Os efeitos da hidratação sobre a pressão arterial (PA) e seus mecanismos hemodinâmicos e autonômicos pós-exercício foram pouco estudados e os resultados são controversos. Esse estudo avaliou esses efeitos, em normotensos jovens após uma sessão de exercício aeróbico. Assim, 16 rapazes submeteram-se a quatro sessões experimentais, realizadas em ordem aleatória: controle sem hidratação, exercício sem hidratação, controle com hidratação e exercício com hidratação. Nas sessões com hidratação, os sujeitos ingeriam 1l de água na noite anterior, 500ml 60min antes da intervenção (exercício ou repouso) e mais 1ml por 1g de massa corporal perdida logo após a intervenção. O exercício foi realizado por 45min em ciclo ergômetro em 50% do VO2pico. Em todas as sessões as PA sistólica (S), média (M) e diastólica (D), o débito cardíaco (DC), a frequência cardíaca (FC) e as variabilidades da FC e da PA foram medidos antes e após as intervenções. O exercício diminuiu a PAS e o volume sistólico (VS) e impediu os aumentos da FC, da PAD, da PAM e da sensibilidade baroreflexa, que ocorreram na sessão controle. A hidratação não modificou as respostas hemodinâmicas e autonômicas após o exercício. Em conclusão, em sujeitos jovens normotensos, a hidratação não modificou o efeito hipotensor promovido pelo exercício aeróbico no período de recuperação, não afetando seus mecanismos hemodinâmicos e autonômicos / The effects of hydration on post-exercise blood pressure (BP) and hemodynamic and autonomic mechanisms were poorly studied and results are controversial. This study evaluated these effects in young normotensives after an acute bout of aerobic exercise. Sixteen young men underwent four sessions in a random order: control without hydration, exercise without hydration, control with hydration and exercise with hydration. In the hydration sessions, subjects drank 1l of water in the night before, 500 ml 60 min before the intervention (rest or exercise) and 1ml for 1g of body mass lost immediately after the intervention. In exercise sessions, they exercised for 45 min on a cycle ergometer at 50% of VO2peak. Systolic (S), diastolic (D) and mean (M) BP, as well as cardiac output (CO), heart rate (HR), and HR and BP variabilities were measured before and after the interventions. Exercise produced a significant reduction in SBP and stroke volume (SV), and abolished the increase in HR, DBP, MBP and baroreflex sensitivity that occurred in the control sessions. Hydration did not change hemodynamic and autonomic responses after exercise. In conclusion, in healthy young subjects, hydration did not modify the hypotensive effect promoted by the aerobic exercise during the recovery period, not affecting its hemodynamic and autonomic mechanisms

This thesis presents four studies investigating the phenomenon of post exercise hypotension in the human condition of pre (borderline)-hypertension. Study one investigated the effects of an acute bout of 30-minutes upright cycling on post exercise haemodynamics and compared the results to a non-exercise control condition. 9 pre-hypertensive males, mean arterial pressure (MAP) = 106 ± 5 mmHg (50 ± 10 yr), not on medication, were studied for 6 hours following 30-minutes of cycle exercise at 70% maximal oxygen consumption and following 30-minutes of seated rest. Results demonstrate that moderate intensity exercise exerts a modest fall (~6 mmHg) in arterial pressure with the hypotension sustained for 6-hours post exercise. The fall in arterial pressure equates to a significantly reduced after load when compared to both pre-exercise baseline and non-exercise control data taken at the same time of day. The arterial pressure responses transcended into a sustained reduction (20%) in systemic vascular resistance and reciprocal increase in vascular conductance for up to 2-hours post-exercise. Venous atrial natriuretic peptide (ANP) demonstrated an elevation (44%) following exercise and a significant decline (33%) in the post-exercise period mirroring the haemodynamic response. This research reveals that acute exercise is capable of sustained reductions in arterial pressure and vascular resistance beyond the usual labile fluctuations and that the octapeptide ANP may exert a modulatory influence over the post-exercise response. Increases in 02 tension beyond the physiological range induces complex effects on the circulatory system with a dominant vasoconstriction following hyperoxia. The purpose of study 2 was to assess the effects of hypoxic (16% 02) and hyperoxic (50% 62) exercise on subsequent haemodynamic control when compared with normoxia. 9 pre-hypertensive males, MAP = 106 ± 5 mmHg (50 ±10 yr), not on medication, performed 30-minutes of cycle exercise at 70% normoxic maximal oxygen consumption in hypoxia (16% O 2 ), hyperoxia (50% O 2) and normoxia(21% O2 ). Hyperoxic exercise blunted post-exercise haemodynamics by significantly attenuating the reductions (from normoxic baseline) in SVR (-45%, PO.05 vs. normoxic & hypoxic exercise immediately post-exercise) that persisted throughout 120-minutes recovery in normoxia (-35% vs. normoxic & hypoxic exercise, during recovery) and elicited a mildly hypertensive effect, with regards to MAP, whereas normoxic and hypoxic exercise elicited a hypotension compared to baseline (P < 0.05). Circulating ANP was decreased in the hyperoxic trial when compared with normoxic and hypoxic exercise [24.3 (13.4) v. 31.5 (16.3) and 29.6 (13.9) pg/ml, respectively; P < 0.05, pooled for state]. Changes in MAP were related to changes in ANP concentration only following hyperoxic exercise (r = 0.50, P < 0.01). These findings indicate that acute modest hyperoxia reflexively induces measurable physiological derangement partly explained by decreased circulating concentrations of ANP. Study three determined the role of free-radical mediated oxidative stress and redox regulation of circulating NO metabolism as a primary modulator of vascular tone following exercise in pre-hypertensive humans. Utilising the same cohort and exercise protocol as in study 1 venous blood was sampled from an antecubital vein. Plasma NO metabolites nitrate (NO" 3 ) and nitrite (NO"2 ) were determined fluorometrically, whilst S-Nitrosothiol (RSNO) concentrations were assayed by the Saville reaction Indirect markers of oxidative stress were determined spectrophotometrically detecting lipid hydroperoxides (LOOH). Exercise led to a delayed increase in LOOH by 60- minutes post-exercise (0.69 ± 0.13 v. 0.86 ± 0.18 umol/1, respectively, P < 0.05), that remained elevated until termination of the trial 6-hours post-exercise. NO'a significantly fell below baseline by 120-minutes post-exercise (10.8 ± 3.3 v. 1.1 ±1.1 u.mol/1, respectively, P < 0.05), remaining attenuated for the remainder of the study.NO'i and RSNO were unmodified in the post-exercise period. In parallel to this finding the data also indicates a significant blunting in the hyperaemic response [SVR decreased from a 31% reduction immediately (within 1-minute) post-exercise to -13 and 8% at 60- and 120-minutes post-exercise, respectively, P < 0.05] and reversal of the hypotension (P < 0.05) over the same time frame as the augmented lipid peroxidation and attenuated circulating NO~3. These results indicate that augmented oxidative stress exerts a deleterious effect on post-exercise haemodynamics and implicates a potential redox regulation pathway of NO as being a mechanism by which free radical-induced oxidative stress blunts the degree of PEH in the recovery period. The final study investigated the potential role of a redox-mediated regulation of circulating NO bioavailability as a modulator of the augmented vasoconstriction following hyperoxic exercise. The same cohort and exercise protocol were employed as in study 2 and venous blood was assayed for NO"3 , NO'a, RSNO, LOOK, & lipid /water-soluble antioxidant concentrations. Similar adverse haemodynamic effects were noted following hyperoxic exercise as reported previously in study 2. RSNO showed a significant increase following hypoxic exercise only (P < Q.Q5, state x time, interaction), whereas NO~3, NO~2 and LOOH failed to differ between conditions (P > 0.05, main effect for state [02] and state x time, interaction effects). Ascorbic acid was mobilised in response to hyperoxic exercise when compared to normoxia (P < 0.05, main effect for state [O2] and state x time, interaction effects) being significantly elevated by 120-minutes post-exercise in hyperoxia compared to normoxia and hypoxia [75.1 (31) v. 39.5 (18.3) v. 46.7 (14.2) |amol/l, respectively, P < 0.05]. This data demonstrates an effective endogenous antioxidant response and argues against a redox regulation pathway of NO metabolism as a primary mediator of blunted vasodilatation in this scenario. This elucidates a more complex regulation of arterial tone, resulting from a metabolic pathway independent of NO in older subjects with pre-hypertension. This work demonstrates that (1) aerobic exercise exerts a hypotensive effect in humans with pre-hypertension, (2) ANP plays a part in the vasodilatation following exercise, (3) Free-radical mediated oxidative stress & subsequent modulation of NO metabolism exerts a deleterious influence on post-exercise haemodynamics (4) Acute hyperoxic exercise induces a sustained vasoconstriction that is mediated via circulating ANP concentration but not by redox regulation of NO metabolism.

abstract: INTRODUCTION: Exercise performed at moderate to vigorous intensities has been shown to generate a post exercise hypotensive response. Whether this response is observed with very low exercise intensities is unclear. PURPOSE: To compare post physical activity ambulatory blood pressure (ABP) response to a single worksite walking day and a normal sedentary work day in pre-hypertensive adults. METHODS: Participants were 7 pre-hypertensive (127 + 8 mmHg / 83 + 8 mmHg) adults (3 male, 4 female, age = 42 + 12 yr) who participated in a randomized, cross-over study that included a control and a walking treatment. Only those who indicated regularly sitting at least 8 hours/day and no structured physical activity were enrolled. Treatment days were randomly assigned and were performed one week apart. Walking treatment consisted of periodically increasing walk time up to 2.5 hours over the course of an 8 hour work day on a walking workstation (Steelcase Company, Grand Rapids, MI). Walk speed was set at 1 mph. Participants wore an ambulatory blood pressure cuff (Oscar 2, SunTech Medical, Morrisville, NC) for 24-hours on both treatment days. Participants maintained normal daily activities on the control day. ABP data collected from 9:00 am until 10:00 pm of the same day were included in statistical analyses. Linear mixed models were used to detect differences in systolic (SBP) and diastolic blood pressure (DBP) by treatment condition over the whole day and post workday for the time periods between 4 -10 pm when participants were no longer at work. RESULTS:BP was significantly lower in response to the walking treatment compared to the control day (Mean SBP 126 +7 mmHg vs.124 +7 mmHg, p=.043; DBP 80 + 3 mmHg vs. 77 + 3 mmHg, p = 0.001 respectively). Post workday (4:00 to 10:00 pm) SBP decreased 3 mmHg (p=.017) and DBP decreased 4 mmHg (p<.001) following walking. CONCLUSION: Even low intensity exercise such as walking on a walking workstation is effective for significantly reducing acute BP when compared to a normal work day. / Dissertation/Thesis / M.S. Exercise and Wellness 2013

Os efeitos da hidratação sobre a pressão arterial (PA) e seus mecanismos hemodinâmicos e autonômicos pós-exercício foram pouco estudados e os resultados são controversos. Esse estudo avaliou esses efeitos, em normotensos jovens após uma sessão de exercício aeróbico. Assim, 16 rapazes submeteram-se a quatro sessões experimentais, realizadas em ordem aleatória: controle sem hidratação, exercício sem hidratação, controle com hidratação e exercício com hidratação. Nas sessões com hidratação, os sujeitos ingeriam 1l de água na noite anterior, 500ml 60min antes da intervenção (exercício ou repouso) e mais 1ml por 1g de massa corporal perdida logo após a intervenção. O exercício foi realizado por 45min em ciclo ergômetro em 50% do VO2pico. Em todas as sessões as PA sistólica (S), média (M) e diastólica (D), o débito cardíaco (DC), a frequência cardíaca (FC) e as variabilidades da FC e da PA foram medidos antes e após as intervenções. O exercício diminuiu a PAS e o volume sistólico (VS) e impediu os aumentos da FC, da PAD, da PAM e da sensibilidade baroreflexa, que ocorreram na sessão controle. A hidratação não modificou as respostas hemodinâmicas e autonômicas após o exercício. Em conclusão, em sujeitos jovens normotensos, a hidratação não modificou o efeito hipotensor promovido pelo exercício aeróbico no período de recuperação, não afetando seus mecanismos hemodinâmicos e autonômicos / The effects of hydration on post-exercise blood pressure (BP) and hemodynamic and autonomic mechanisms were poorly studied and results are controversial. This study evaluated these effects in young normotensives after an acute bout of aerobic exercise. Sixteen young men underwent four sessions in a random order: control without hydration, exercise without hydration, control with hydration and exercise with hydration. In the hydration sessions, subjects drank 1l of water in the night before, 500 ml 60 min before the intervention (rest or exercise) and 1ml for 1g of body mass lost immediately after the intervention. In exercise sessions, they exercised for 45 min on a cycle ergometer at 50% of VO2peak. Systolic (S), diastolic (D) and mean (M) BP, as well as cardiac output (CO), heart rate (HR), and HR and BP variabilities were measured before and after the interventions. Exercise produced a significant reduction in SBP and stroke volume (SV), and abolished the increase in HR, DBP, MBP and baroreflex sensitivity that occurred in the control sessions. Hydration did not change hemodynamic and autonomic responses after exercise. In conclusion, in healthy young subjects, hydration did not modify the hypotensive effect promoted by the aerobic exercise during the recovery period, not affecting its hemodynamic and autonomic mechanisms

Accelerometers are objective monitors of physical activity (PA) that can be used to estimate energy expenditure (EE). Most accelerometer EE estimation equations are based on steady-state data and do not consider excess post-exercise oxygen consumption (EPOC) after exercise. PURPOSE: To quantify the error in accelerometer EE estimates due to EPOC after varying durations of high-intensity treadmill running. METHODS: Nine young, healthy, recreationally active males participated in three study visits. Visit 1 included a treadmill VO2 peak test to determine the treadmill speed correlating to 80% VO2 peak for visits 2 and 3. Visit 2 included a seated 20-min baseline and three short (30s, 60s, 120s) vigorous treadmill running bouts each followed by 20 minutes of seated rest. Visit 3 included a supine 60-min baseline and a 30-min treadmill running bout followed by 3 hours of supine rest. Twelve EE estimation equations each using either a non-dominant wrist or right hip ActiGraph GT3X+ accelerometer were compared to the true EE measured by the Parvomedics TrueOne 2400 indirect calorimeter. RESULTS: The Freedson 1998 EE estimation equation overestimated EE during the 20min post-exercise period after each exercise bout (mean kCals [95% CIs]; 30s: 19.3 [11.4, 27.2], 60s: 16.6 [8.5, 24.7], 120s: 13.4 [5.74, 21.1], 30min: 15.1 [6.69, 23.5]). The Crouter 2009 branching algorithm underestimated EE during the 20min post-exercise period after each exercise bout (mean kCals [95% CIs]; 30s: -8.59 [-10.6, -6.62], 60s: -11.6 [-13.7, -9.38], 120s: -15.0 [-18.1, -11.8], 30min: -11.0 [-14.3, -7.77]), but was partially corrected by adding in the measured EPOC. CONCLUSION: Estimated EE during lying or seated rest from linear accelerometer equations was heavily dependent on the y-intercept of the equation, which represents the estimated resting EE of the wearer, with the Crouter calibration study being the only one to directly measure resting EE. More sophisticated approaches, like the Crouter 2009 and newer machine learning algorithms, have better potential to more accurately estimate EE across various activity types. New accelerometer EE estimations should include resting in their calibration protocols in order to more accurately estimate EE during rest.

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No description available.

Estudo de abordagem quantitativa e delineamento quase-experimental com o objetivo de comparar os efeitos dos exercícios dinâmicos contínuo e intervalado sobre a magnitude e duração da resposta hipotensora em hipertensos. A amostra foi composta por 20 idosos hipertensos de um município do interior paulista. As variáveis estudadas foram agrupadas nas categorias: sociodemográficas, antropométricas e hemodinâmicas. Cada participante foi submetido duas sessões de exercício físico, com intervalo de uma semana entre os treinos. As sessões de exercício contínuo foram realizadas a intensidade do limiar anaeróbio. Nas sessões de exercício intervalado, os indivíduos trabalharam no limiar de compensação respiratória por 4 minutos durante a fase ativa; na fase de recuperação, trabalharam a 40% do consumo máximo de oxigênio por 2 minutos. O tempo total de cada sessão foi de 42 minutos. Para obtenção dos dados hemodinâmicos, os participantes realizaram três exames de Monitorização Ambulatorial da Pressão Arterial (MAPA), com duração de 24 horas: MAPA controle, MAPA após exercício contínuo e MAPA após exercício intervalado. As análises descritivas, com cálculo de frequências absolutas e porcentagens e descrição das médias, desvio padrão e medianas, foram realizadas por meio do pacote estatístico SPSS, versão 15.0. A descrição das diferenças proporcionais entre os grupos foi realizada primordialmente por meio de aplicação do teste estatístico não paramétrico de Wilcoxon. Em todas as análises, foi adotado o nível de significância estatística de 5% (p&lt;0,05).Quando comparamos os resultados da MAPA realizada após o exercício contínuo aos valores derivados da MAPA controle, encontramos diferença estatisticamente significante para as variáveis Pressão Arterial Sistólica (PAS) vigília (p&lt;0,001), PAS sono (p&lt;0,001), Pressão Arterial Diastólica (PAD) vigília (p&lt;0,001), PAD sono (p&lt;0,001), Pressão Arterial Média (PAM) vigília (p&lt;0,001), PAD sono (p&lt;0,001), Frequência cardíaca (FC) sono (p&lt;0,03) e Duplo Produto (DP) vigília (p&lt;0,002) e sono (p&lt;0,001), sendo que todos os índices mostraram redução após a prática do exercício contínuo. À comparação dos resultados da MAPA após exercício intervalado aos resultados da MAPA controle, constatamos que, após a prática de exercício, houve redução nos valores de PAS vigília (p&lt;0,001), PAS sono (p&lt;0,001), PAD vigília (p&lt;0,001), PAD sono (p&lt;0,001), PAM vigília (p&lt;0,001), PAM sono (p&lt;0,001) e DP vigília (p&lt;0,001) e DP sono (p&lt;0,001). Na comparação do exercício contínuo ao intervalado, encontramos diferença estatisticamente significante para as variáveis PAS vigília (p&lt;0,001) e sono (p&lt;0,01), PAD vigília (p&lt;0,001), PAM vigília (p&lt;0,001), PAM sono (p&lt;0,01), DP vigília (p&lt;0,01) e DP sono (p&lt;0,001), que se mostraram mais reduzidas após a prática do exercício intervalado. Concluímos que a prática de exercício físico contínuo e intervalado promove a hipotensão pós-exercício (HPE) ao longo das 20 horas subsequentes à atividade. O exercício intervalado gera maior magnitude de HPE e menor sobrecarga cardiovascular em comparação ao exercício contínuo. / Quantitative study with a quasi-experimental design to compare the effect of continuous and interval dynamic exercises on the magnitude and length of the hypotensive response in hypertensive patients. The sample consisted of 20 hypertensive elderly patients from a city in the interior of the State of São Paulo, Brazil. The study variables were grouped in the following categories: sociodemographic, anthropometric and hemodynamic. Each participant was submitted to two physical exercise sessions with a one-week interval between the training. The continuous exercise sessions were held at the intensity level of the anaerobic threshold. In the interval exercise sessions, the participants exercised at the respiratory compensation threshold for four minutes during the active phase; in the recovery phase, they worked at 40% of the maximum oxygen consumption for two minutes. The total length of each session was 42 minutes. To obtain the hemodynamic data, the participants undertook three outpatient Ambulatory Blood Pressure Monitoring (ABPM) tests, which took 24 hours: control ABPM, ABPM after continuous exercise and ABPM after interval exercise. For the descriptive analyses, including the calculation of absolute frequencies and percentages and the description of means, standard deviations and medians, the statistical software SPSS version 15.0 was used. The description of the proportional differences between the groups was mainly based on the application of Wilcoxon\'s non-parametric statistical test. In all analyses, statistical significance was set at 5% (p&lt;0,05).When comparing the ABPM results after continuous exercise with the results of the control ABPM, a statistically significant difference was found for the variables Systolic Blood Pressure (SBP) wake (p&lt;0.001), SBP sleep (p&lt;0.001), Diastolic Blood Pressure (DBP) wake (p&lt;0.001), DBP sleep (p&lt;0.001), Mean Blood Pressure (MBP) wake (p&lt;0.001), MBP sleep (p&lt;0.001), Heart frequency (HF) sleep (p&lt;0.03) and Double Product (DP) wake (p&lt;0.002) and sleep (p&lt;0.001). All indices showed a drop after continuous exercise. In the comparison between the ABPM results after interval exercise with the control ABPM results, after the exercise, the following levels dropped: SBP wake (p&lt;0.001), SBP sleep¬ (p&lt;0.001), DBP wake (p&lt;0.001), DBP sleep (p&lt;0.001), MBP wake (p&lt;0.001), MBP sleep (p&lt;0.001) and DP wake (p&lt;0.001) and DP sleep (p&lt;0.001). In the comparison between the continuous and interval exercises, a statistically significant difference was found for the variables SBP wake (p&lt;0.001) and sleep (p&lt;0.01), DBP wake (p&lt;0.001), MBP wake (p&lt;0.001), MBP sleep (p&lt;0.01), DP wake (p&lt;0.01) and DP sleep (p&lt;0.001), which were lower after the interval exercise sessions. In conclusion, the practice of continuous and interval physical exercise promotes post-exercise hypotension (PEH) during the 20 hours after the exercise. Interval exercises lead to a larger HPE and less cardiovascular burden in comparison with continuous exercise.

Este estudo teve como objetivo comparar o efeito agudo de três métodos de recuperação pós-exercício (recuperação ativa, passiva e crioterapia) sobre o desempenho físico, marcadores fisiológicos, psicológicos, bioquímicos e imunológicos, bem como os sentidos atribuídos por sujeitos treinados. Doze corredores treinados em provas de meio-fundo e fundo, voluntários, do gênero masculino (idade: 20,6 ± 1,7 anos; Massa corporal: 64,1 ± 5,6 Kg; Estatura: 1,74 ± 0,05 m.; Gordura corporal: 6,8 ± 2,7 %; VO2máx: 57,0 ± 5,9 mL.Kg-1.min-1; vVO2máx: 15,7 ± 1,7 Km/h; Tlim: 603 ± 243 s.) realizaram três corridas de 30 minutos, em esteira rolante, a 80% da vVO2max, estimado através de teste incremental. Em seguida foram aplicados os métodos de recuperação ativa (corrida a 40% da vVO2max), passiva (sentado em uma cadeira) e crioterapia (imersão em água com gelo quebrado a 5° [±1º] até a altura da crista ilíaca) por 20 minutos, em ordem contrabalanceada. Logo após, os sujeitos realizaram um teste de corrida (Tlim) a 100% da vVO2max. Uma semana antes da realização dos testes, foi realizado um procedimento de familiarização com os métodos de recuperação a serem aplicados. As taxas dos marcadores tempo limite de corrida, distúrbio de humor total, razão fadiga/vigor, percepção subjetiva de esforço, frequência cardíaca, lactato, IL-6, TNF-, leucócitos, neutrófilos, monócitos e linfócitos foram mensuradas no momento anterior a corrida (M1), após a corrida na esteira rolante (M2), imediatamente após a aplicação dos métodos recuperativos (M3) e após a aplicação do teste de corrida tempo limite (M4), exceto a PSE que foi mensurado no M1 e M4, e o Tlim e a entrevista (para análise de representações sociais) que foram realizadas no M4. Foram retirados 18ml de sangue venoso, em cada momento de coleta, para realização dos procedimentos de análise sanguínea. Após os resultados concluímos que o uso dos métodos de recuperação ativa, passiva ou crioterapia durante 20 minutos após uma corrida de 30 minutos a 80%vVO2máx não afetou o desempenho subsequente de corrida a 100%vVO2máx até a exaustão. A crioterapia promove maior queda na frequência cardíaca e menor remoção de lactato após exercício a 80%vVO2máx comparada aos métodos de recuperação ativa e passiva, promovendo maior produção de lactato e menor resposta cronotrópica durante corrida subsequente a 100%vVO2máx até a exaustão e que o uso da crioterapia não interfere na percepção de esforço e nas respostas psicológicas após o esforço, mas induz uma maior perturbação sobre os marcadores imunológicos, especificamente, sobre leucócitos e linfócitos. Na perspectiva qualitativa, verificou-se uma variedade discursiva sobre a escolha do melhor método de recuperação. Os sentidos que mais se destacaram foram: uma maior leveza do corpo, acalmando a musculatura e fica mais... assim, relaxado na crioterapia; ação natural do corpo e quando se está cansado paramos para descansar na recuperação passiva e; continuidade de movimentos, operabilidade, manutenção do ritmo e da normalidade na recuperação ativa / This study aimed at comparing the acute effect of three post-exercise recovering methods (active, passive and cryotherapy recovering) on the physical performance, physiological, psychological, biochemical, immunological, performance and sense markers attributed by trained subjects. Twelve male volunteer runners (aged 20.6 + 1.7 years old; Body mass: 64.1 + 5.6 kg; Height: 1.74 + 0.05 m; Body fat 6.8 + 2.7%; VO2máx: 57,0 ± 5,9 mL.Kg-1.min-1; vVO2máx: 15,7 ± 1,7 Km/h; Tlim: 603 ± 243 s.) trained in middle-distance and distance races have accomplished three 30-minute runnings on a treadmill at 80% of the vVO2, estimated through an incremental test. After that, the active (running at 40 % of the vVO2max), passive (sitting on a chair) and cryotherapy (immersion in water with broken ice at 5° [+ 1°] until the height of the iliac crest) recovering methods were applied for 20 minutes in counterbalanced order. Then, the subjects carried out a running test (Tlim) at 100% of the vVO2max. One week before the accomplishment of the tests, a procedure in order to familiarize them with the recovering methods to be applied was carried out. The running limit time markers, total humor disturb, fatigue/vigor ratio, subjective perception of effort, heart rate, lactate, IL-6, tnf-, leucocytes, neutrophils and lymphocytes rates were measured at the moment before the running (M1), after running on the treadmill (M2), immediately after applying the recovering methods (M3) and after doing the limit time running test (M4), except the PSE, which was measured in M1 and M4, and the Tlim and the interview (to analyze the social representations), which were carried out in M4. 18 ml of venous blood were taken, in each moment of the blood collecting so as to carry out the blood analysis procedures. After the results, we reached the conclusion that the use of active, passive and cryotherapy recovering methods within 20 minutes after a 30-minute running at 80%vVO2máx hasnt affect the performance of a following running at 100%vVO2máx until exhaustion. The cryotherapy promotes a higher fall in the heart rate and a smaller lactate removal after the exercise at 80%vVO2máx, compared to the active and passive recovering methods, thus promoting higher production of lactate and a smaller chronotropic response during the follow-up running at 100%vVO2máx until exhaustion; and that the use of cryotherapy does not interfere in the effort perception or in the psychological responses after effort, but it leads to a higher disorder on the immunologic markers, specifically on the leucocytes and lymphocytes. Within the qualitative perspective, it was verified a discursive variety about the choice of the best recovering method. The senses which were highlighted most were, a larger lightness of the body, calming the muscles down and it gets sort of, relaxed in cryotherapy; natural action of the body and when youre tired we stop to rest in the passive recovering; and, continuity of movement, operability, keeping the rhythm and the normality in the active recovering

Uma sessão de exercícios resistidos promove hipotensão pós-exercício em hipertensos (HT). Devido às alterações cardiovasculares impostas pela doença, é possível que os HT apresentem mecanismos hipotensores diferentes dos observados em normotensos (NT). Além disso, os HT utilizam medicamentos anti-hipertensivos que podem afetar as respostas fisiológicas pós-exercício. O objetivo desta tese foi avaliar, em homens HT, o efeito de uma sessão de exercício resistido sobre a pressão arterial (PA) e seus os mecanismos hemodinâmicos e autonômicos, comparando este efeito com o observado em NT e verificando o efeito do uso do captopril sobre estas respostas. Participaram do estudo, 12 HT (50±3anos) e 14 NT (44±3anos). Os hipertensos foram estudados em duas situações: após 4 semanas de placebo ou captopril (3 x 50mg/dia) administrados em formato crossover e de forma duplo-cega. Os NT foram estudados apenas 1 vez sem nenhum medicamento. Em cada grupo/situação experimental os voluntários realizaram 2 sessões experimentais conduzidas em ordem aleatória: Controle (repouso) e Exercício (6 exercícios, 3 séries até a fadiga moderada, 50% de 1RM). As variáveis foram medidas antes e em 2 momentos pós-intervenções: Pós1 (entre 30-80min) e Pós2 (após 7h). Além disso, a PA foi medida por 24h em condições ambulatoriais. No Pós1, a PA sistólica diminuiu de forma similar nos grupos/situações (NT=-8±2; HT não medicado=-13±2; HT medicado=-12±2mmHg). A PA diastólica também diminuiu, mas a queda foi maior nos HT não medicados em comparação com os NT (-9±1 vs. -4±1mmHg, respectivamente) e foi igual nos hipertensos com e sem medicamento. Em cada grupo/situação, a hipotensão pós-exercício se acompanhou de redução do débito cardíaco (DC) em parte dos voluntários e da resistência vascular periférica (RVP) na outra parte. O volume sistólico (VS) diminuiu (NT=-14±5; HT não medicado=-11±5; HT medicado=-17±5ml) e a FC aumentou (NT=+13±3; HT não medicados=+13±2; HT medicados=+13±2bpm) pós-exercício de forma similar nos grupos/situações. Também de forma similar, o balanço simpatovagal cardíaco aumentou (NT=+1,9±0,4; HT não medicados=+1,4±0,3; HT medicados=+1,8±0,3) e a sensibilidade barorreflexa diminuiu (NT=-5±1; HT não medicados=-4±2; HT medicados=+3±1mmHg/bpm) pós-exercício. No Pós2, não houve efeito do exercício sobre nenhuma variável. A PA ambulatorial foi semelhante em todos os grupos/situações. Em conclusão, uma sessão de exercício resistido promove efeito hipotensor no ambiente laboratorial em NT e HT medicados ou não, mas este efeito não se mantém em condições ambulatoriais. Nos HT, a magnitude de queda da PA diastólica é maior que nos NT. Os mecanismos hemodinâmicos e autonômicos da hipotensão pós-exercício são semelhantes em NT e HT medicados ou não. O determinante hemodinâmico (DC ou RVP) da hipotensão pós-exercício varia de um indivíduo para outro, mas a redução da PA se acompanha de redução do VS e aumento da FC, sendo este último resultante do aumento do balanço simpatovagal cardíaco e da redução da SB / A session of resistance exercise promotes post-exercise hypotension in hypertensive subjects (HT). Due to the cardiovascular alterations imposed by the disease, it is possible that HT present hypotensive mechanisms different from those observed in normotensive subjects (NT). Moreover, HT frequently receive antihypertensive medications that might affect post-exercise responses. The aim of this thesis was to evaluate, in HT men, the effects of resistance exercise session on blood pressure (BP) and its hemodynamic and neural mechanisms, comparing these effects with the responses observed in NT and verifying the effect of captopril use on these responses. Twelve HT (50±3 years) and 14 NT (44±3 years) participated in the study. HT were studied in two situations, after 4 weeks of placebo and captopril (3 x 50mg/day) administered in a crossover double-blind design. NT was studied only once without any medication. At each group/situation, subjects underwent 2 experimental sessions performed in a random order: Control (rest) and Exercise (6 resistance exercises, 3 sets until moderated fatigue, 50% of 1RM). Measurements were taken before and in 2 post-intervention moments (Post1 - between 30-80min and Post2 - after 7pm). Moreover, ambulatory BP was measured after the sessions. In Post1, systolic BP decreased similarly in all groups/situations (NT=-8±2; unmedicated HT=-13±2; medicated HT=-12±2mmHg). Diastolic BP also decreased, but this decrease was greater in unmedicated HT compared with NT (-9±1 vs. -4±1mmHg, respectively), and were similar in HT with and without medication. Regardless of group/situation, exercise promoted a decrease in cardiac output (CO) in some subjects and a reduction in systemic vascular resistance (SVR) in others. Stroke volume (SV) decreased (NT=-14±5; unmedicated HT=-11±5; medicated HT=-17±5ml) and HR increased (NT=13±3; unmedicated HT=13±2; medicated HT=13±2bpm) after exercise similarly in all groups/situations. Also similarly between groups/situations, cardiac sympathovagal balance increased (NT=+1,9±0,4, unmedicated HT=+1.4±0.3, medicated HT=+1,8±0,3) and BS decreased (NT=-5±1; unmedicated HT=-4±2; medicated HT=+3±1mmHg/bpm) post-exercise. In Post2, in all groups/situations, exercise did not affect any variable. In addition, ambulatory BP was similar after the control and exercise sessions in all group/situation. In conclusion, a single bout of resistance exercise session promotes post-exercise hypotension in the laboratory in NT and HT subjects receiving or not captopril, but this hypotensive effect is not maintained under ambulatory conditions. The magnitude of BP decrease is greater in non-medicated HT than in NT, and it was not changed by captopril. Autonomic and hemodynamic mechanisms of post-exercise hypotension are similar in NT and HT receiving medication or not. The hemodynamic determinant (CO or SVR) of post-exercise hypotension varies from one subject to another. However, BP reduction is accompanied by decrease in SV and an increase in HR that results from an increase in cardiac sympathovagal balance and decrease in BS