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Fructose overconsumption is a worldwide trend, and it has been found to cause metabolic disorders in parents and their offspring. Additionally, metabolic syndrome has been closely associated with increased cardiovascular risk. In this study, we hypothesized that the chronic fructose consumption by parents could trigger autonomic dysfunction and cardiometabolic disorders in their offspring. Wistar rats undergo an intake of 10% of fructose in drinking water or regular water for 60 days before mating. Their offspring, control (C) and fructose (F) groups, were evaluated 30 days after weaning. Lower birth weight, increased levels of blood triglycerides and insulin resistance were observed in F compared to C group. The offspring of the fructose parents showed increased mean arterial pressure (C: 104 ± 1 vs. F: 111 ± 2 mmHg) and baroreflex sensitivity impairment, characterized by reduced bradycardic (C: -1.6 ± 0.06 vs. F: -1.3 ± 0.06 bpm/mmHg) and tachycardic responses (C: -4.0 ± 0.1 vs. F: -3.1 ± 0.2 bpm/mmHg). Finally, a higher baroreflex-induced tachycardia was associated with lower insulin tolerance (r = -0.55, P < 0.03) and higher systolic arterial pressure (r = 0.54, P < 0.02). In conclusion, our findings indicate that the excessive consumption of fructose by parents is associated with early autonomic, cardiovascular, and metabolic derangement in the offspring, favoring an increased cardiometabolic risk when they reach adulthood.
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Doenças Cardiovasculares , Resistência à Insulina , Ratos , Animais , Pressão Arterial , Barorreflexo , Frutose/efeitos adversos , Ratos Wistar , Glicemia/metabolismo , Pressão SanguíneaRESUMO
PURPOSE OF REVIEW: Resistant Hypertension (RH) poses a significant public health challenge, contributing to increased mortality, cardiovascular events and organ damage. Both clinical and experimental research are striving for higher standards in a translational manner to integrate new findings and confirm hypotheses. Considering that many are the aspects of RH that are still under investigation, this review aims to shed light on the advances made in experimental research concerning RH. It seeks to underscore the pivotal role of experimental studies in shaping clinical practices and also explore future perspectives. RECENT FINDINGS: It is important to emphasize the significance of experimental models, primarily for advancing our understanding: experimental models have greatly contributed to our comprehension of the underlying mechanisms in RH, including factors like sympathetic activation, endothelial dysfunction and structural vessel abnormalities. Secondly, for assessing treatment approaches: animal models have also played a crucial role in evaluating the potential effectiveness of diverse treatment approaches for RH. These encompass both pharmacological options, involving combinations of established drugs or novel pharmaceuticals, and non-pharmacological alternatives, which include surgical procedures like renal denervation, medical devices like baroreceptor stimulators, and lifestyle modifications. The most lacking component in translational research is the fact that there is no well-established animal model that perfectly replicates RH. Consequently, alternative strategies, including the combination of models, must be considered. What remains clear is that the development of animal models closely mimicking RH holds the promise of providing valuable insights into the essential mechanisms and responses necessary to combat or slow the global progression of RH.
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Previous studies show that COVID-19 survivors have elevated muscle sympathetic nerve activity (MSNA), endothelial dysfunction, and aortic stiffening. However, the neurovascular responses to mental stress and exercise are still unexplored. We hypothesized that COVID-19 survivors, compared with age- and body mass index (BMI)-matched control subjects, exhibit abnormal neurovascular responses to mental stress and physical exercise. Fifteen severe COVID-19 survivors (aged: 49 ± 2 yr, BMI: 30 ± 1 kg/m2) and 15 well-matched control subjects (aged: 46 ± 3 yr, BMI: 29 ± 1 kg/m2) were studied. MSNA (microneurography), forearm blood flow (FBF), and forearm vascular conductance (FVC, venous occlusion plethysmography), mean arterial pressure (MAP, Finometer), and heart rate (HR, ECG) were measured during a 3-min mental stress (Stroop Color-Word Test) and during a 3-min isometric handgrip exercise (30% of maximal voluntary contraction). During mental stress, MSNA (frequency and incidence) responses were higher in COVID-19 survivors than in controls (P < 0.001), and FBF and FVC responses were attenuated (P < 0.05). MAP was similar between the groups (P > 0.05). In contrast, the MSNA (frequency and incidence) and FBF and FVC responses to handgrip exercise were similar between the groups (P > 0.05). MAP was lower in COVID-19 survivors (P < 0.05). COVID-19 survivors exhibit an exaggerated MSNA and blunted vasodilatory response to mental challenge compared with healthy adults. However, the neurovascular response to handgrip exercise is preserved in COVID-19 survivors. Overall, the abnormal neurovascular control in response to mental stress suggests that COVID-19 survivors may have an increased risk to cardiovascular events during mental challenge.
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COVID-19 , Força da Mão , Adulto , Humanos , Pessoa de Meia-Idade , Pressão Sanguínea/fisiologia , Hemodinâmica , Exercício Físico/fisiologia , Frequência Cardíaca/fisiologia , Sistema Nervoso Simpático , Antebraço/irrigação sanguínea , Músculo Esquelético/inervaçãoRESUMO
The aim of this study was to compare the effects of continuous-moderate vs. high-intensity interval aerobic training on cardiovascular and metabolic parameters in ovariectomized high-fat-fed mice. C57BL/6 female ovariectomized were divided into four groups (n=8): low-fat-fed sedentary (SLF); high-fat-fed sedentary (SHF); high-fat-fed moderate-intensity continuous trained (MICT-HF); and high-fat-fed high-intensity interval aerobic trained (HIIT-HF). The high-fat diet lasted 10 weeks. Ovariectomy was performed in the fourth week. The exercise training was carried out in the last four weeks of protocol. Fasting glycemia, oral glucose tolerance, arterial pressure, baroreflex sensitivity, and cardiovascular autonomic modulation were evaluated. Moderate-intensity continuous training prevented the increase in arterial pressure and promoted a reduction in HR at rest, associated with an improvement in the sympathovagal balance in MICT-HF vs. SHF. The high-intensity interval training reduced blood glucose and glucose intolerance in HIIT-HF vs. SHF and MICT-HF. In addition, it improved sympathovagal balance in HIIT-HF vs. SHF. Moderate-intensity continuous training was more effective in promoting cardiovascular benefits, while high-intensity interval training was more effective in promoting metabolic benefits.
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Doenças Cardiovasculares , Treinamento Intervalado de Alta Intensidade , Camundongos , Animais , Feminino , Camundongos Obesos , Camundongos Endogâmicos C57BL , Glicemia/metabolismo , Coração , Treinamento Intervalado de Alta Intensidade/métodosRESUMO
BACKGROUND: Air pollution causes negative impacts on health. Systemic lupus erythematosus (SLE) is an autoimmune disease with diverse clinical manifestations and multifactorial etiology. Recent studies suggest that air pollution can trigger SLE and induce disease activity. However, this association has not been deeply investigated. Thus, the aim of this study was to evaluate whether exposure to fine particulate matter (PM2.5) exacerbates SLE manifestations, focusing on renal complications, in a lupus-prone animal model. Female NZBWF1 mice were exposed daily to 600 µg/m3 of inhaled concentrated ambient particles (CAP) or filtered air (FA). Survival rate, body weight, weight of organs (kidney, spleen, thymus, liver and heart), blood cell count, proteinuria, kidney stereology, renal histopathology, gene expression and oxidative stress were analyzed. RESULTS: Female NZBW mice exposed to CAP showed decreased survival, increased circulating neutrophils, early onset of proteinuria and increased kidney weight with renal cortex enlargement when compared to NZBW mice exposed to FA. CONCLUSIONS: This work shows that air pollution aggravates some SLE manifestations in lupus-prone mice. These results reinforce the need of reducing air pollutant levels in order to promote a better quality of life for individuals diagnosed with SLE.
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Poluentes Atmosféricos , Poluição do Ar , Lúpus Eritematoso Sistêmico , Poluentes Atmosféricos/análise , Poluentes Atmosféricos/toxicidade , Poluição do Ar/análise , Poluição do Ar/estatística & dados numéricos , Animais , Feminino , Camundongos , Material Particulado/análise , Qualidade de VidaRESUMO
Physical exercise is one of the most important factors improving quality of life, but it is not feasible for patients with morbidity or limited mobility. Most previous studies focused on high-intensity or long-term exercise that causes metabolic stress or physiological adaption, respectively. Here, we studied how moderate-intensity swimming affects systemic inflammation in 6-8â¯week old C57BL/6J male mice during endotoxemia. One-hour swimming prevented hypokalemia, hypocalcemia, attenuated serum levels of inflammatory cytokines, increased anti-inflammatory cytokines but affected neither IL6 nor glycemia before or after the endotoxic challenge. Exercise attenuated serum TNF levels by inhibiting its production in the spleen through a mechanism mediated by the subdiaphragmatic vagus nerve but independent of the splenic nerve. Exercise increased serum levels of dopamine, and adrenalectomy prevented the potential of exercise to induce dopamine and to attenuate serum TNF levels. Dopaminergic agonist type-1, fenoldopam, inhibited TNF production in splenocytes. Conversely, dopaminergic antagonist type-1, butaclamol, attenuated exercise control of serum TNF levels. These results suggest that vagal induction of dopamine may contribute to the anti-inflammatory potential of physical exercise.
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Dopamina/metabolismo , Condicionamento Físico Animal/fisiologia , Nervo Vago/fisiologia , Animais , Anti-Inflamatórios/farmacologia , Citocinas/metabolismo , Dopamina/sangue , Endotoxemia/terapia , Inflamação/terapia , Lipopolissacarídeos/farmacologia , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Sepse/metabolismo , Fator de Necrose Tumoral alfa/metabolismoRESUMO
Increase in oxidative/nitrosative stress is one of the mechanisms associated with the development of cardiotoxicity due to doxorubicin (Dox), a potent chemotherapy drug. Previously, we reported mitigation of Dox-induced oxidative/nitrosative stress and apoptosis by vitamin C (Vit C) in isolated cardiomyocytes. In the present in vivo study in rats, we investigated the effect of prophylactic treatment with Vit C on Dox-induced apoptosis, inflammation, oxidative/nitrosative stress, cardiac dysfunction, and Vit C transporter proteins. Dox (cumulative dose: 15 mg/kg) in rats reduced systolic and diastolic cardiac function and caused structural damage. These changes were associated with a myocardial increase in reactive oxygen species, reduction in antioxidant enzyme activities, increased expression of apoptotic proteins, and inflammation. Dox also caused an increase in the expression of proapoptotic proteins Bax, Bnip-3, Bak, and caspase-3. An increase in oxidative/nitrosative stress attributable to Dox was indicated by an increase in superoxide, protein carbonyl formation, lipid peroxidation, nitric oxide (NO), NO synthase (NOS) activity, protein nitrosylation, and inducible NOS protein expression. Dox increased the levels of cardiac proinflammatory cytokines TNF-α, IL-1ß, and IL-6, whereas the expression of Vit C transporter proteins (sodium-ascorbate cotransporter 2 and glucose transporter 4) was reduced. Prophylactic and concurrent treatment with Vit C prevented all these changes and improved survival in the Vit C + Dox group. Vit C also improved Dox-mediated systolic and diastolic dysfunctions and structural damage. These results suggest a cardioprotective role of Vit C in Dox-induced cardiomyopathy by reducing oxidative/nitrosative stress, inflammation, and apoptosis, as well as improving Vit C transporter proteins.NEW & NOTEWORTHY This in vivo study provides novel data that vitamin C improves cardiac structure and function in doxorubicin-induced cardiomyopathy by reducing oxidative/nitrosative stress, apoptosis, and inflammation along with upregulation of cardiac vitamin C transporter proteins. The latter may have a crucial role in improving antioxidant status in this cardiomyopathy.
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Anti-Inflamatórios não Esteroides/farmacologia , Antibióticos Antineoplásicos , Antioxidantes/farmacologia , Ácido Ascórbico/farmacologia , Cardiomiopatias/induzido quimicamente , Cardiomiopatias/tratamento farmacológico , Cardiotônicos/farmacologia , Doxorrubicina , Estresse Oxidativo/efeitos dos fármacos , Estresse Fisiológico/efeitos dos fármacos , Animais , Citocinas/biossíntese , Eletrocardiografia/efeitos dos fármacos , Masculino , Óxido Nítrico Sintase/biossíntese , Óxido Nítrico Sintase/metabolismo , Consumo de Oxigênio/efeitos dos fármacos , Ratos , Ratos Wistar , Espécies Reativas de Nitrogênio , Análise de SobrevidaRESUMO
A rapid rise in obesity, as well as physical inactivity, in industrialized countries is associated with fructose-consumption-mediated metabolic syndrome having a strong association with cardiovascular disease. Although insulin resistance is thought to be at the core, visceral obesity, hypertension, and hypertriglyceridemia are also considered important components of this metabolic disorder. In addition, various other abnormalities such as inflammation, oxidative stress, and elevated levels of uric acid are also part of this syndrome. Lifestyle changes through improved physical activity, as well as nutrition, are important approaches to minimize metabolic syndrome and its deleterious effects.
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Açúcares da Dieta/efeitos adversos , Frutose/efeitos adversos , Inflamação/etiologia , Síndrome Metabólica/etiologia , Estresse Oxidativo , Animais , Pressão Sanguínea , Estilo de Vida Saudável , Humanos , Hipertensão/sangue , Hipertensão/etiologia , Hipertensão/fisiopatologia , Hiperuricemia/sangue , Hiperuricemia/etiologia , Hiperuricemia/metabolismo , Inflamação/sangue , Inflamação/fisiopatologia , Inflamação/terapia , Mediadores da Inflamação/sangue , Síndrome Metabólica/sangue , Síndrome Metabólica/fisiopatologia , Síndrome Metabólica/terapia , Prognóstico , Fatores de Risco , Comportamento de Redução do Risco , Ácido Úrico/sangueRESUMO
Hypertensive patients have a higher risk of developing health complications, particularly cardiovascular (CV) events, than individuals with normal blood pressure (BP). Severity of complications depends on the magnitude of BP elevation and other CV risk factors associated with the target organ damage. Therefore, BP control and management of organ damage may contribute to reduce this risk. BP variability (BPV) has been considered a physiological marker of autonomic nervous system control and may be implicated in increased CV risk in hypertension. This review will present some evidence relating BPV and target organ damage in hypertension in clinical and experimental settings.
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Pressão Sanguínea , Hipertensão/fisiopatologia , Animais , Anti-Hipertensivos/uso terapêutico , Sistema Nervoso Autônomo/fisiopatologia , Determinação da Pressão Arterial , Humanos , Hipertensão/tratamento farmacológico , Fatores de RiscoRESUMO
It is now well established that after menopause cardiometabolic disorders become more common. Recently, resistance exercise has been recommended as a complement to aerobic (combined training, CT) for the treatment of cardiometabolic diseases. The aim of this study was to evaluate the effects of CT in hypertensive ovariectomized rats undergoing fructose overload in blood pressure variability (BPV), inflammation, and oxidative stress parameters. Female rats were divided into the following groups (n = 8/group): sedentary normotensive Wistar rats (C), and sedentary (FHO) or trained (FHOT) ovariectomized spontaneously hypertensive rats undergoing and fructose overload. CT was performed on a treadmill and ladder adapted to rats in alternate days (8 wk; 40-60% maximal capacity). Arterial pressure (AP) was directly measured. Oxidative stress and inflammation were measured on cardiac and renal tissues. The association of risk factors (hypertension + ovariectomy + fructose) promoted increase in insulin resistance, mean AP (FHO: 174 ± 4 vs. C: 108 ± 1 mmHg), heart rate (FHO: 403 ± 12 vs. C: 352 ± 11 beats/min), BPV, cardiac inflammation (tumor necrosis factor-α-FHO: 65.8 ± 9.9 vs. C: 23.3 ± 4.3 pg/mg protein), and oxidative stress cardiac and renal tissues. However, CT was able to reduce mean AP (FHOT: 158 ± 4 mmHg), heart rate (FHOT: 303 ± 5 beats/min), insulin resistance, and sympathetic modulation. Moreover, the trained rats presented increased nitric oxide bioavailability, reduced tumor necrosis factor-α (FHOT: 33.1 ± 4.9 pg/mg protein), increased IL-10 in cardiac tissue and reduced lipoperoxidation, and increased antioxidant defenses in cardiac and renal tissues. In conclusion, the association of risk factors promoted an additional impairment in metabolic, cardiovascular, autonomic, inflammatory, and oxidative stress parameters and combined exercise training was able to attenuate these dysfunctions.
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Sistema Nervoso Autônomo/fisiopatologia , Hipertensão/terapia , Inflamação/terapia , Menopausa , Síndrome Metabólica/terapia , Estresse Oxidativo , Treinamento Resistido , Animais , Pressão Arterial , Sistema Nervoso Autônomo/metabolismo , Biomarcadores/sangue , Modelos Animais de Doenças , Feminino , Frutose , Frequência Cardíaca , Hipertensão/sangue , Hipertensão/fisiopatologia , Inflamação/sangue , Inflamação/fisiopatologia , Mediadores da Inflamação/sangue , Resistência à Insulina , Rim/metabolismo , Peroxidação de Lipídeos , Menopausa/sangue , Síndrome Metabólica/sangue , Síndrome Metabólica/fisiopatologia , Miocárdio/metabolismo , Ovariectomia , Ratos Endogâmicos SHR , Ratos Wistar , Comportamento Sedentário , Fatores de TempoRESUMO
BACKGROUND: We evaluated cardiac autonomic modulation in women with chronic ischemic stroke (at least 4 years post-stroke) at rest and in response to submaximal exercise test. METHODS: Fourteen post-stroke women (S group) and 10 healthy women (C group) participated in this study. Autonomic modulation (using linear and nonlinear analysis), blood pressure and metabolic variables at rest were evaluated immediately after the exercise test and during the recovery period (20 min). All participants underwent submaximal exercise test on cycle ergometer with gas analysis. RESULTS: At rest, the S group displayed higher lactate concentration, systolic (SBP) and diastolic blood pressure (DBP) values when compared to C group. Furthermore, the S group had lower heart rate variability (HRV) in time domain (SDNN: S = 30 ± 5 vs. 40 ± 8 ms; rMSSD: S = 14 ± 2 vs. C = 34 ± 3 ms), decreased high frequency band of pulse interval (S = 8.4 ± 2 vs. 33.1 ± 9 %) and 2V pattern of symbolic analysis (S = 17.3 ± 1 vs. 30 ± 3 %) (both indicators of cardiac vagal modulation) when compared to C group. Immediately after exercise, S group presented higher values of lactate, SBP, DBP and double product when compared to C group, as well as decreased heart rate recovery (HRR) measured at the first, second and third minutes. At recovery time, all HRV parameters in time and frequency domains improved in the S group; however, HF band remained lower when compared to C group. CONCLUSIONS: After the exercise test, women with chronic stroke presented reduced heart rate variability, reduced cardiac vagal modulation, as well as reduced HRR, while displayed an improvement of heart rate variability and cardiac vagal modulation when compared to their baseline. These results reinforce the importance of a physically active lifestyle for cardiovascular autonomic disorders observed in chronic stroke women.
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Teste de Esforço/métodos , Coração/inervação , Acidente Vascular Cerebral/fisiopatologia , Nervo Vago/fisiopatologia , Idoso , Glicemia/metabolismo , Pressão Sanguínea/fisiologia , Doença Crônica , Feminino , Seguimentos , Frequência Cardíaca/fisiologia , Humanos , Ácido Láctico/sangue , Pessoa de Meia-IdadeRESUMO
BACKGROUND: Previous research has demonstrated that hyperglycemia may protect the heart against ischemic injury. The aim of the present study was to investigate the association between hyperglycemia and myocardial infarction on cardiovascular autonomic modulation and cardiac oxidative stress profile in rats. Male Wistar rats were divided into: control (C), diabetic (D), myocardial infarcted (MI) and diabetic infarcted rats (DMI). METHODS: Diabetes was induced by streptozotocin (STZ, 50 mg/Kg) at the beginning of the protocol and MI was induced by left coronary occlusion 15 days after STZ. Thirty days after streptozocin-induced diabetes, cardiovascular autonomic modulation was evaluated by spectral analysis, and oxidative stress profile was determined by antioxidant enzyme activities and superoxide anion, together with protein carbonylation and redox balance of glutathione (GSH/GSSG). RESULTS: The diabetic and infarcted groups showed decreased heart rate variability and vagal modulation (p < 0.05); however, sympathetic modulation decreased only in diabetic groups (p < 0.05). Sympatho/vagal balance and vascular sympathetic modulation were increased only in the MI group (p < 0.05). Diabetes promoted an increase in catalase concentration (p < 0.05). Glutathione peroxidase activity was increased only in DMI when compared to the other groups (p < 0.05). Superoxide anion and protein carbonylation were increased only in MI group (p < 0.05). Cardiac redox balance, as evaluated by GSH/GSSG, was lower in the MI group (p < 0.05). CONCLUSIONS: These data suggest that hyperglycemia promotes compensatory mechanisms that may offer protection against ischemia, as demonstrated by increased antioxidants, decreased pro-oxidants and protein damage, possibly related to the improvements in both redox balance and sympathetic modulation to the heart.
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Diabetes Mellitus Experimental/metabolismo , Hiperglicemia/metabolismo , Infarto do Miocárdio/metabolismo , Estresse Oxidativo , Animais , Antioxidantes/farmacologia , Diabetes Mellitus Experimental/induzido quimicamente , Glutationa/metabolismo , Masculino , Infarto do Miocárdio/fisiopatologia , Estresse Oxidativo/efeitos dos fármacos , Ratos Wistar , Espécies Reativas de Oxigênio/metabolismo , EstreptozocinaRESUMO
BACKGROUND: Metabolic syndrome is characterized by the association of 3 or more risk factors, including: abdominal obesity associated with an excess of abdominal fat, insulin resistance, type 2 diabetes, dyslipidemia and hypertension. Moreover, the prevalence of hypertension and metabolic dysfunctions sharply increases after the menopause. However, the mechanisms involved in these changes are not well understood. Thus, the aim of this study was to assess the effects of fructose overload on cardiovascular autonomic modulation, inflammation and cardiac oxidative stress in an experimental model of hypertension and menopause. METHODS: Female SHR rats were divided into (n = 8/group): hypertensive (H), hypertensive ovariectomized (HO) and hypertensive ovariectomized undergoing fructose overload (100 g/L in drinking water) (FHO). Arterial pressure (AP) signals were directly recorded. Cardiac autonomic modulation was evaluated by spectral analysis. Oxidative stress was evaluated in cardiac tissue. RESULTS: AP was higher in the FHO group when compared to the other groups. Fructose overload promoted an increase in body and fat weight, triglyceride concentration and a reduction in insulin sensitivity. IL-10 was reduced in the FHO group when compared to the H group. TNF-α was higher in the FHO when compared to all other groups. Lipoperoxidation was higher and glutathione redox balance was reduced in the FHO group when compared to other groups, an indication of increased oxidative stress. A negative correlation was found between IL-10 and adipose tissue. CONCLUSION: Fructose overload promoted an impairment in cardiac autonomic modulation associated with inflammation and oxidative stress in hypertensive rats undergoing ovarian hormone deprivation.
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Sistema Nervoso Autônomo/fisiopatologia , Coração/inervação , Hipertensão/fisiopatologia , Menopausa/fisiologia , Síndrome Metabólica/fisiopatologia , Estresse Oxidativo/fisiologia , Adiposidade , Animais , Biomarcadores/sangue , Glicemia/metabolismo , Peso Corporal , Modelos Animais de Doenças , Feminino , Frutose , Hemodinâmica , Inflamação/fisiopatologia , Síndrome Metabólica/induzido quimicamente , Ratos Endogâmicos SHR , Triglicerídeos/sangueRESUMO
BACKGROUND: It has been suggested that exercise training (ET) protects against the pathological remodeling and ventricular dysfunction induced by myocardial infarction (MI). However, it remains unclear whether the positive adjustments on baroreflex and cardiac autonomic modulations promoted by ET may afford a cardioprotective mechanism. The aim of this study was to evaluate the effects of aerobic ET, prior to MI, on cardiac remodeling and function, as well as on baroreflex sensitivity and autonomic modulation in rats. METHODS: Male Wistar rats were divided into 4 groups: sedentary rats submitted to Sham surgery (C); trained rats submitted to Sham surgery (TC); sedentary rats submitted to MI (I), trained rats submitted to MI (TI). Sham and MI were performed after ET period. After surgeries, echocardiographic, hemodynamic and autonomic (baroreflex sensitivity, cardiovascular autonomic modulation) evaluations were conducted. RESULTS: Prior ET prevented an additional decline in exercise capacity in TI group in comparison with I. MI area was not modified by previous ET. ET was able to increase the survival and prevent additional left ventricle dysfunction in TI rats. Although changes in hemodynamic evaluations were not observed, ET prevented the decrease of baroreflex sensitivity, and autonomic dysfunction in TI animals when compared with I animals. Importantly, cardiac improvement was associated with the prevention of cardiac autonomic impairment in studied groups. CONCLUSIONS: Prior ET was effective in changing aerobic capacity, left ventricular morphology and function in rats undergoing MI. Furthermore, these cardioprotective effects were associated with attenuated cardiac autonomic dysfunction observed in trained rats. Although these cause-effect relationships can only be inferred, rather than confirmed, our study suggests that positive adaptations of autonomic function by ET can play a vital role in preventing changes associated with cardiovascular disease, particularly in relation to MI.
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Sistema Nervoso Autônomo/fisiopatologia , Terapia por Exercício , Infarto do Miocárdio/terapia , Disfunção Ventricular Esquerda/prevenção & controle , Função Ventricular Esquerda , Adaptação Fisiológica , Animais , Barorreflexo , Modelos Animais de Doenças , Tolerância ao Exercício , Hemodinâmica , Masculino , Infarto do Miocárdio/diagnóstico por imagem , Infarto do Miocárdio/fisiopatologia , Ratos Wistar , Comportamento Sedentário , Fatores de Tempo , Ultrassonografia , Disfunção Ventricular Esquerda/diagnóstico por imagem , Disfunção Ventricular Esquerda/fisiopatologia , Remodelação VentricularRESUMO
The cardiovascular autonomic imbalance in patients after myocardial infarction (MI) provides a significant increase in mortality rate, and seems to precede metabolic, hormonal, and immunological changes. Moreover, the reduction in the parasympathetic function has been associated with inflammatory response in different pathological conditions. Over the years, most of the studies have indicated the exercise training (ET) as an important nonpharmacological tool in the management of autonomic dysfunction and reduction in inflammatory profile after a myocardial infarction. In this work, we reviewed the effects of ET on autonomic imbalance after MI, and its consequences, particularly, in the post-MI inflammatory profile. Clinical and experimental evidence regarding relationship between alterations in autonomic regulation and local or systemic inflammation response after MI were also discussed.
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Vias Autônomas/fisiologia , Exercício Físico/fisiologia , Infarto do Miocárdio/metabolismo , Infarto do Miocárdio/fisiopatologia , HumanosRESUMO
BACKGROUND: Progressive exercise intolerance is a hallmark of pulmonary hypertension (pH), severely impacting patients' independence and quality of life (QoL). Accumulating evidence over the last decade shows that combined abnormalities in peripheral reflexes and target organs contribute to disease progression and exercise intolerance. OBJECTIVE: The aim of this study was to review the literature of the last decade on the contribution of the cardiovascular, respiratory, and musculoskeletal systems to pathophysiology and exercise intolerance in pH. METHODS: A systematic literature search was conducted using specific terms in PubMed, SciELO, and the Cochrane Library databases for original pre-clinical or clinical studies published between 2013 and 2023. Studies followed randomized controlled/non-randomized controlled and pre-post designs. RESULTS: The systematic review identified 25 articles reporting functional or structural changes in the respiratory, cardiovascular, and musculoskeletal systems in pH. Moreover, altered biomarkers in these systems, lower cardiac baroreflex, and heightened peripheral chemoreflex activity seemed to contribute to functional changes associated with poor prognosis and exercise intolerance in pH. Potential therapeutic strategies acutely explored involved manipulating the baroreflex and peripheral chemoreflex, improving cardiovascular autonomic control via cardiac vagal control, and targeting specific pathways such as GPER1, GDF-15, miR-126, and the JMJD1C gene. CONCLUSION: Information published in the last 10 years advances the notion that pH pathophysiology involves functional and structural changes in the respiratory, cardiovascular, and musculoskeletal systems and their integration with peripheral reflexes. These findings suggest potential therapeutic targets, yet unexplored in clinical trials, that could assist in improving exercise tolerance and QoL in patients with pH.
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Family history of hypertension is associated with early autonomic dysfunction and increased oxidative stress. These alterations have been found to be reinforced by the overweight factor. Conversely, an active lifestyle is effective in improving the mechanisms regulating blood pressure control. Hence, we ought to investigate the effects of an active lifestyle on the hemodynamic, autonomic and oxidative stress parameters in individuals carrying both family history of hypertension and overweight risk factors. Fifty-six normotensive males were divided into four groups: eutrophic offspring of normotensive parents (EN, n = 12), eutrophic and inactive with hypertensive parents (EH, n = 14), overweight and inactive with hypertensive parents (OH, n = 13), and overweight and physically active with hypertensive parents (OAH, n = 17). Cardiovascular autonomic modulation was assessed by heart rate (HRV) and blood pressure (BPV) variability indexes. Oxidative stress included pro/antioxidant markers and nitrite concentration. Inactive offspring of hypertensive parents (EH and OH) showed higher LFSBP (vs EN), an indicator of sympathetic outflow to the vasculature and reduced anti-oxidant activity (vs EN), while higher pro-oxidant markers were found exclusively in OH (vs EN and EH). Conversely, the OAH group showed bradycardia, higher vagally-mediated HFabs index (vs OH and EN), lower sympathovagal balance (vs OH) and preserved LFSBP. Yet, the OAH showed preserved pro/antioxidant markers and nitrite levels. Our findings indicates that overweight offspring of hypertensive parents with an active lifestyle have improved hemodynamic, cardiac autonomic modulation and oxidative stress parameters compared to their inactive peers.
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Sistema Nervoso Autônomo , Pressão Sanguínea , Frequência Cardíaca , Hipertensão , Sobrepeso , Estresse Oxidativo , Humanos , Masculino , Hipertensão/fisiopatologia , Hipertensão/genética , Sistema Nervoso Autônomo/fisiopatologia , Adulto , Sobrepeso/fisiopatologia , Sobrepeso/complicações , Exercício Físico , Pessoa de Meia-Idade , Fatores de RiscoRESUMO
Recent studies have found increased cardiovascular mortality risk in patients with type 1 diabetes when compared to normoglycemic people, even when they were kept under good glycemic control. However, the mechanisms underlying this condition have yet to be fully understood. Using streptozotocin (STZ)-induced diabetic rats, we evaluated the effects of insulin replacement therapy on cardiac, autonomic, inflammatory, and oxidative stress parameters. Daily treatment with insulin administrated subcutaneously in the STZ-diabetic rats showed a reduction in hyperglycemia (>250 mg/dL) to normalized values. The insulin treatment was effective in preventing alterations in cardiac morphometry and systolic function but had no impact on diastolic function. Also, the treatment was not able to prevent the impairment of baroreflex-tachycardic response and systolic arterial pressure variability (SAP-V). A correlation was found between improvement of these autonomic parameters and higher levels of IL-10 and lower levels of oxidized glutathione. Our findings show that insulin treatment was not able to prevent diastolic, baroreflex, and SAP-V dysfunction, suggesting an outstanding cardiovascular risk, even after obtaining a good glycemic control in STZ-induced diabetic rats. This study shed light on a relatively large population of diabetic patients in need of other therapies to be used in combination with insulin treatment and thus more effectively manage cardiovascular risk.
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OBJECTVE: The purpose of the research was to investigate the effects of aerobic training on renal function, oxidative stress, intrarenal renin-angiotensin system, and mortality of hypertensive and diabetic (SHR-STZ) rats. MATERIALS AND METHODS: Blood pressure, creatinine, urea levels, urinary glucose, urine volume, and protein excretion were reduced in trained SHR-STZ rats. RESULTS: Aerobic training not only attenuated oxidative stress but also elevated the activity of antioxidant enzymes in the kid'ney of SHR-STZ rats. Training increased intrarenal levels of angiotensin-converting enzymes (ACE and ACE2) as well as the neprilysin (NEP) activity, along with decreased intrarenal angiotensin II (Ang II) levels. Aerobic training significantly improved the survival of STZ-SHR rats. CONCLUSION: The protective role of aerobic training was associated with improvements in the renal antioxidative capacity, reduced urinary protein excretion along with reduced intrarenal Ang II and increased NEP activity. These findings might reflect a better survival under the combined pathological conditions, hypertension, and diabetes.
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AIM: Physical activity attenuates hypertension in older adults, but its impact on pulmonary function and mechanics in hypertensive older adults is unknown. The study seeks to understand whether a physically active lifestyle can improve respiratory capacity, the mechanical efficiency of the lungs, and, consequently, the quality of life of these individuals, comparing data between groups of active and sedentary hypertensive older adults. METHODS: This is a cross-sectional study. We evaluated 731 older adults, stratified into two initial groups: hypertensive older adults (HE; n = 445) and non-hypertensive older adults (NHE; n = 286). For a secondary analysis, we used the International Physical Activity Questionnaire to sub-stratify HE and NHE into four groups: physically inactive hypertensive (PIH; n = 182), active hypertensive (AH; n = 110), physically inactive non-hypertensive (PINH; n = 104), and active non-hypertensive (ANH; n = 65). Lung function was measured by spirometry, and lung mechanics were assessed by impulse oscillometry. RESULTS: Hypertensive older adults presented reduced lung function compared to non-hypertensive older adults, and physical inactivity accentuated this decline. Regarding pulmonary mechanics, hypertensive older adults had higher resistance of the entire respiratory system (R5 Hz), the central airways (R20 Hz), and peripheral airways (R5-20 Hz), which may trigger bronchoconstriction. CONCLUSIONS: Hypertension is associated with impaired lung function and mechanics in older adults, and a physically active lifestyle attenuates these dysfunctions.