Orientadores: Carla Roberta O. Carvalho, Debora de Queiroz Tavares / Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Engenharia de Alimentos / Made available in DSpace on 2018-07-25T16:35:41Z (GMT). No. of bitstreams: 1 Bezerra_RosangelaMariaNeves_D.pdf: 3623488 bytes, checksum: d3f1edf07d469480dc4fd305aa42682f (MD5) Previous issue date: 1999 / Resumo: A interação da insulina com o seu receptor, estimula a porção tiro sina quinase do receptor, levando à autofosforilação e a fosforilação de substratos citossólicos, substrato 1 do receptor de insulina (IRS-1) e substrato 2 do receptor de insulina (IRS-2). Estes substratos fosforilados associam-se a proteínas com domínio SH2. Ratos alimentados com dieta rica em frutose são um modelo experimental já descrito de resistência à insulina, hipertriacilgliceridemia, hiperinsulinemia e hipertensão. Entretanto, o mecanismo molecular envolvido na resistência à insulina ainda não foi totalmente esclarecido. Neste estudo, utilizando da técnica de imunoprecipitação e "im.munoblotting", avaliamos a quantidade protéica e o grau de fosforilação, após estimulo insulínico, do receptor de insulina (IR) e do IRS-l, bem como a associação do IRS-1 com a PI 3-quinase e IRS-1 com a fosfotirosina fostatase (SHP2) em figado e músculo de ratos alimentados com dieta rica em frutose. Não houve mudanças na concentração do receptor de insulina e do IRS-l em figado e músculo dos animais alimentados com dieta rica em frutose. Entretanto, o grau de fosforilação do receptor de insulina foi reduzido para 71 ± 2% (P<0,05) nas amostras de figado do grupo fru.tose. Nas amostras imunoprecipitadas com anticorpo anti-IRS-1 e incubadas com anticorpo antifosfotirosina, houve diminuição do grau de fosforilação para 70 ± 6% (P<0,05) e 76 ± 5% (P<0,05) respectivamente, em figado e músculo dos ratos com dieta rica em frutose. A associação IRS-1 /PI 3-quinase reduziu para 84 ± 3% (P<0,05) no figado e para 84 ± 4% (P<0,05) no músculo do grupo frutose. A associação IRS-1jSHP2, foi reduzida para 79 ± 5% (P<0,05) no figado dos animais alimentados com frutose. Esses dados sugerem que alterações nas etapas iniciais da via de sinalização da insulina podem ter significado importante no mecanismo de resistência à insulina encontrada neste modelo. Os animais alimentados por 28 dias com dieta rica em frutose apresentaram moderada resistência à insulina, demonstrada pela diminuição da velocidade de redução da glicose, e um aumento significativo da concentração de triacilglicerol sérico. Entretanto, diferentemente da maioria dos estudos, não houve alteração na concentração de insulina nem na pressão arterial destes animais comparados ao grupo controle. Como existe uma heterogeneidade na composição de gordura e sódio destas dietas, foi avaliada a influência da adição de sódio na dieta rica em frutose, na sensibilidade à insulina, na pressão arterial e no grau de fosforilação do IRS-1 no figado destes animais. A adição de sódio não teve efeito na sensibilidade à insulina medida pelo teste de tolerância à insulina curto, nem na fosforilação induzida pela insulina do IRS-l, como demonstrada pela técnica de "immunoblotting". Entretanto, a adição de sódio promoveu um aumento significativo na pressão arterial indireta dos animais controle e com dieta rica em frutose (C: 117±3 mmHg x C-Na: 141± 4 mmHg, P O,05 e F: 118 ± 3 mmHg x F-Na: 132 ± 4 mmHg, P<0,05). Esses resultados demonstram que a alimentação por 28 dias com dieta rica em frutose, não induz a hiperinsulinemia, nem a hipertensão. Essas observações sugerem que a gordura saturada e a quantidade de sódio na dieta podem agir sinergisticamente com as alterações metabólicas induzidas pela frutose, favorecendo a elevação da insulina sérica e da pressão arterial neste modelo animal. / Abstract: The abstract is available with the full electronic document / Doutorado / Doutor em Ciência da Nutrição

Master of Science / Department of Kinesiology / Carl Ade / Background – Chemotherapy-induced left ventricular cardiotoxicity is associated with many cancer treatments; however, what is less known is how these treatments affect vascular health and autonomic control of blood pressure. Arterial stiffness and cardiovagal baroreflex sensitivity (BRS) are indicators of cardiovascular health and may provide insight into the adverse effects of anti-cancer chemotherapy. Therefore, the primary aims of the present study were to evaluate carotid artery stiffness and arterial BRS in cancer patients currently being treated with adjuvant chemotherapy. Methods – We performed a cross-sectional, case-control study involving 9 cancer patients and 9 age- and sex-matched controls. Carotid artery stiffness was assess via 2D ultrasonography. Cardiovagal BRS was assessed from the spontaneous changes in beat-to-beat time series of R-R interval and systolic blood pressure via the cross correlation technique. Results – Our findings indicated a significant decrease in cardiovagal BRS in cancer patients compared to controls (4.7 ± 0.6 vs 9.2 ± 1.7 msec mmHg⁻¹ respectively, P = 0.02). Carotid artery β-Stiffness was significantly higher in the cancer patients compared to control participants (9.2 ± 1.2 vs 6.6 ± 0.74 U respectively, P = 0.05). Conclusions – These data suggest that anti-cancer chemotherapy elicits significant decreases in the autonomic control of blood pressure and arterial stiffness, leaving cancer survivors with an increased risk of future cardiovascular disease.

Orthostatic intolerance following exposure to simulated or actual microgravity is observed following spaceflight and extended periods of bed rest, and is not always associated with simultaneous hypotension. Differential adaptation of cephalic and caudal arterial vasculatures (as a result of removal of the normal hydrostatic gradient) is proposed as a potential mechanism underlying this phenomenon. A potential role for changes to the L-arginine/nitric oxide pathway in such adaptations has been suggested, predominantly from previous in vitro studies; using an established model of simulated microgravity (head-down tilt; HDT). This thesis investigates whether findings in isolated vessels are reflected by in vivo measurements of cephalic and caudal vascular function. Using carotid or iliac artery flow normalized to mean arterial pressure as an index of cerebral or hind limb vascular conductance, autoregulatory cerebral vasodilatation in response to lower body negative pressure was found to be impaired following HDT. In addition, α¬1-adrenoceptor agonist-mediated vasoconstriction was decreased in the cerebral vasculature and increased in the peripheral and hind limb vasculature. Administration of acetylcholine or the non-selective nitric oxide synthase (NOS) inhibitor Nω-nitro-L-arginine methyl ester (L-NAME) demonstrated a decreased contribution of NOS to cerebrovascular tone, but an increased contribution of NOS to peripheral vascular resistance and tone of the hind limb vasculature. Together with a lack of difference in the response to the selective inducible NOS (iNOS) inhibitor 1400W, these results suggest that differential adaptation of eNOS may account for the observed differences between control and HDT animals. Further investigation of the changes to the L-arginine/nitric oxide pathway suggest that these changes are not associated with changes in eNOS expression, but may be related to altered activity of eNOS. Furthermore, the bioavailability (as measured by pharmacokinetic half life) or the vascular effector mechanisms (as measured by the haemodynamic response to exogenously administered nitric oxide) responsible for the effects of nitric oxide were also shown to be unaffected by HDT. These findings suggest that differential adaptation of the L-arginine/nitric oxide pathway may contribute to the inability to raise total peripheral resistance and impaired cerebral autoregulation following HDT, thereby representing a mechanism of orthostatic intolerance following exposure to microgravity. / Medicine, Faculty of / Anesthesiology, Pharmacology and Therapeutics, Department of / Graduate

Orientador: Jose Antonio Rocha Gontijo / Dissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia / Made available in DSpace on 2018-08-03T15:37:28Z (GMT). No. of bitstreams: 1 Suedekum_ElenWhiteMateus_M.pdf: 8584327 bytes, checksum: 8f11b1956a8a970839181b78f49bb35b (MD5) Previous issue date: 2003 / Resumo: Alterações morfológicas e funcionais de diferentes sistemas e aparelhos e a hipertensão arterial têm sido demonstrados freqüentemente na evolução da diabetes mellitus. Dentre estas alterações funcionais, destacam-se aquelas manifestações relacionadas à modificação de manipulação tubular de sódio e do balanço hidrossalino. Pouco se conhece sobre o envolvimento da angiotensina 11 e da atividade neural nesta alteração, bem como da importância destas na modulação de uma resposta contra-reguladora durante a depleção volêmica induzida pela furosemida. O objetivo do estudo foi avaliar o efeito do bloqueio de receptores A T1 da angiotensina II e da atividade neural renal sobre a pressão arterial e a manipulação tubular renal de sódio, após a administração aguda ou crônica de furosemida, na diabetes mel/itus experimental. Para a avaliação do papel dos receptores A T1 da angiotensina 11 e da atividade neural renal, comparamos oito grupos de animais: 1) controle; 2) controle tratado com losartan; 3) diabetes mellitus induzida por estreptozotocina, 4) diabetes mellitus induzida por estreptozotocina e tratado com losartan, 5) controle submetido à cirurgia simulada de denervação renal bilateral; 6) controle submetido à denervação renal bilateral, 7) diabetes mel/itus induzida por estreptozotocina e submetido à cirurgia simulada de denervação renal bilateral; e 8) diabetes mellitus induzida por estreptozotocina e submetido à denervação renal bilateral. A pressão arterial foi aferida semanalmente através do método de plestimografia de cauda e o estudo funcional renal foi estimado através dos clearances de creatinina endógeno e de lítio, em ratos Wistar-Hannover acordados em gaiolas metabólicas individuais. Nossos resultados mostram que: 1) uma progressiva elevação da pressão arterial ocorreu em animais diabéticos, que foi atenuada pela denervação renal bilateral; 2) losartan 10 mg/kg/dia reduz a pressão arterial em animais-controle; todavia, perde a sua eficácia hipotensora em animais diabéticos, após a administração crônica de furosemida; 3) a administração oral aguda de furosemida promoveu uma natriurese em animais-controle e diabéticos, por elevar a excreção de sódio em segmentos proximais e pós-proximais do néfron; 4) o tratamento crônico de furosemida promoveu uma significativa atenuação nesta resposta natriurética por promover uma queda na fração de excreção de sódio, principalmente em segmentos pós-proximais do néfron, associada também à queda da taxa de filtração glomerular em animais controles e diabéticos; 5) losartan atenua a resposta diurética induzida pela administração aguda e cônica de furosemida em animais diabéticos; 6) losartan não modificou a resposta natriurética observada principalmente em segmentos pós-proximais do néfron em animais controles; 7) o bloqueio de receptores A T1 da angiotensina causa elevação da taxa de filtração glomerular associada à queda da fração de excreção proximal de sódio em animais diabéticos; 8) a denervação renal bilateral atenuou a resposta natriurética à administração aguda de furosemida por reduzir a excreção de sódio em segmentos pós-proximais do néfron; 9) a denervação renal não aboliu a resposta natriurética induzi da por furosemida administrada cronicamente. Portanto, nosso estudo mostra que na diabetes mellitus ocorre uma elevação significativa da pressão arterial sistêmica, que é atenuada pela denervação renal bilateral, e sugere que mecanismos contra-regulatórios . à depleção do volume sangüíneo ocorrem independentemente da ação de angiotensina 11 e da atividade neural renal / Abstract: Functional and morphological modification of the different animal systems and apparatus, and arterial blood pressure has been demonstrated in the evolution of the diabetes mellitus. Among these dysfunctions, detach to these related to the modifications of sodium tubular handling and the hydro-saline homeostasis. The studies evaluating the evolving of angiotensin 11 and renal nerve activity in this pathophysiological situation are not wide at the moment, as well as the importance these in the modulation of a counter-regulatory answer during depletion's volume that was induce by furosemide. The objective of study was evaluate the influence of the blockade of the A T1 angiotensin receptors and of the renal nerve activity on the arterial blood pressure and sodium renal tubular handling, after acute and chronic administration of furosemide, in diabetes mellitus animal model induced by streptozotocin i. v administration in rats. To examine the role of AT1 angiotensin receptors and of the renal nerve activity, we compared eight groups of animais: 1) contol rats, 2) losartan treated rats; 3) streptozotocin-induced DM rats; 4) losartan treated streptozotocin-induced DM rats; 5) sham-operated rats; 6) denervated rats; 7) sham-operated streptozotocin-induced DM rats, e 8) denervated streptozotocininduced DM rats. The arterial blood pressure was measured weekly by tail plethysmography method and renal function test was estimated by lithium and creatinine clearance, in concious and unrestrained rats and individual metabolic cages. The results of present study demostrate that: 1) a progressive elevation of the arterial pressure occured in diabetic animais that is attenuaded by bilateral renal denervation; 2) losartan 10 mg/kg/day reduced the arterial pressure in controls animais; but it lose its efficacy in diabetic animais, after the chronic administration of furosemide; 3) the acute oral administration of furosemide promoted a natriurese, in controls and diabetic animais, by elevate the sodium excretion in proximal and post-proximal nefron segment.; 4) the chronic tratment of furosemide promoted a significant attenuation in this natriuretic response by induced a fali in sodium excretion fraction, mainly in post-proximal segment of nefron associated toa to the fali of the glomerular filtration rate in controls and diabetic animais. 5) losartan attenuate the diuretic response induced by acute and chronic of furosemide in diabetic animais; 6) losartan no modified the natriurese response observed principally in post-proximal segment of nefron in controls animais; 7) the blockade of A T1 receptors of angiotensin 11 causes an elevation of the glomerular filtration rate associated to the a fali of the sodium proximal excretion fraction in diabetic animal; 8) the bilateral renal denervation attenuated the natriuretic response to acute administration of furosemide by reduce the sodium excrection in post-proximal segment nefron; 9) the renal denervation no abolished a natriuretic response induced by chronic administration of furosemide. Therefore, our study demonstrate that in diabetes mellitus occurs a significant elevation of the systemic arterial pressure that is attenuated by bilateral renal denervation. And, it suggests that contra-regulatory mechanisms to the blood volume depletion occur independently of angiotensin 11 and renal nerve activity / Mestrado / Fisiologia / Mestre em Biologia Funcional e Molecular

A hipertensão arterial sistêmica (HAS) pós-transplante é frequente e está associada com aumento da morbimortalidade cardiovascular e subsequente disfunção do enxerto, sendo relatada como consequência ao uso de imunossupressores, especialmente os inibidores da calcineurina. Este estudo pretende avaliar o impacto da hipertensão arterial sobre a rigidez arterial calculada utilizando o índice ambulatorial de rigidez arterial (IARA) como desfecho substituto obtido pela monitorização ambulatorial da pressão arterial (MAPA) em pacientes transplantados de coração. Trata-se de um estudo prospectivo, observacional, analítico, com grupo controle, realizado no Hospital de Messejana Dr. Carlos Alberto Studart Gomes, hospital público do estado do Ceará, especializado em doenças cardiopulmonares e de referência em transplante de coração. Foram selecionados pacientes adultos transplantados do coração, os quais passaram por exames clínicos e complementares, e um grupo controle com pacientes não transplantados hipertensos. Todos foram submetidos a MAPA e obtenção do IARA com o objetivo de estimar o risco de rigidez arterial. Foram realizados testes estatísticos de significância e regressão logística para controle de confundimento. A média de idade dos transplantados foi de 55 anos, contra 48 dos não transplantados. A hipertensão prévia foi mais frequente em não transplantados, mas diabetes e doença arterial coronariana foram mais frequentes em transplantados. A média diastólica dos transplantados (82) é significativamente maior que a dos não transplantados (74) e o descenso sistólico é praticamente inexistente em pacientes transplantados (-0,18) que no grupo-controle (9,45). A condição de transplantado do paciente não é determinante de rigidez arterial, mas a hipertensão arterial sistólica na primeira avaliação, a média sistólica em 24h, a média diastólica em 24h, o descenso sistólico, o descenso diastólico e o IARA (parâmetros da MAPA) o são. Este estudo encontrou que num grupo de transplantados de coração adultos, a hipertensão arterial sistêmica está independentemente associada com a rigidez arterial estimada pelo IARA, que é um novo método, não invasivo, de fácil execução e de baixo custo. A evidência demonstrada por este estudo pode auxiliar no direcionamento de tratamento dos pacientes transplantados, contribuindo com melhoria do prognóstico / Hypertension post cardiac transplant is frequent and is associated with increased cardiovascular morbidity and mortality and graft dysfunction, being reported because of the use of immunosuppressant, especially the calcineurin inhibitors. This study aims to evaluate the impact of hypertension on the arterial stiffness calculated using the IARA as surrogate outcome obtained by the Home Blood Pressure Monitoring in heart transplanted patients. This is an observational study, analytical, with the control group, in Heart and Lung Messejana´s Hospital, a public institution in the State of Ceará, which is specialized in cardiopulmonary diseases and especially in heart transplant, with adult patients cardiac transplanted, which underwent clinical and complementary exams, from which were obtained the IARA. Statistical significance tests and logistic regression to control for confounding were performed. The average age of transplanted was 55 years, against 48 of the non-transplanted. Hypertension was more frequent in prior not transplanted, but diabetes and coronary artery disease were more frequent in transplanted. The average diastolic of transplanted (82) is significantly higher than the non-transplanted (74) and decrease systolic is virtually nonexistent in transplant patients (-0.18) than in the control group (9.45). The condition of the transplanted patient is not determinant of arterial stiffness (p = 0.105), but are the systolic hypertension in the first evaluation, the average systolic, diastolic average in 12:0 am 12:0 am, systolic, diastolic descent and the IARA (parameters of the HBPM). This study showed that in a group of adult cardiac transplanted, hypertension is independently associated with arterial stiffness estimated by IARA, which is a new method, non-invasive, easy to perform and inexpensive. The evidence demonstrated by this study may assist in treatment of transplanted patients, contributing to improving the prognosis

No description available.

No description available.

Background. Stroke affects over 80 million individuals worldwide. Elevated arterial stiffness has emerged as a novel independent risk marker for stroke. While arterial stiffness is improved after chronic aerobic training, a single bout of aerobic exercise leads to transient increases that typically resolve within 5 minutes of recovery. Elevated arterial stiffness may persist for up to 30 minutes following exercise in populations with cardiovascular disease. However, no study has examined the effect of acute aerobic exercise on arterial stiffness and central hemodynamics in individuals with stroke. Moreover, no study has explored the clinical significance of these responses. Objectives. The primary objective of this thesis was to characterize the response and recovery of arterial stiffness and central hemodynamics to peak aerobic exercise in individuals ≥ 6 months post-stroke. The secondary objective was to explore the relationships between the exercise response and recovery of arterial stiffness and central hemodynamics, with cardiorespiratory fitness and walking ability. Results. This cross-sectional study recruited 10 adults with stroke (mean ± SD age=56.9 ± 11.8; median [IQR]= 2.9 [1.9] years post-stroke; n=4 females). After peak aerobic exercise, cfPWV increased from rest and remained elevated for 20 minutes (p<0.05). Heart rate increased and remained elevated for 10 minutes post-exercise (p<0.05), while systolic blood pressure decreased and remained reduced for 15 minutes (p<0.05). Positive associations were found between cardiorespiratory fitness and heart rate reserve (r=0.74, p=0.02), and with each phase of heart rate recovery (HR60s r=0.80, p=0.005, HR120s r=0.79, p=0.006; HR300s r=0.72, p=0.02; and HR600s r=0.75, p=0.01). There were no relationships between response and recovery of hemodynamic variables with walking ability. Conclusion. Individuals with chronic stroke may have impaired arterial stiffness and heart rate recovery following peak aerobic exercise. Moreover, heart rate reserve and all phases of heart rate recovery were related to cardiorespiratory fitness, but not walking ability. / Thesis / Master of Science Rehabilitation Science (MSc) / Arterial stiffness has been recently identified as an important risk marker for stroke. Aerobic exercise reduces the risk of stroke by lowering arterial stiffness. But during exercise, there is an increase in arterial stiffness that usually subsides by 5 minutes. Lengthy exposure to arterial stiffness can cause damage to organs like the kidneys and liver. The purpose of this thesis was to measure the arterial stiffness and cardiovascular response to exercise in people with stroke. We also studied the relationship between the responses, fitness and walking ability. Ten people with stroke participated in this study. After aerobic exercise, arterial stiffness stayed high above resting levels and did not recover after 20 minutes. Also, heart rate recovery was related to fitness but not walking ability. This study tells us that people with stroke have an weakened ability to recover from aerobic exercise and that higher fitness levels can improve exercise recovery.

Cardiovascular disease (CVD) is the leading cause of death in the United States. Recently, the gut microbiota has been implicated in the pathophysiology and progression of CVD. Experimental evidence suggests that high fat feeding alters the functional composition of the gut microbiota (dysbiosis); leading to increased translocation of the pro-inflammatory, endotoxin, and increased production of the pro-atherogenic, trimethylamine-N-oxide (TMAO). Together, these changes are hypothesized to accelerate CVD progression. Conversely, administration of gut microbiota modulating agents, such as antibiotics and probiotics, attenuate high fat feeding induced CVD in rodent models. In humans, the capacity to produce TMAO following L-carnitine or phosphatidylcholine challenges is abolished after receiving broad spectrum antibiotics for a period of one week. However, whether gut modulation over a longer period of time decreases fasting serum endotoxin, fasting plasma TMAO, and CVD risk in response to high fat feeding has been unexplored in humans. To address these issues we conducted a randomized, placebo controlled, parallel group designed, controlled feeding study in healthy, non-obese males receiving the multi-strain probiotic, VSL #3 (or placebo), while a consuming a high fat diet for 4-weeks. First, we tested the hypothesis that VSL #3 would attenuate the rise in serum endotoxin and consequent arterial stiffening following high fat feeding in healthy, non-obese males. Second, we tested the hypothesis that VSL #3 would attenuate the rise in plasma TMAO concentrations following high fat feeding in healthy, non-obese males. In contrast to our first hypotheses, serum endotoxin concentrations and arterial stiffness did not change in response to high fat feeding or with VSL#3 treatment. Interestingly, VSL #3 significantly attenuated the increase in body mass (+ 1.4±0.4 vs. +2.3±0.3 kg; P < 0.05) and fat mass (+0.7±0.1 vs. + 1.4±0.3 kg; P < 0.05) following high fat feeding compared to the placebo. In contrast to our second hypothesis, probiotic supplementation did not attenuate the rise in plasma TMAO following high fat feeding. Future studies are necessary to elucidate the mechanisms responsible for the prevention of body mass and fat mass gain with VSL#3 supplementation following high fat feeding. In addition, studies are needed to determine whether higher doses of VSL #3, other single or multispecies probiotics, prebiotics, or synbiotics attenuate the production of the proatherogenic, TMAO. / Ph. D.

O objetivo deste estudo foi avaliar os efeitos da intensidade do exercício na sensibilidade do barorreflexo pós-exercício. Vinte homens normotensos entre 19 a 30 anos foram analisados: a) 45 minutos de exercício em cicloergômetro em 30%, 50% e 70% do consumo pico de oxigênio; e b) 45 minutos de repouso sentado; realizado de maneira aleatória. O controle barorreflexo foi avaliado através da infusão intravenosa de fenilefrina (1 mg/kg) e nitroprussiato de sódio (1 mg/kg). Independentemente da intensidade do exercício, a pressão arterial sistólica e diastólica estavam significantemente diminuídas durante o período de recuperação, do que no repouso. A frequência cardíaca foi significantemente maior no período de recuperação nas sessões 50% e 70% do consumo pico de oxigênio, sendo essa queda mais acentuada na sessão de 70% do consumo pico de oxigênio. A sensibilidade do barorreflexo foi significantemente menor após o exercício em 70% do consumo pico de oxigênio do que na sessão controle, não havendo alterações nas outras. O controle cardiopulmonar estava significantemente reduzido após a sessão em 70% do consumo pico de oxigênio através da aplicação da câmara de pressão negativa e inalterada da elevação das pernas. Em conclusão, a intensidade do exercício não influenciou na redução da pressão arterial no período pós-exercício e somente o exercício intenso diminuiu a sensibilidade do barorreflexo e cardiopulmonar / This study was designed to evaluate the aftereffects of exercise intensity on baroreflex sensitivity. Twenty normotensive men between 19 and 30 years were examined after: a) 45 min of leg cycling performed at 30%, 50% and 70% of peak oxygen uptake , and b) 45 min of seated rest; performed in a random order. During this period, baroreflex control was evaluated by intravenous infusion of phenylephrine (1 mg/kg) and sodium nitroprusside (1 mg/kg). Independently of exercise intensity, systolic and diastolic blood pressures were significantly lower during the recovery period than pre-exercise.. Heart rate was significantly higher after exercise performed at 50% and 70% of peak oxygen uptake, and this increase was greater after exercise at 70% of peak oxygen uptake. The baroreflex sensitivity was significantly lower after exercise at 70% peak oxygen uptake than during control session and showed no change in the other sessions. In conclusion, exercise intensity did not influence post-exercise blood pressure reduction and only high intensity exercise decreased baroreflex sensitivity