Maternal low-protein diet reduces skeletal muscle protein synthesis and mass via Akt-mTOR pathway in adult rats.

Several studies have demonstrated that a maternal low-protein diet induces long-term metabolic disorders, but the involved mechanisms are unclear. This study investigated the molecular effects of a low-protein diet during pregnancy and lactation on glucose and protein metabolism in soleus muscle isolated from adult male rats. Female rats were fed either a normal protein diet or low-protein diet during gestation and lactation. After weaning, all pups were fed a normal protein diet until the 210th day postpartum. In the 7th month of life, mass, contractile function, protein and glucose metabolism, and the Akt-mTOR pathway were measured in the soleus muscles of male pups. Dry weight and contractile function of soleus muscle in the low-protein diet group rats were found to be lower compared to the control group. Lipid synthesis was evaluated by measuring palmitate incorporation in white adipose tissue. Palmitate incorporation was higher in the white adipose tissue of the low-protein diet group. When incubated soleus muscles were stimulated with insulin, protein synthesis, total amino acid incorporation and free amino acid content, glucose incorporation and uptake, and glycogen synthesis were found to be reduced in low-protein diet group rats. Fasting glycemia was higher in the low-protein diet group. These metabolic changes were associated with a decrease in Akt and GSK-3ß signaling responses to insulin and a reduction in RPS6 in the absence of the hormone. There was also notably lower expression of Akt in the isolated soleus muscle of low-protein diet group rats. This study is the first to demonstrate how maternal diet restriction can reduce skeletal muscle protein and mass by downregulating the Akt-mTOR pathway in adulthood.

Housekeeping proteins: How useful are they in skeletal muscle diabetes studies and muscle hypertrophy models?

The use of Western blot analysis is of great importance in research, and the measurement of housekeeping proteins is commonly used for loading controls. However, Ponceau S staining has been shown to be an alternative to analysis of housekeeping protein levels as loading controls in some conditions. In the current study, housekeeping protein levels were measured in skeletal muscle hypertrophy and streptozotocin-induced diabetes experimental models. The following housekeeping proteins were investigated: glyceraldehyde-3-phosphate dehydrogenase (GAPDH), ß-actin, α-tubulin, γ-tubulin, and α-actinin. Evidence is presented that Ponceau S is more reliable than housekeeping protein levels for specific protein quantifications in Western blot analysis.

Overload-induced skeletal muscle hypertrophy is not impaired in STZ-diabetic rats.

The aim of this study was to evaluate the effect of overload-induced hypertrophy on extensor digitorum longus (EDL) and soleus muscles of streptozotocin-induced diabetic rats. The overload-induced hypertrophy and absolute tetanic and twitch forces increases in EDL and soleus muscles were not different between diabetic and control rats. Phospho-Akt and rpS6 contents were increased in EDL muscle after 7 days of overload and returned to the pre-overload values after 30 days. In the soleus muscle, the contents of total and phospho-Akt and total rpS6 were increased in both groups after 7 days. The contents of total Akt in controls and total rpS6 and phospho-Akt in the diabetic rats remained increased after 30 days. mRNA expression after 7 days of overload in the EDL muscle of control and diabetic animals showed an increase in MGF and follistatin and a decrease in myostatin and Axin2. The expression of FAK was increased and of MuRF-1 and atrogin-1 decreased only in the control group, whereas Ankrd2 expression was enhanced only in diabetic rats. In the soleus muscle caused similar changes in both groups: increase in FAK and MGF and decrease in Wnt7a, MuRF-1, atrogin-1, and myostatin. Differences between groups were observed only in the increased expression of follistatin in diabetic animals and decreased Ankrd2 expression in the control group. So, insulin deficiency does not impair the overload-induced hypertrophic response in soleus and EDL muscles. However, different mechanisms seem to be involved in the comparable hypertrophic responses of skeletal muscle in control and diabetic animals.

Short-term creatine supplementation decreases reactive oxygen species content with no changes in expression and activity of antioxidant enzymes in skeletal muscle.

The effect of short-term creatine (Cr) supplementation upon content of skeletal muscle-derived-reactive oxygen species (ROS) was investigated. Wistar rats were supplemented with Cr (5 g/kg BW) or vehicle, by gavage, for 6 days. Soleus and extensor digitorum longus (EDL) muscles were removed and incubated for evaluation of ROS content using Amplex-UltraRed reagent. The analysis of expression and activity of antioxidant enzymes (superoxide dismutase 1 and 2, catalase and glutathione peroxidase) were performed. Direct scavenger action of Cr on superoxide radical and hydrogen peroxide was also investigated. Short-term Cr supplementation attenuated ROS content in both soleus and EDL muscles (by 41 and 33.7%, respectively). Cr supplementation did not change expression and activity of antioxidant enzymes. Basal TBARS content was not altered by Cr supplementation. In cell-free experiments, Cr showed a scavenger effect on superoxide radical in concentrations of 20 and 40 mM, but not on hydrogen peroxide. These results indicate that Cr supplementation decreases ROS content in skeletal muscle possibly due to a direct action of Cr molecule on superoxide radical.

Metabolic and functional effects of beta-hydroxy-beta-methylbutyrate (HMB) supplementation in skeletal muscle.

Beta-hydroxy-beta-methylbutyrate (HMB) is a metabolite derived from leucine. The anti-catabolic effect of HMB is well documented but its effect upon skeletal muscle strength and fatigue is still uncertain. In the present study, male Wistar rats were supplemented with HMB (320 mg/kg per day) for 4 weeks. Placebo group received saline solution only. Muscle strength (twitch and tetanic force) and resistance to acute muscle fatigue of the gastrocnemius muscle were evaluated by direct electrical stimulation of the sciatic nerve. The content of ATP and glycogen in red and white portions of gastrocnemius muscle were also evaluated. The effect of HMB on citrate synthase (CS) activity was also investigated. Muscle tetanic force was increased by HMB supplementation. No change was observed in time to peak of contraction and relaxation time. Resistance to acute muscle fatigue during intense contractile activity was also improved after HMB supplementation. Glycogen content was increased in both white (by fivefold) and red (by fourfold) portions of gastrocnemius muscle. HMB supplementation also increased the ATP content in red (by twofold) and white (1.2-fold) portions of gastrocnemius muscle. CS activity was increased by twofold in red portion of gastrocnemius muscle. These results support the proposition that HMB supplementation have marked change in oxidative metabolism improving muscle strength generation and performance during intense contractions.

Local injections of adipose-derived mesenchymal stem cells modulate inflammation and increase angiogenesis ameliorating the dystrophic phenotype in dystrophin-deficient skeletal muscle.

The effects of adipose-derived mesenchymal stem cells (ADMSC) transplantation on degeneration, regeneration and skeletal muscle function were investigated in dystrophin-deficient mice (24-week-old). ADMSC transplantation improved muscle strength and, resistance to fatigue. An increase in fiber cross-sectional area and in the number of fibers with centralized nuclei and augment of myogenin content were observed. In ADMSC-treated muscles a decrease in muscle content of TNF-α, IL-6 and oxidative stress measured by Amplex(®) reagent were observed. The level of TGF-ß1 was lowered whereas that of VEGF, IL-10 and IL-4 were increased by ADMSC treatment. An increase in markers of macrophage M1 (CD11 and F4-80) and a decrease in T lymphocyte marker (CD3) and arginase-1 were also observed in ADMSCs-treated dystrophic muscle. No change was observed in iNOS expression. Increased phosphorylation of Akt, p70S6k and 4E-BP1 was found in dystrophic muscles treated with ADMSC. These results suggest that ADMSC transplantation modulates inflammation and improves muscle tissue regeneration, ameliorating the dystrophic phenotype in dystrophin-deficient mice.

[Regulation of glucose and fatty acid metabolism in skeletal muscle during contraction]. / Regulação do metabolismo de glicose e ácido graxo no músculo esquelético durante exercício físico.

The glucose-fatty acid cycle explains the preference for fatty acid during moderate and long duration physical exercise. In contrast, there is a high glucose availability and oxidation rate in response to intense physical exercise. The reactive oxygen species (ROS) production during physical exercise suggests that the redox balance is important to regulate of lipids/carbohydrate metabolism. ROS reduces the activity of the Krebs cycle, and increases the activity of mitochondrial uncoupling proteins. The opposite effects happen during moderate physical activity. Thus, some issues is highlighted in the present review: Why does skeletal muscle prefer lipids in the basal and during moderate physical activity? Why does glucose-fatty acid fail to carry out their effects during intense physical exercise? How skeletal muscles regulate the lipids and carbohydrate metabolism during the contraction-relaxation cycle?

Regulação do metabolismo de glicose e ácido graxo no músculo esquelético durante exercício físico / Regulation of glucose and fatty acid metabolism in skeletal muscle during contraction

O ciclo glicose-ácido graxo explica a preferência do tecido muscular pelos ácidos graxos durante atividade moderada de longa duração. Em contraste, durante o exercício de alta intensidade, há aumento na disponibilidade e na taxa de oxidação de glicose. A produção de espécies reativas de oxigênio (EROs) durante a atividade muscular sugere que o balanço redox intracelular é importante na regulação do metabolismo de lipídios/carboidratos. As EROs diminuem a atividade do ciclo de Krebs e aumentam a atividade da proteína desacopladora mitocondrial. O efeito oposto é esperado durante a atividade moderada. Assim, as questões levantadas nesta revisão são: Por que o músculo esquelético utiliza preferencialmente os lipídios no estado basal e de atividade moderada? Por que o ciclo glicose-ácido graxo falha em exercer seus efeitos durante o exercício intenso? Como o músculo esquelético regula o metabolismo de lipídios e carboidratos em regime envolvendo o ciclo contração-relaxamento.

The glucose-fatty acid cycle explains the preference for fatty acid during moderate and long duration physical exercise. In contrast, there is a high glucose availability and oxidation rate in response to intense physical exercise. The reactive oxygen species (ROS) production during physical exercise suggests that the redox balance is important to regulate of lipids/carbohydrate metabolism. ROS reduces the activity of the Krebs cycle, and increases the activity of mitochondrial uncoupling proteins. The opposite effects happen during moderate physical activity. Thus, some issues is highlighted in the present review: Why does skeletal muscle prefer lipids in the basal and during moderate physical activity? Why does glucose-fatty acid fail to carry out their effects during intense physical exercise? How skeletal muscles regulate the lipids and carbohydrate metabolism during the contraction-relaxation cycle?.

Amino acids and diabetes: implications for endocrine, metabolic and immune function.

Aberrant alterations in glucose and lipid concentrations and their pathways of metabolism are a hallmark of diabetes. However, much less is known about alterations in concentrations of amino acids and their pathways of metabolism in diabetes. In this review we have attempted to highlight, integrate and discuss common alterations in amino acid metabolism in a wide variety of cells and tissues and relate these changes to alterations in endocrine, physiologic and immune function in diabetes.

Regulation of glycolysis and expression of glucose metabolism-related genes by reactive oxygen species in contracting skeletal muscle cells.

Contractile activity induces a marked increase in glycolytic activity and gene expression of enzymes and transporters involved in glucose metabolism in skeletal muscle. Muscle contraction also increases the production of reactive oxygen species (ROS). In this study, the effects of treatment with N-acetylcysteine (NAC), a potent antioxidant compound, on contraction-stimulated glycolysis were investigated in electrically stimulated primary rat skeletal muscle cells. The following parameters were measured: 2-[(3)H]deoxyglucose (2-DG) uptake; activities of hexokinase, phosphofructokinase (PFK), and glucose-6-phosphate dehydrogenase (G6PDH); lactate production; and expression of the glucose transporter 4 (GLUT4), hexokinase II (HKII), and PFK genes after one bout of electrical stimulation in primary rat myotubes. NAC treatment decreased ROS signal by 49% in resting muscle cells and abolished the muscle contraction-induced increase in ROS levels. In resting cells, NAC decreased mRNA and protein contents of GLUT4, mRNA content and activity of PFK, and lactate production. NAC treatment suppressed the contraction-mediated increase in 2-DG uptake; lactate production; hexokinase, PFK, and G6PDH activities; and gene expression of GLUT4, HKII, and PFK. Similar to muscle contraction, exogenous H(2)O(2) (500 nM) administration increased 2-DG uptake; lactate production; hexokinase, PFK, and G6PDH activities; and gene expression of GLUT4, HKII, and PFK. These findings support the proposition that ROS endogenously produced play an important role in the changes in glycolytic activity and gene expression of GLUT4, HKII, and PFK induced by contraction in skeletal muscle cells.

Effect of short-term creatine supplementation on markers of skeletal muscle damage after strenuous contractile activity.

The protective effect of short-term creatine supplementation (CrS) upon markers of strenuous contractile activity-induced damage in human and rat skeletal muscles was investigated. Eight Ironman triathletes were randomized into the placebo (Pl; n = 4) and creatine-supplemented (CrS; n = 4) groups. Five days prior to the Ironman competition, the CrS group received creatine monohydrate (20 g day(-1)) plus maltodextrin (50 g) divided in two equal doses. The Pl group received maltodextrin (50 g day(-1)) only. The effect of CrS (5 g day(-1)/kg body weight for 5 days) was also evaluated in a protocol of strenuous contractile activity induced by electrical stimulation in rats. Blood samples were collected before and 36 and 60 h after the competition and were used to determine plasma activities of creatine kinase (CK), lactate dehydrogenase (LDH), aldolase (ALD), glutamic oxaloacetic acid transaminase (GOT), glutamic pyruvic acid transaminase (GPT), and C-reactive protein (CRP) level. In rats, plasma activities of CK and LDH, muscle vascular permeability (MVP) using Evans blue dye, muscle force and fatigue were evaluated. Activities of CK, ALD, LDH, GOT, GTP, and levels of CRP were increased in the Pl group after the competition as compared to basal values. CrS decreased plasma activities of CK, LDH, and ALD, and prevented the rise of GOT and GPT plasma activities. In rats, CrS delayed the fatigue, preserved the force, and prevented the rise of LDH and CK plasma activities and MVP in the gastrocnemius muscle. CrS presented a protective effect on muscle injury induced by strenuous contractile activities.

Exercise prevents cardiometabolic alterations induced by chronic use of glucocorticoids.

BACKGROUND: Chronically, glucocorticoids induce adverse cardiometabolic alterations including insulin resistance, diabetes, dyslipidemia, liver steatosis and arterial hypertension. OBJECTIVES: To evaluate the effect of regular practice of aerobic exercise on cardiometabolic alterations induced by chronic administration of dexamethasone (Dex - 0.5 mg/kg/day ip) in rats. METHODS: Male Wistar rats (n = 24) were divided in four groups: Control group; Trained group; Treated with Dex group and Treated with Dex and trained group. The exercise training (initiated 72 hours after the first dose of Dex) was carried out three times a week until the end of the treatment. At the end of this period, the following biochemical assessments were performed: fasting glycemia, oral glucose tolerance test and analysis of the blood lipid profile that included total cholesterol (TC), LDL-c, HDL-c, VLDL-c and triglycerides (TG). The weight of the gastrocnemius muscle, the histopathological analysis of the liver and cardiometabolic indices (TC/HDL-c, LDL-c/HDL-c and TG/HDL-c) were also performed. RESULTS: Hyperglycemia, lower glucose tolerance, increased TC, LDL-c, VLDL-c, TG, CT/HDL-c, LDL-c/HDL-c and TG/HDL-c, decreased HDL-c, presence of liver steatosis and muscular hypotrophy were observed in the animals treated with Dex. The exercise training reduced hyperglycemia, improved glucose tolerance, decreased dyslipidemia and prevented liver steatosis, muscular hypotrophy and reduced CT/HDL-c, LDL-c/HDL-c and TG/HDL-c ratios. However, there was no significant effect on HDL-c. CONCLUSION: The aerobic exercise training have a protective effect against the cardiometabolic alterations induced by the chronic use of glucocorticoids.

Exercício físico previne alterações cardiometabólicas induzidas pelo uso crônico de glicocorticóides / Exercise prevents cardiometabolic alterations induced by chronic use of glucocorticoids

FUNDAMENTO: Cronicamente, os glicocorticóides induzem alterações cardiometabólicas adversas, incluindo resistência à insulina, diabete, dislipidemia, esteatose hepática e hipertensão arterial. OBJETIVOS: Avaliar o efeito da prática regular de exercício físico aeróbio sobre as alterações cardiometabólicas induzidas por administração crônica de dexametasona (Dex - 0,5 mg/kg/dia i.p) em ratos. MÉTODOS: Ratos Wistar machos (n = 24) foram divididos em quatro grupos: Grupo controle; Grupo treinado; Grupo tratado com Dex e Grupo tratado com Dex e treinado. O treinamento físico (iniciado 72 horas após a primeira dose de Dex) foi realizado 3 vezes por semana, até o final do tratamento. Ao final desse período, realizaram-se as seguintes avaliações bioquímicas: glicemia em jejum, teste de tolerância à glicose e análise do perfil lipídico no sangue que incluiu colesterol total (CT), LDL-c, HDL-c, VLDL-c e triglicerídeos (TG). O peso do músculo gastrocnêmio, análise histopatológica do fígado e os índices cardiometabólicos (CT/HDL-c, LDL-c/HDL-c e TG/HDL-c) também foram avaliados. RESULTADOS: Observou-se hiperglicemia, menor tolerância à glicose, elevação do CT, LDL-c, VLDL-c e TG, diminuição do HDL-c, presença de esteatose hepática, hipotrofia muscular e elevação dos índices CT/HDL-c, LDL-c/HDL-c e TG/HDL-c nos animais tratados com Dex. O exercício físico reduziu a hiperglicemia, melhorou a tolerância à glicose, reduziu a dislipidemia e preveniu a esteatose hepática , a hipotrofia muscular e reduziu os índices CT/HDL-c, LDL-c/HDL-c e TG/HDL-c. Entretanto, não houve efeito significante do treinamento físico sobre o HDL-c. CONCLUSÃO: O exercício físico aeróbio tem efeito protetor contra as alterações cardiometabólicas induzidas pelo uso crônico de glicocorticóides.

BACKGROUND: Chronically, glucocorticoids induce adverse cardiometabolic alterations including insulin resistance, diabetes, dyslipidemia, liver steatosis and arterial hypertension. OBJECTIVES: To evaluate the effect of regular practice of aerobic exercise on cardiometabolic alterations induced by chronic administration of dexamethasone (Dex - 0.5 mg/kg/day ip) in rats. METHODS: Male Wistar rats (n = 24) were divided in four groups: Control group; Trained group; Treated with Dex group and Treated with Dex and trained group. The exercise training (initiated 72 hours after the first dose of Dex) was carried out three times a week until the end of the treatment. At the end of this period, the following biochemical assessments were performed: fasting glycemia, oral glucose tolerance test and analysis of the blood lipid profile that included total cholesterol (TC), LDL-c, HDL-c, VLDL-c and triglycerides (TG). The weight of the gastrocnemius muscle, the histopathological analysis of the liver and cardiometabolic indices (TC/HDL-c, LDL-c/HDL-c and TG/HDL-c) were also performed. RESULTS: Hyperglycemia, lower glucose tolerance, increased TC, LDL-c, VLDL-c, TG, CT/HDL-c, LDL-c/HDL-c and TG/HDL-c, decreased HDL-c, presence of liver steatosis and muscular hypotrophy were observed in the animals treated with Dex. The exercise training reduced hyperglycemia, improved glucose tolerance, decreased dyslipidemia and prevented liver steatosis, muscular hypotrophy and reduced CT/HDL-c, LDL-c/HDL-c and TG/HDL-c ratios. However, there was no significant effect on HDL-c. CONCLUSION: The aerobic exercise training have a protective effect against the cardiometabolic alterations induced by the chronic use of glucocorticoids.

Updating the effects of fatty acids on skeletal muscle.

In this review we updated the fatty acid (FA) effects on skeletal muscle metabolism. Abnormal FA availability induces insulin resistance and accounts for several of its symptoms and complications. Efforts to understand the pathogenesis of insulin resistance are focused on disordered lipid metabolism and consequently its effect on insulin signaling pathway. We reviewed herein the FA effects on metabolism, signaling, regulation of gene expression and oxidative stress in insulin resistance. The elevated IMTG content has been associated with increased intracellular content of diacylglycerol (DAG), ceramides and long-chain acyl-coenzyme A (LCA-CoA). This condition has been shown to promote insulin resistance by interfering with phosphorylation of proteins of the insulin pathway including insulin receptor substrate-1/2 (IRS), phosphatidylinositol-3-kinase, (PI3-kinase) and protein kinase C. Although the molecular mechanism is not completely understood, elevated reactive oxygen (ROS) and nitrogen species (RNS) are involved in this process. Elevated ROS/RNS activates nuclear factor-kappaB (NFkB), which promotes the transcription of proinflammatory tumoral necrosis factor alpha (TNFalpha), decreasing the insulin response. Therefore, oxidative stress induced by elevated FA availability may constitute one of the major causes of insulin resistance in skeletal muscle.

Uso do ioga como recurso não-farmacológico no tratamento da hipertensão arterial essencial / Use of the yoga as a non-pharmacologic resource in the treatment of essential arterial hypertension

Os tratamentos não-farmacológicos são importantes no contexto terapêutico da hipertensão arterial. Estudos prévios têm mostrado os benefícios do ioga na redução dos níveis de estresse, reatividade vascular e função autonômica cardíaca em populações orientais. Objetivos: Avaliar os efeitos da prática do Hatha Yoga como recurso complementar no tratamento e controle da pressão arterial em pacientes com hipertensão arterial essencial atendidos em nível ambulatorial. Métodos: Foram estudados 16 pacientes (10 mulherese 6 homens) durante um mês com sessões semanais de ioga. O protocolo de iogaterapia envolveu exercícios de controle respiratório (pranayamas) e shavasana, uma postura associada às técnicas de relaxamento durante 60 minutos diários. As variáveis analisadas foram a variabilidade da freqüência cardíaca (VFC) no domínio do tempo, a pressão arterial sistólica (PAS), a pressão arterial diastólica (PAD) e o duplo-produto (DP). Os dados foram submetidos à análise estatística descritiva e ao teste t de Student pareado para análise do pûvalor. Resultados: Foram observadas redução da PAS (p < 0,01), da PAD (p < 0,05) e do DP (p < 0,01) sendo essas alterações associadas à melhora na VFC (índice SDNN p < 0,001). Conclusões: O Hatha Yoga poderia ser utilizado como recurso complementar no tratamento da hipertensão arterial, uma vez que sua prática está associada à melhora na função autonômica cardíaca, na redução da pressão arterial e da sobrecarga cardíaca em hipertensos.

Spontaneous respiratory modulation improves cardiovascular control in essential hypertension.

BACKGROUND: Recent studies show that controlled breathing improves baroreflex and heart rate variability and lowers blood pressure in hypertensive patients. OBJECTIVE: To evaluate the effects of slow breathing training on cardiorespiratory system modulation of patients (n=10, men and women, ages ranging from 45 to 60) with essential hypertension seen in an outpatient setting. METHODS: According to the study design, each patient was used as his/her own control, and data were collected before and after the intervention. The following parameters were assessed: heart rate variability (HRV), systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial blood pressure (MAP), respirometry, chest expansion measurement, and statistical data analysis. Respiratory training was performed in 30-minute sessions held twice a week over one month using slow breathing exercises. RESULTS: Our results were as follows: a reduction in SBP, DPB, and MAP (p < 0.05 vs control); an increase in heart rate variability, as evidenced by greater RR interval variation and SDNN index; a decline in respiratory rate (p < 0.01 vs control); and an increase in tidal volume (p < 0.01 vs control) and thoracic expansibility (p < 0.01 vs control). CONCLUSION: Respiratory retraining using the slow breathing technique appears to be a useful adjunctive for cardiorespiratory control in hypertensive patients.

Modificação do padrão respiratório melhora o controle cardiovascular na hipertensão essencial / Spontaneous respiratory modulation improves cardiovascular control in essential hypertension

FUNDAMENTO: Estudos recentes apontam os benefícios do controle da respiração na melhoria do barorreflexo, variabilidade da freqüência cardíaca e redução da pressão arterial em pacientes hipertensos. OBJETIVO: Avaliar os efeitos do treinamento com técnica de respiração lenta na modulação dos sistemas cardiovascular e respiratório de pacientes (n=10, homens e mulheres, com 45 a 60 anos de idade) com hipertensão arterial essencial, assistidos em ambulatório. MÉTODOS: No delineamento do estudo, cada paciente foi utilizado como controle de si mesmo, sendo a coleta de dados realizada antes e após o período de intervenção. Foram avaliados parâmetros como variabilidade da freqüência cardíaca, pressão arterial sistólica, pressão arterial diastólica, pressão arterial média, ventilometria, cirtometria torácica e análise estatística dos dados. O treinamento respiratório utilizou exercícios de baixa freqüência e foi realizado duas vezes por semana durante um mês. Cada sessão teve duração de 30 minutos. RESULTADOS: Os resultados demonstraram redução da pressão arterial sistólica, da pressão arterial diastólica e da pressão arterial média (p < 0,05 vs controle), aumento da variabilidade da freqüência cardíaca evidenciado pelo aumento da variância dos intervalos RR e índice SDNN, redução da freqüência respiratória (p < 0,01 vs controle), aumento do volume corrente (p < 0,01 vs controle), e aumento da expansibilidade torácica apical (p < 0,01 vs controle). CONCLUSÃO: A reeducação respiratória com a técnica de respiração lenta parece ser um bom recurso complementar para o controle tanto cardiovascular como respiratório em pacientes hipertensos.

BACKGROUND: Recent studies show that controlled breathing improves baroreflex and heart rate variability and lowers blood pressure in hypertensive patients. OBJECTIVE: To evaluate the effects of slow breathing training on cardiorespiratory system modulation of patients (n=10, men and women, ages ranging from 45 to 60) with essential hypertension seen in an outpatient setting. METHODS: According to the study design, each patient was used as his/her own control, and data were collected before and after the intervention. The following parameters were assessed: heart rate variability (HRV), systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial blood pressure (MAP), respirometry, chest expansion measurement, and statistical data analysis. Respiratory training was performed in 30-minute sessions held twice a week over one month using slow breathing exercises. RESULTS: Our results were as follows: a reduction in SBP, DPB, and MAP (p < 0.05 vs control); an increase in heart rate variability, as evidenced by greater RR interval variation and SDNN index; a decline in respiratory rate (p < 0.01 vs control); and an increase in tidal volume (p < 0.01 vs control) and thoracic expansibility (p < 0.01 vs control). CONCLUSION: Respiratory retraining using the slow breathing technique appears to be a useful adjunctive for cardiorespiratory control in hypertensive patients.