<p>There is a prevalent belief that acute hormone responses to resistance exercise mediate adaptations in skeletal muscle hypertrophy; however, there is little supporting evidence. We conducted studies to examine the relationship between acute hormonal increases after resistance exercises and subsequent changes in muscle anabolism.</p> <p>We tested the hypothesis that exercise-induced responses of anabolic hormones—growth hormone (GH) and testosterone—would enhance rates of myofibrillar protein synthesis (MPS) after an acute bout of resistance exercise, and would augment muscle hypertrophy after training. We concluded, however, that resistance exercise-induced increases in putative anabolic hormones do not enhance MPS or hypertrophy.</p> <p>We also examined whether rates of MPS would be attenuated in women (compared with men) after resistance exercise, due to their lack of post-exercise testosteronemia. We reported similar increases in MPS in men and women; post-exercise testosterone responses in women, which were 45-fold lower than men, did not attenuate elevations in MPS.</p> <p>Collectively, our work leads to the conclusion that the acute rise in hormones such as testosterone and GH has very little bearing on MPS and hypertrophy responses to resistance exercise. Instead, the rise in these hormones appears to be a non-specific response to exercise stress rather than a response that is important for muscle anabolism. Contrary to widely used principles, our data suggests that exercise programs should not be designed based on nuances in the post-exercise hormonal milieu. Alternatively, understanding local mechanotransduction, which is directly linked to muscle fibre loading, will reveal the processes that drive human exercise-mediated muscle hypertrophy.</p> / Doctor of Philosophy (PhD)

<p>Introduction: Mitochondrial dysfunction and oxidative stress increase with aging and may contribute to age-associated muscle atrophy (sarcopenia). Resistance exercise (RE) can promote the accretion of muscle mass, increase strength, and ultimately improve function in the elderly. Such beneficial effects are thought to be mitigated solely by increased muscle mass and strength; however, the contribution of the mitochondria to the beneficial effects of RE in aging have not been thoroughly characterized. While mitochondrial benefits have been established separately in both young and aged adults following chronic RE, the acute effects have not been well characterized. Methods: Sedentary young and aged adult males completed either an acute bout of fatiguing RE or endurance exercise (EE), and muscle biopsies were obtained at 3, 24 and 48 h post- exercise depending on the study. Results: Despite equivalent lean-body mass, increased age was associated with elevated mtDNA deletions, indicating potential for mitochondrial dysfunction. RE was associated with reduced mitochondrial content (transcripts, protein, and mtDNA copy number) at 48 h post-exercise, a response that did not differ with increasing age. Paradoxically, reduced mitochondrial content occurred alongside elevated total peroxisome proliferator-activated receptor γ coactivator one α (PGC-1α) mRNA; however, RE altered only the PGC-1α4 isoform post-exercise, a transcript that regulates myostatin and insulin-like growth factor one (IGF1) signalling and ultimately muscle hypertrophy and not mitochondrial adaptations. In addition, PGC-1α modulates the unfolded protein response (UPR), and RE was subsequently shown to elevate endoplasmic reticulum stress and elicit the UPR. Conclusion: PGC-1α mRNA increases regardless of exercise mode; however, differential expression or regulation of alternate PGC-1α isoforms or transcriptional binding partners co-activated by PGC-1α may dictate the specific phenotypic adaptations that occur following divergent modes of exercise. Furthermore, RE acutely decreases mitochondrial content despite elevated PGC-1α mRNA, and this response is not influenced by age.</p> / Doctor of Philosophy (Medical Science)

<p>A comprehensive understanding of the mechanisms regulating vascular structure and function may assist in designing effective strategies to decrease cardiovascular disease risk. The current studies were designed to investigate a) relationships between collagen markers and arterial stiffness and markers of vasoconstriction and inflammation and endothelial function in humans with a wide range of vascular health, including overweight women, elderly healthy men, individuals with coronary artery disease, individuals with spinal cord injury and young healthy men and b) changes in arterial structure and function and circulating serum markers of type I collagen synthesis and degradation, vasoconstriction and inflammation in overweight pre-menopausal women before and after a 16- week diet and exercise intervention. Resting brachial artery flow mediated dilation (FMD), upper limb and/or central pulse wave velocity (PWV_c-r and PWV_c-f) and carotid artery distensibility were assessed at baseline in all groups and, in the overweight population, after the 16-week intervention. Pro-collagen type I C-peptide (PIP), C-telopeptide of type I collagen (CTX), markers of collagen synthesis and degradation respectively, endothelin-1 (ET-1) a vasoconstrictor and interleukin-6 (IL-6) an inflammatory marker were measured. In the spectrum of vascular health, a negative relationship exists between collagen markers and central PWV (CTX–PWV_c-f: r = -0.41, p = 0.001 and PIP – PWV_c-f: r = -0.32, p = 0.01) and a positive relationship between markers and carotid distensibility (CTX: r = 0.59, pc-r increased over time in the overweight population (FMD pre: 4.1 ± 0.5 % vs. post: 6.9 ± 0.7 %, pc-r pre: 8.1 ± 0.3 m/s vs. post: 8.9 ± 0.3 m/s, p</p> / Doctor of Philosophy (PhD)

<p>Amino acids are key nutritional stimuli that are both substrate for muscle protein synthesis (MPS), and signaling molecules that regulate the translational machinery. There is a dose-dependent relationship between protein intake and MPS that differs between young and elderly subjects. The current thesis contains results from three separate studies that were conducted to examine to potential to enhance smaller doses of protein, known to be suboptimal in their capacity to stimulate MPS, through supplementation with specific amino acids, namely leucine and citrulline.</p> <p>The first two studies examined the potential to enhance the muscle protein synthetic capacity of a smaller, suboptimal dose of whey protein with leucine. In study one, we concluded that leucine supplementation of a suboptimal dose of protein could render it as effective at enhancing rates of MPS as ~four times as much protein (25 g) under resting conditions, but not following resistance exercise. In study two, we examined the potential of leucine and branched-chain amino acids to enhance the MPS response of a suboptimal dose of protein within the context of mixed macronutrient ingestion. We concluded that supplementation with a relatively high dose of leucine could render it as effective at enhancing MPS rates as ~four times as much protein (25 g) under both resting and post-exercise conditions.</p> <p>In study three, we examined the potential of citrulline supplementation to enhance blood flow, microvascular circulation, and MPS in response to a suboptimal dose of whey protein in elderly subjects. We concluded that supplementation of a suboptimal dose of protein with citrulline did not augment bulk blood flow or muscle microvascular circulation. The major findings from the works presented in this thesis is that smaller doses of protein that normally elicit a suboptimal increase in MPS can be made more anabolic when supplemented with specific amino acids.</p> / Doctor of Philosophy (PhD)

<p>What a ride it has been. The ups and downs of the McMaster graduate program has been a sweet one. It has been a pleasure working with the Exercise Metabolism Research Group for the past 2 years, and I will miss being around the work that goes on in the trenches around the lab. I have leaned on many people for all types of guidance through this journey, and would like to thank everyone for their unprecedented support. I have grown as a person and student and will use everything I have learned at this fine establishment I’m sure at one point or another along the great path of life. I must thank my amazing parents, family, friends and of coarse Ashley for putting up with my work ethic throughout my studies; the long days that I would go missing. Without their support none of this would have been possible. I have to specially mention Melanie Wolfe for recommending myself, and ultimately Stu Phillips for presenting this opportunity that is coming to a close. I have had great senior support from Cam Mitchell, Tyler Churchward-Venne, Todd Prior and Michaela Devries in putting this document together, and would not be submitting this without their selfless assistance. It’s been a journey getting to this point, but I wouldn’t change it for the world, to the next chapter in life, cheers and God Bless.</p> / <p>Higher dietary protein intake, greater than the Recommended Dietary Allowance (RDA; 0.8 g protein/kg/d), coupled with resistive exercise has been shown to aid in preservation of muscle mass during hypocaloric diet-induced weight loss. We examined the impact of dietary protein supplementation at two levels (1.2 and 2.4 g/kg/d) on body composition during a 4wk hypocaloric dietary intervention that included 6d/wk of high intensity resistance exercise and interval training. In a single blind study, forty young men consumed 33±1.1 kcal/LBM (~40% reduction versus estimated energy requirements), and were randomly assigned to a group that consumed either 1.2g/kg/d protein or 2.4g/kg/d. Body composition was determined using DXA, Bod Pod, and Bio-impedance pre- and post-intervention to derive a 4-compartment model for body composition. Both groups retained lean mass (LM), but retention was greater in the higher protein group (p</p> / Master of Science (MSc)

<p> Protein digestibility, a function of the source of amino acids consumed, can differentially affect postprandial protein anabolism at rest. We investigated the effect of ingesting whey and casein proteins, in isolation and in combination, after an acute bout of unilateral resistance exercise on muscle protein synthesis in eight healthy resistance trained men (24.4 ± 4.8 yr; 177.4 ± 4.2 cm; 85.5 ± 14.8 kg; means± SD). On three occasions, participants performed a unilateral bout of resistance exercise following which they consumed a drink containing whey, whey and casein (1:1), or casein protein. Each drink provided 10 g of essential amino acids. Mixed muscle protein fractional synthetic rate (FSR) was determined by pulse-tracer injections of L-[ring-2H5]phenylalanine and L-[15N]phenylalanine 120-180 min after protein ingestion. The pattern of amino acid appearance in the blood after consuming the protein drinks was not different. Consequently, while consumption of the protein drinks stimulated a larger increase in FSR in the exercised leg compared to the rested leg (p < 0.05), there were no differences between the drinks. Thus, while the source of amino acids may affect protein turnover at rest, this effect is not apparent after resistance exercise. Therefore, we conclude that the ingestion of whey and casein proteins, in isolation or combination, stimulates mixed muscle protein synthesis to similar degrees after an acute bout of resistance exercise.</p> / Thesis / Master of Science (MSc)

<p> We aimed to determine the effectiveness of a low volume of high-intensity resistance exercise, alone (EX) or in combination with a whey protein supplement (WHY +EX), on prevention of muscle mass and strength loss following 14 days of knee immobilization in humans. Seventeen recreationally active (i.e., exercise ≤ 2-3 d·wk^-1) participants (23.9±5.0 yr; BMI = 25.4±3.6 kg·m^-2) were divided into three groups: exercise (EX; n=6), whey protein supplementation with exercise (WHY+EX; n=6), and control (CON; n=5). All subjects wore a knee-immobilization brace such that one leg was completely non-weight bearing for 14d. The resistance exercise (RE) were performed unilaterally and consisted of one set of ten repetitions of leg press (with plantar flexion at full extension), knee extension, and seated calf raises every other day during the 14d immobilization period, at 80% of one repetition maximum. Subjects in the WHY+EX group consumed two 30g boluses of whey protein daily while EX and CON consumed isocaloric carbohydrate beverages. Immobilization induced a significant reduction (p<0.05) in thigh cross-sectional area (CSA), isometric knee extensor strength, and isometric plantar flexion strength in CON but not in EX and WHY+EX. There were significant losses in lower leg CSA for all three groups, with a tendency for losses to be mitigated in both the EX and WHY+EX groups versus CON (p=0.065). The two constituent muscles of the triceps surae muscle group showed a differential response to the RE training with the gastrocnemius showing reductions in CSA almost uniformly across the three groups whereas soleus CSA was significantly reduced in the CON (p<0.05) but not in the EX and WHY+EX groups. We conclude that a relatively low volume of high-intensity resistance exercise is an effective countermeasure against atrophy of the thigh and the soleus muscle, as well as against knee extension and plantar flexion strength loss during 14d of leg immobilization. As a countermeasure to immobilization, there is no additional benefit of consumption of a daily whey protein supplement in combination with resistance exercise in maintaining muscle mass or strength.</p> / Thesis / Master of Science (MSc)

A máxima fase estável do lactato (MFEL) é considerada uma intensidade critica em exercício dinâmico e sua intensidade é específica do grupo etário. No entanto, apesar da relação existente entre a intensidade de esforço e os ajustes cardiovasculares, metabólicos e ventilatórios durante o exercício resistido, a MFEL foi muito pouco estudada neste tipo de exercício. O objetivo do estudo foi verificar e comparar a existência de MFEL nos exercícios leg press (LP) e supino reto (SR) em dois grupos: jovens e idosos. Além disso, analisar o comportamento das variáveis ergoespirométricas (VE, VO2 e VCO2), lactacidemia, freqüência cardíaca (FC), pressão arterial (PA) e percepção subjetiva de esforço (PSE) na intensidade da MFEL. Foram avaliados 13 homens jovens (26,1 +/- 2,9 anos) e 11 idosos (68,9 +/- 4,0 anos) saudáveis e com experiência mínima de 6 meses em treinamento resistido, que passaram por teste de 1 repetição máxima (1RM), teste crescente para determinação do limiar anaeróbio (LAn) e mais três sessões para a determinação da MFEL. Todas as sessões foram realizadas no mesmo horário do dia, separadas por 48 a 72 horas de intervalo. O LAn, expresso em %1RM, foi significativamente superior no LP em relação ao SR para os dois grupos estudados (LP: 27,8 +/- 3,6 %1RM nos jovens e 27,9 +/- 5,0% 1RM nos idosos; SR: 24,0 +/- 3,0% 1RM nos jovens e 21,5 +/- 3,1% 1RM nos idosos). Não foram observadas diferenças estatisticamente significativas na intensidade do LAn entre os grupos em cada aparelho. A lactacidemia na intensidade do LAn foi significativamente inferior no LP (1,86 +/- 0,63 mmol/L nos jovens e 1,23 +/- 0,34 mmol/L nos idosos) em relação ao SR (2,08 +/- 0,41 mmol/L nos jovens e 1,91 +/- 0,40 mmol/L nos idosos). A intensidade da MFEL no grupo de jovens foi 29,2 +/- 6,7% 1RM no LP e 21,7 +/- 4,4% 1RM no SR. No grupo e idosos, a MFEL ocorreu a 30,9 +/- 4,9% 1RM no LP e 23,3 +/- 6,6% 1RM no SR. A MFEL ocorre em intensidade significativamente menor no aparelho SR para os dois grupos (p < ou = 0,05), sem diferenças estatisticamente significativas entre os grupos. Não houve diferença significativa entre as intensidades do LAn e da MFEL para os dois grupos nos dois aparelhos. Durante a realização do exercício na MFEL, ocorreu a estabilização dos parâmetros ergoespirométricos, FC, PA e PSE entre a série 9 e série 15. Estes resultados demonstram que é possível determinar MFEL nos exercícios LP e SR para as duas populações estudadas. A MFEL ocorre em intensidades superiores no exercício LP. A intensidade da MFEL, expressa em percentual de 1RM, é semelhante à intensidade do LAn. / The maximal lactate steady state (MLSS) is considered a critical intensity of dynamic exercise and its intensity is specific to the age group. However, despite the relationship between exercise intensity and cardiovascular, metabolic and ventilatory adjustments during resistance exercise, the MLSS was unknown in this type of exercise. The purpose of the study was to verify and to compare if there is a maximal lactate steady state (MLSS) for leg press (LP) and bench press (BP) exercises in two different groups: young and older people. Furthermore, to evaluate the ventilatory responses (VE, VO2 e VCO2, blood lactate concentration (BLC), heart rate (HR), blood pressure and rate of perceived exertion (RPE) to those exercises performed on MLSS intensity. 13 young men (26,1 +/- 2,9 years) and 11 elderly healthy men (68,9 +/- 4,0 years) with a minimal experience of 6 months of resistance training volunteered for the study. Volunteers underwent a 1 repetition maximum test (1RM), an incremental test to determine anaerobic threshold (AT) and three more sessions to determine MLSS. Session were performed on the same time of day and separated by a 48-72 h interval. AT intensity (%1RM) was significantly higher for LP than BP for the two groups studied (LP: 27,8 +/- 3,6% 1RM for young group and 27,9 +/- 5,0% 1RM for elderly; BP: 24,0 +/- 3,0%1RM for young group and 21,5 +/- 3,1%1RM for elderly). There was no significant difference between groups in the AT intensity. BLC on AT was significantly lower for LP (1,86 +/- 0,63 mmol/L for young group and 1,23 +/- 0,34 mmol/L for elderly) than BP (2,08 +/- 0,41 mmol/L for young and 1,91 +/- 0,40 mmol/L for elderly). MLSS intensity for young group was 29,2 +/- 6,7% 1RM in LP and 21,7 +/- 4,4% 1RM in BP. For elderly, MLSS was 30,9 +/- 4,9% 1RM in LP and 23,3 +/- 6,6% 1RM in BP. MLSS intensity was significantly lower in BP for both groups (p < or = 0,05), with no statistical differences between groups. There was no significant difference between AT and MLSS intensities on both groups. During exercise on MLSS, ventilatory parameters, HR, blood pressure and RPE stabilized between set 9 and set 15. These results show that it is possible to identify MLSS on the LP and BP exercises for both populations. MLSS intensity is higher in LP exercise, when compared to BP. MLSS intensity is similar to the AT intensity.

INTRODUÇÃO: A atividade física faz parte do tratamento do portador de diabetes mellitus tipo 1 (DM1), devendo ser encorajada pelas mesmas razões que é em não portadores. Os portadores de DM1, como evidenciam os estudos, apresentam póstreino: redução dos fatores de risco para o desenvolvimento de doenças cardiovasculares, melhora do condicionamento físico, da sensibilidade à ação da insulina e do bem-estar. Mas é fundamental realizar a monitorização glicêmica, adequar alimentação e dose de insulina para a prática de exercícios, a fim de evitar hipo ou hiperglicemias antes, durante ou após as sessões, e consequentemente, obter melhora ou manutenção do controle glicêmico. Além disso, o nível de atividade física relaciona-se inversamente ao aparecimento de complicações do diabetes e risco de mortalidade em portadores de DM1. Porém, poucos estudos demonstram o comportamento da glicemia destes pacientes em diferentes tipos de exercícios. O conhecimento da variação glicêmica durante o exercício é fundamental para a conduta terapêutica do médico, para a prescrição e orientação segura de exercícios pelos professores de educação física. OBJETIVOS: Analisar a variação da glicose de DM1, submetidos às sessões de exercício aeróbio, exercícios resistidos e teste ergoespirométrico, utilizando o Sistema de Monitorização Contínua da Glicose (CGMS) e o glicosímetro portátil para monitorização da glicemia capilar. E como objetivo secundário, analisar a acurácia do CGMS e as respostas agudas e crônicas às sessões de exercícios aeróbio, resistidos e teste ergoespirométrico por portadores de DM 1. CASUÍSTICA E MÉTODOS: Dez portadores de DM1, de ambos os sexos, com idade entre 16 e 45 anos, sem complicações da doença. Os pacientes foram submetidos ao teste ergoespirométrico máximo (TE) e a 40 sessões de exercícios aeróbios (A) ou resistidos (R). As sessões foram realizadas no período pós-prandial do almoço e nestes dias, os pacientes foram orientados pela equipe médica a reduzir: 1U (se dose <20U) ou 2U (se dose >20U) da insulina basal (NPH) da manhã e 50 a 75% da insulina pré-prandial ultra-rápida (UR) do almoço; não houve redução para o TE. Os pacientes mediam a glicemia capilar antes, durante (se, necessário) e após as sessões. RESULTADOS: Os exercícios aeróbios promoveram uma queda maior na GC (67 mg/dL), quando comparada a queda causada pelos exercícios resistidos (37mg/dL) (p=0,047). A correlação entre os dados obtidos pelo CGMS e pelo glicosímetro durante o exercício é significativa (p<0,001), positiva e direta (r=+0,925). A freqüência cardíaca e a pressão arterial sistólica apresentaram aumento durante A (p<0,001), não apresentando diferença para R. A pressão arterial diastólica não mostrou diferença em nenhum dos dois grupos. A freqüência média de consumo [(A=19,8) e (R=16,7)] e a quantidade de gel [(A=28,2) e (R=21,3)] utilizada durante o período de treinamento foram similares em ambos os grupos. A freqüência de hipoglicemias foi igual em ambos os grupos [(A=1,5) e (R=1,5)] durante o treinamento, não apresentando diferenças em relação às reduções de dose de insulina UR ou período de treinamento. As respostas crônicas foram obtidas ao final do período de treinamento (40 sessões): o controle glicêmico (HbA1c), o perfil lipídico (colesterol total, triglicérides, HDL, LDL, VLDL) e os parâmetros antropométricos não foram influenciados pelo treinamento. Os níveis médios de microalbuminúria em repouso não modificaram, mas os níveis médios de microalbuminúria induzida pelo exercício praticamente dobraram. CONCLUSÕES: O grupo A apresentou maior declínio da glicose quando comparado ao grupo R. O CGMS pode ser considerado um método acurado para a sua utilização durante o exercício. O comportamento da freqüência cardíaca e pressão arterial foram similares aos não portadores de diabetes. O protocolo de redução de insulina se mostrou efetivo durante o período de treinamento. Houve mudanças na composição corporal detectadas pelo DEXA / Background and Aims: For type 1 diabetes patients is essential self monitoring of blood glucose and adjustment of carbohydrate intake and insulin dose for exercise practice. The aim of this study was to assess glucose variability during: spiroergometric test (ST) and aerobic (A) and resistance exercises(R). Materials and Methods: 10 DM1 patients performed ST, and 40 A and R bouts and they reduced their insulin dose in A and R exercise days. Results: Glycemia variation groups were: A=67mg/dL and R=37mg/dL. Heart rate and systolic blood pressure increased during A. Diastolic blood pressure was not modified. Glycemic control, lipids and body measurements were not influenced by training. Conclusions: Aerobic and resistance exercise produced glycemia reduction but glycemia fall was higher during aerobic exercise bouts when compared with resistance exercise bouts

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