evaluations, all participants were allocated into three groups according to their GFFI: G1 (regular), G2 (good) and G3 (very good).Results: Baseline blood pressure was higher in G1 when compared to G3 (+12% and +11%, for SBP and DBP, respectively, p

Made available in DSpace on 2013-08-12T18:40:24Z (GMT). No. of bitstreams: 0 Previous issue date: 2011-09-01 Made available in DSpace on 2013-09-30T18:04:11Z (GMT). No. of bitstreams: 0 Previous issue date: 2011-09-01 Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-20T13:26:06Z No. of bitstreams: 0 Made available in DSpace on 2014-05-20T13:26:06Z (GMT). No. of bitstreams: 0 Previous issue date: 2011-09-01 There is accumulating evidence that physical inactivity, associated with the modern sedentary lifestyle, is a major determinant of hypertension. It represents the most important modifiable risk factor for cardiovascular diseases, which are the leading cause of morbidity and mortality for both men and women. In addition to involving sympathetic overactivity that alters hemodynamic parameters, hypertension is accompanied by several abnormalities in the skeletal muscle circulation including vessel rarefaction and increased arteriole wall-to-lumen ratio, which contribute to increased total peripheral resistance. Low-intensity aerobic training is a promising tool for the prevention, treatment and control of high blood pressure, but its efficacy may differ between men and women and between male and female animals. This review focuses on peripheral training-induced adaptations that contribute to a blood pressure-lowering effect, with special attention to differential responses in male and female spontaneously hypertensive rats (SHR). Heart, diaphragm and skeletal muscle arterioles (but not kidney arterioles) undergo eutrophic outward remodeling in trained male SHR, which contributed to a reduction of peripheral resistance and to a pressure fall. In contrast, trained female SHR showed no change in arteriole wall-to-lumen ratio and no pressure fall. on the other hand, training-induced adaptive changes in capillaries and venules (increased density) were similar in male and female SHR, supporting a similar hyperemic response to exercise. Univ São Paulo, Inst Ciencias Biomed, Dept Fisiol & Biofis, BR-05508000 São Paulo, Brazil Univ Estadual Paulista, Dept Educ Fis, Fac Ciencias, Bauru, SP, Brazil Universidade Federal de São Carlos (UFSCar), Dept Ciencias Fisiol, Programa Interinst Posgrad UNESP UFSCAR, BR-13560 São Carlos, SP, Brazil Univ Estadual Paulista, Dept Educ Fis, Fac Ciencias, Bauru, SP, Brazil Universidade Federal de São Carlos (UFSCar), Dept Ciencias Fisiol, Programa Interinst Posgrad UNESP UFSCAR, BR-13560 São Carlos, SP, Brazil

Modelo : Estudo de prevalência. Objetivos: Avaliar a presença de hipertensão arterial auto-referida e comparar com os níveis de pressão arterial aferidos. Além sso, o trabalho se propôs a avaliar o grau de informação dos funcionários da saúde e determinar se o setor onde trabalha o funcionário influencia a Pressão Arterial (PA). Métodos: Foram avaliados 349 funcionários (46±10 anos) das cidades de Bauru e Jaú, que responderam uma anamnese (dados pessoais, condição socioeconômica, presença de doenças, prática de exercícios físicos e setor ocupacional) e foram submetidos a uma avaliação da PA. Os avaliados se auto-referiram normotensos ou hipertensos. Valores de PA Sistólica >140 mmHg e/ou PA diastólica >90 mmHg foram considerados elevados. Dentre os avaliados, 198 foram submetidos à avaliações antropométricas e bioquímicas. Os resultados são apresentados como média ± desvio padrão e distribuição de frequência. Utilizou-se teste “T- student” (p

This study investigated whether exercise training could prevent the negative side effects of dexamethasone. Rats underwent a training period and were either submitted to a running protocol (60% physical capacity, 5 days/week for 8 weeks) or kept sedentary. After this training period, the animals underwent dexamethasone treatment (1 mg/kg per day, i.p., 10 days). Glycemia, insulinemia, muscular weight and muscular glycogen were measured from blood and skeletal muscle. Vascular endothelial growth factor (VEGF) protein was analyzed in skeletal muscles. Dexamethasone treatment evoked body weight loss (−24%), followed by muscular atrophy in the tibialis anterior (−25%) and the extensor digitorum longus (EDL, −15%). Dexamethasone also increased serum insulin levels by 5.7-fold and glucose levels by 2.5-fold compared to control. The exercise protocol prevented atrophy of the EDL and insulin resistance. Also, dexamethasone-treated rats showed decreased muscular glycogen (−41%), which was further attenuated by the exercise protocol. The VEGF protein expression decreased in the skeletal muscles of dexamethasone-treated rats and was unaltered by the exercise protocol. These data suggest that exercise attenuates hyperglycemia and may also prevent insulin resistance, muscular glycogen loss and muscular atrophy, thus suggesting that exercise may have some benefits during glucocorticoid treatment.

Submitted by Guilherme Lemeszenski (guilherme@nead.unesp.br) on 2013-08-22T18:52:47Z No. of bitstreams: 1 S0100-879X2008000500012.pdf: 930162 bytes, checksum: f1ada3e5aa9531cc4d2868f7787b2ef5 (MD5) Made available in DSpace on 2013-08-22T18:52:47Z (GMT). No. of bitstreams: 1 S0100-879X2008000500012.pdf: 930162 bytes, checksum: f1ada3e5aa9531cc4d2868f7787b2ef5 (MD5) Previous issue date: 2008-05-01 Made available in DSpace on 2013-09-30T18:04:18Z (GMT). No. of bitstreams: 2 S0100-879X2008000500012.pdf: 930162 bytes, checksum: f1ada3e5aa9531cc4d2868f7787b2ef5 (MD5) S0100-879X2008000500012.pdf.txt: 32101 bytes, checksum: aeaaddd39455d43ec28d289aaf8317d4 (MD5) Previous issue date: 2008-05-01 Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-20T13:26:09Z No. of bitstreams: 2 S0100-879X2008000500012.pdf: 930162 bytes, checksum: f1ada3e5aa9531cc4d2868f7787b2ef5 (MD5) S0100-879X2008000500012.pdf.txt: 32101 bytes, checksum: aeaaddd39455d43ec28d289aaf8317d4 (MD5) Made available in DSpace on 2014-05-20T13:26:09Z (GMT). No. of bitstreams: 2 S0100-879X2008000500012.pdf: 930162 bytes, checksum: f1ada3e5aa9531cc4d2868f7787b2ef5 (MD5) S0100-879X2008000500012.pdf.txt: 32101 bytes, checksum: aeaaddd39455d43ec28d289aaf8317d4 (MD5) Previous issue date: 2008-05-01 Exercise-induced vessel changes modulate arterial pressure (AP) in male spontaneously hypertensive rats (SHR). Vascular endothelial growth factor (VEGF) is important for angiogenesis of skeletal muscle. The present study evaluated the time course of VEGF and angiogenesis after short- and long-term exercise training of female SHR and Wistar Kyoto (WKY) rats, 8-9 weeks (200-250 g). Rats were allocated to daily training or remained sedentary for 3 days (N = 23) or 13 weeks (N = 23). After training, the carotid artery was catheterized for AP measurements. Locomotor (tibialis anterior and gracilis) and non-locomotor skeletal muscles (temporalis) were harvested and prepared for histologic and protein expression analyses. Training increased treadmill performance by all groups (SHR = 28%, WKY = 64%, 3 days) and (SHR = 141%, WKY = 122%, 13 weeks). SHR had higher values of AP than WKY (174 ± 4 vs 111 ± 2 mmHg) that were not altered by training. Three days of running increased VEGF expression (SHR = 28%, WKY = 36%) simultaneously with an increase in capillary-to-fiber ratio in gracilis muscle (SHR = 19%, WKY = 15%). In contrast, 13 weeks of training increased gracilis capillary-to-fiber ratio (SHR = 18%, WKY = 19%), without simultaneous changes in VEGF expression. Training did not change VEGF expression and capillarity of temporalis muscle. We conclude that training stimulates time- and tissue-dependent VEGF protein expression, independent of pressure levels. VEGF triggers angiogenesis in locomotor skeletal muscle shortly after the exercise starts, but is not involved in the maintenance of capillarity after long-term exercise in female rats. Universidade Estadual Paulista Júlio de Mesquita Filho Faculdade de Ciências de Bauru Departamento de Educação Física Universidade de São Paulo Instituto de Ciências Biomédicas Departamento de Fisiologia e Biofísica Universidade Estadual Paulista Júlio de Mesquita Filho Faculdade de Ciências de Bauru Departamento de Educação Física

Angiogenesis, under normal conditions, is a tightly regulated balance between pro- and antiangiogenic factors. The goal of this study was to investigate the mechanisms involved in the control of the skeletal muscle angiogenic response induced by electrical stimulation during the suppression of plasma renin activity (PRA) with a high-salt diet. Rats fed 0.4% or 4% salt diets were exposed to electrical stimulation for 7 days. The tibialis anterior (TA) muscles from stimulated and unstimulated hindlimbs were removed and prepared for gene expression analysis, CD31-terminal deoxynucleotide transferase-mediated dUTP nick-end labeling (TUNEL) double-staining assay, and Bcl-2 and Bax protein expression by Western blot. Rats fed a low-salt diet showed a dramatic angiogenesis response in the stimulated limb compared with the unstimulated limb. This angiogenesis response was significantly attenuated when rats were placed on a high-salt diet. Microarray analysis showed that in the stimulated limb of rats fed a low-salt diet many genes related to angiogenesis were upregulated. In contrast, in rats fed a high-salt diet most of the genes upregulated in the stimulated limb function in apoptosis and cell cycle arrest. Endothelial cell apoptosis, as analyzed by CD31-TUNEL staining, increased by fourfold in the stimulated limb compared with the unstimulated limb. There was also a 48% decrease in the Bcl-2-to-Bax ratio in stimulated compared with unstimulated limbs of rats fed a high-salt diet, confirming severe apoptosis. This study suggests that the increase in endothelial cell apoptosis in TA muscle might contribute to the attenuation of angiogenesis response observed in rats fed a high-salt diet.

Objective To investigate mechanisms underlying the training-induced blood pressure-lowering effect we analyzed the hemodynamic responses and morphometric changes of the skeletal muscle microcirculation of spontaneously hypertensive (SHR) and normotensive Wistar–Kyoto (WKY) rats during an exercise training program. Design Training (50–60% VO2 max) was performed on a treadmill for 13 weeks and control groups were kept sedentary over the same period of time. Trained and sedentary rats were chronically instrumented for hindlimb flow and arterial pressure (AP) recordings under conscious unrestrained conditions. Gracilis and myocardial muscle samples were obtained for morphometric analysis after transcardiac perfusion of fixative. Results SHR, when compared to WKY presented an elevated blood pressure, an increased relative hindlimb vascular resistance, capillary rarefaction in both gracilis and myocardium and an increased wall-to-lumen ratio of gracilis arterioles. Training increased significantly both capillary density and capillary/fiber ratio in the gracilis and myocardium of WKY and SHR groups, causing a complete reversal of capillary rarefaction in trained SHR. In SHR, training also reduced resting blood pressure and caused normalization of both relative hindlimb vascular resistance and gracilis arterioles wall-to-lumen ratio. Regression analysis revealed strong positive correlation between hindlimb vascular resistance and mean AP (MAP) and between arterioles wall-to-lumen ratio and MAP. Conclusions The results suggest that low-intensity training can significantly reduce pressure in SHR while normalizing both the arteriole morphology and the resistance of the skeletal muscle microcirculation.

The objective of the present study was to validate the transit-time technique for long-term measurements of iliac and renal blood flow in rats. Flow measured with ultrasonic probes was confirmed ex vivo using excised arteries perfused at varying flow rates. An implanted 1-mm probe reproduced with accuracy different patterns of flow relative to pressure in freely moving rats and accurately quantitated the resting iliac flow value (on average 10.43 +/- 0.99 ml/min or 2.78 +/- 0.3 ml min-1 100 g body weight-1). The measurements were stable over an experimental period of one week but were affected by probe size (resting flows were underestimated by 57% with a 2-mm probe when compared with a 1-mm probe) and by anesthesia (in the same rats, iliac flow was reduced by 50-60% when compared to the conscious state). Instantaneous changes of iliac and renal flow during exercise and recovery were accurately measured by the transit-time technique. Iliac flow increased instantaneously at the beginning of mild exercise (from 12.03 +/- 1.06 to 25.55 +/- 3.89 ml/min at 15 s) and showed a smaller increase when exercise intensity increased further, reaching a plateau of 38.43 +/- 1.92 ml/min at the 4th min of moderate exercise intensity. In contrast, exercise-induced reduction of renal flow was smaller and slower, with 18% and 25% decreases at mild and moderate exercise intensities. Our data indicate that transit-time flowmetry is a reliable method for long-term and continuous measurements of regional blood flow at rest and can be used to quantitate the dynamic flow changes that characterize exercise and recovery.