Síncope Neurocardiogênica e Exercício

A síncope neurocardiogênica acomete, na grande maioria das vezes, pessoas jovens, aparentemente normais, e que, com a recorrência de sintomas, passam a apresentar limitaçoes quanto às atividades de vida diária e profissional. O tratamento convencional, realizado com base nas medidas gerais (aumento na ingestao de líquidos, evitar situaçoes desencadeantes e outras), e drogas, como beta-bloqueadores, fludrocortisona e inibidores de recaptaçao de serotonina, nem sempre é eficaz em diminuir a freqüência e a intensidade dos episódios sincopais. Cada vez mais, buscam-se, em todo o mundo, medidas de caráter nao-farmacológico para minimizar a ocorrência de sintomas. Nesse aspecto, e com base na fisiopatologia das síncopes neuromediadas, recursos como

Síncope Neurocardiogênica e Exercício

A síncope neurocardiogênica acomete, na grande maioria das vezes, pessoas jovens, aparentemente normais, e que, com a recorrência de sintomas, passam a apresentar limitaçoes quanto às atividades de vida diária e profissional. O tratamento convencional, realizado com base nas medidas gerais (aumento na ingestao de líquidos, evitar situaçoes desencadeantes e outras), e drogas, como beta-bloqueadores, fludrocortisona e inibidores de recaptaçao de serotonina, nem sempre é eficaz em diminuir a freqüência e a intensidade dos episódios sincopais. Cada vez mais, buscam-se, em todo o mundo, medidas de caráter nao-farmacológico para minimizar a ocorrência de sintomas. Nesse aspecto, e com base na fisiopatologia das síncopes neuromediadas, recursos como

Comparison of Electrocardiographic Criteria for Identifying Left Ventricular Hypertrophy in Athletes from Different Sports Modalities

OBJECTIVES: In athletes, isolated electrocardiogram high voltage criteria are widely used to evaluate left ventricular hypertrophy, but positive findings are thought to represent normal electrocardiogram alterations. However, which electrocardiogram criterion can best detect left ventricular hypertrophy in athletes of various sport modalities remains unknown. METHODS: Five electrocardiogram criteria used to detect left ventricular hypertrophy were tested in 180 male athletes grouped according to their sport modality: 67% low-static and high-dynamic components and 33% high-static and high-dynamic components of exercise. The following echocardiogram parameters are the gold standard for diagnosing left ventricular hypertrophy: left ventricular mass index ≥134 g.m-2, relative wall thickness ≥0.42 mm, left ventricular diastolic diameter index ≥32 mm.m-2, septum wall thickness ≥13 mm, and posterior wall thickness ≥13 mm. Results for the various criteria were compared using the kappa coefficient. Significance was established at

Effects of Exercise Training on Circulating and Skeletal Muscle Renin-Angiotensin System in Chronic Heart Failure Rats

Background: Accumulated evidence shows that the ACE-AngII-AT1 axis of the renin-angiotensin system (RAS) is markedly activated in chronic heart failure (CHF). Recent studies provide information that Angiotensin (Ang)-(1-7), a metabolite of AngII, counteracts the effects of AngII. However, this balance between AngII and Ang-(1-7) is still little understood in CHF. We investigated the effects of exercise training on circulating and skeletal muscle RAS in the ischemic model of CHF.Methods/Main Results: Male Wistar rats underwent left coronary artery ligation or a Sham operation. They were divided into four groups: 1) Sedentary Sham (Sham-S), 2) exercise-trained Sham (Sham-Ex), sedentary CHF (CHF-S), and exercise-trained CHF (CHF-Ex). Angiotensin concentrations and ACE and ACE2 activity in the circulation and skeletal muscle (soleus and plantaris) were quantified. Skeletal muscle ACE and ACE2 protein expression, and AT1, AT2, and Mas receptor gene expression were also evaluated. CHF reduced ACE2 serum activity. Exercise training restored ACE2 and reduced ACE activity in CHF. Exercise training reduced plasma AngII concentration in both Sham and CHF rats and increased the Ang-(1-7)/AngII ratio in CHF rats. CHF and exercise training did not change skeletal muscle ACE and ACE2 activity and protein expression. CHF increased AngII levels in both soleus and plantaris muscle, and exercise training normalized them. Exercise training increased Ang-(1-7) in the plantaris muscle of CHF rats. the AT1 receptor was only increased in the soleus muscle of CHF rats, and exercise training normalized it. Exercise training increased the expression of the Mas receptor in the soleus muscle of both exercise-trained groups, and normalized it in plantaris muscle.Conclusions: Exercise training causes a shift in RAS towards the Ang-(1-7)-Mas axis in skeletal muscle, which can be influenced by skeletal muscle metabolic characteristics. the changes in RAS circulation do not necessarily reflect the changes occurring in the RAS of skeletal muscle.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Fundacao ZerbiniCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Univ São Paulo, Sch Med, Heart Inst InCor HCFMUSP, São Paulo, BrazilUniv São Paulo, Sch Phys Educ & Sport, São Paulo, BrazilUniv São Paulo, Inst Biomed Sci, Dept Physiol & Biophys, São Paulo, BrazilUniversidade Federal de São Paulo, Kidney & Hypertens Hosp, Div Nephrol, São Paulo, BrazilUniversidade Federal de São Paulo, Kidney & Hypertens Hosp, Div Nephrol, São Paulo, BrazilFAPESP: FAPESP-2010/50048-1Web of Scienc

Testing a global standard for quantifying species recovery and assessing conservation impact.

Recognizing the imperative to evaluate species recovery and conservation impact, in 2012 the International Union for Conservation of Nature (IUCN) called for development of a "Green List of Species" (now the IUCN Green Status of Species). A draft Green Status framework for assessing species' progress toward recovery, published in 2018, proposed 2 separate but interlinked components: a standardized method (i.e., measurement against benchmarks of species' viability, functionality, and preimpact distribution) to determine current species recovery status (herein species recovery score) and application of that method to estimate past and potential future impacts of conservation based on 4 metrics (conservation legacy, conservation dependence, conservation gain, and recovery potential). We tested the framework with 181 species representing diverse taxa, life histories, biomes, and IUCN Red List categories (extinction risk). Based on the observed distribution of species' recovery scores, we propose the following species recovery categories: fully recovered, slightly depleted, moderately depleted, largely depleted, critically depleted, extinct in the wild, and indeterminate. Fifty-nine percent of tested species were considered largely or critically depleted. Although there was a negative relationship between extinction risk and species recovery score, variation was considerable. Some species in lower risk categories were assessed as farther from recovery than those at higher risk. This emphasizes that species recovery is conceptually different from extinction risk and reinforces the utility of the IUCN Green Status of Species to more fully understand species conservation status. Although extinction risk did not predict conservation legacy, conservation dependence, or conservation gain, it was positively correlated with recovery potential. Only 1.7% of tested species were categorized as zero across all 4 of these conservation impact metrics, indicating that conservation has, or will, play a role in improving or maintaining species status for the vast majority of these species. Based on our results, we devised an updated assessment framework that introduces the option of using a dynamic baseline to assess future impacts of conservation over the short term to avoid misleading results which were generated in a small number of cases, and redefines short term as 10 years to better align with conservation planning. These changes are reflected in the IUCN Green Status of Species Standard

Sleep-related changes in hemodynamic and autonomic regulation in human hypertension

Objectives The present study investigates the hemodynamic and autonomic regulation during sleep-awake transitions and across different sleep cycles in patients with essential hypertension. Methods Nineteen individuals free of sleep apnea (10 normotensive and nine hypertensive matched for age, sex, and body mass index) underwent a standard polysomnography, with simultaneous electrocardiography and beat-to-beat blood pressure monitoring (Portapres). All measurements were determined while awake (before and after sleep), as well as in the beginning and at end of the sleep cycle (first/last cycle of nonrapid and rapid eye movement stages). Results Systolic blood pressure was higher in hypertensives and exhibited a similar reduction to the normotensives ones in initial nonrapid eye movement sleep. This reduction was because of different mechanisms: a significant fall in cardiac output in normotensives, whereas in hypertensives was also dependent of a decrease in peripheral vascular resistance. Hypertensive patients presented lower heart rate variation and attenuated baroreflex sensitivity during sleep but not immediately before and after sleep. Spectral analysis suggested a higher sympathetic activity in the sleep stages in hypertension. Additionally, a progressive sympathetic predominance (final rapid eye movement> initial rapid eye movement and awake period postsleep> awake period presleep) was observed in both groups. Conclusion Hypertension is associated with depressed baroreflex sensitivity and increased sympathetic activation during sleep. The greater sympathetic predominance at the end of night (preceding the morning surge of sympathetic activity) could be implicated in the occurrence of cardiovascular events. J Hypertens 27: 1655-1663 (C) 2009 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.FAPESPCNPqFundacao Zerbini

Comparison of Electrocardiographic Criteria for Identifying Left Ventricular Hypertrophy in Athletes from Different Sports Modalities

OBJECTIVES: In athletes, isolated electrocardiogram high voltage criteria are widely used to evaluate left ventricular hypertrophy, but positive findings are thought to represent normal electrocardiogram alterations. However, which electrocardiogram criterion can best detect left ventricular hypertrophy in athletes of various sport modalities remains unknown. METHODS: Five electrocardiogram criteria used to detect left ventricular hypertrophy were tested in 180 male athletes grouped according to their sport modality: 67% low-static and high-dynamic components and 33% high-static and high-dynamic components of exercise. The following echocardiogram parameters are the gold standard for diagnosing left ventricular hypertrophy: left ventricular mass index ≥134 g.m-2, relative wall thickness ≥0.42 mm, left ventricular diastolic diameter index ≥32 mm.m-2, septum wall thickness ≥13 mm, and posterior wall thickness ≥13 mm. Results for the various criteria were compared using the kappa coefficient. Significance was established at p<0.05. RESULTS: Fifty athletes (28%) presented with left ventricular hypertrophy according to electrocardiogram findings, with the following sensitivities and specificities, respectively: 38-53% and 79-83% (Perugia), 22-40% and 89-91% (Cornell), 24-29% and 90% (Romhilt-Estes), 68-87% and 20-23% (Sokolow-Lyon), and 0% and 99% (Gubner). The Perugia and Cornell criteria had higher negative predictive values for the low-static and high-dynamic subgroup. Kappa coefficients were higher for Romhilt-Estes, Cornell and Perugia criteria than for Sokolow-Lyon and Gubner criteria. CONCLUSION: All five evaluated criteria are inadequate for detecting left ventricular hypertrophy, but the Perugia, Cornell and Romhilt-Estes criteria are useful for excluding its presence. The Perugia and Cornell criteria were more effective at excluding left ventricular hypertrophy in athletes involved in a sport modality with low-static and high-dynamic component predominance

Aerobic exercise training in heart failure: impact on sympathetic hyperactivity and cardiac and skeletal muscle function

Heart failure is a common endpoint for many forms of cardiovascular disease and a significant cause of morbidity and mortality. Chronic neurohumoral excitation (i.e., sympathetic hyperactivity) has been considered to be a hallmark of heart failure and is associated with a poor prognosis, cardiac dysfunction and remodeling, and skeletal myopathy. Aerobic exercise training is efficient in counteracting sympathetic hyperactivity and its toxic effects on cardiac and skeletal muscles. In this review, we describe the effects of aerobic exercise training on sympathetic hyperactivity, skeletal myopathy, as well as cardiac function and remodeling in human and animal heart failure. We also discuss the mechanisms underlying the effects of aerobic exercise training.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Univ Sao Paulo, Dept Biodinam Movimento Corpo Humano, Escola Educ Fis & Esporte, BR-05508900 Sao Paulo, BrazilUniv Fed Sao Paulo, Dept Biociencias, Santos, SP, BrazilStanford Univ, Dept Chem & Syst Biol, Palo Alto, CA 94304 USAUniv Sao Paulo, Fac Med, Inst Coracao, BR-05508900 Sao Paulo, BrazilUniv Fed Sao Paulo, Dept Biociencias, Santos, SP, BrazilFAPESP: 2002/04558-8FAPESP: 2005/59740-7FAPESP: 2006/61523-7FAPESP: 2008/50777-3FAPESP 2009/03143-1CNPq: 473251/2009-4CNPq: BPQ 301519/2008-0Web of Scienc

Exercise Training and Caloric Restriction Prevent Reduction in Cardiac Ca2+-Handling Protein Profile in Obese Rats

Previous studies show that exercise training and caloric restriction improve cardiac function in obesity. However, the molecular mechanisms underlying this effect on cardiac function remain unknown. Thus, we studied the effect of exercise training and/or caloric restriction on cardiac function and Ca2+ handling protein expression in obese rats. To accomplish this goal, male rats fed with a high-fat and sucrose diet for 25 weeks were randomly assigned into 4 groups: high-fat and sucrose diet, high-fat and sucrose diet and exercise training, caloric restriction, and exercise training and caloric restriction. An additional lean group was studied. The study was conducted for 10 weeks. Cardiac function was evaluated by echocardiography and Ca2+ handling protein expression by Western blotting. Our results showed that visceral fat mass, circulating leptin, epinephrine, and norepinephrine levels were higher in rats on the high-fat and sucrose diet compared with the lean rats. Cardiac nitrate levels, reduced/oxidized glutathione, left ventricular fractional shortening, and protein expression of phosphorylated Ser(2808)-ryanodine receptor and Thr(17-)phospholamban were lower in rats on the high-fat and sucrose diet compared with lean rats. Exercise training and/or caloric restriction prevented increases in visceral fat mass, circulating leptin, epinephrine, and norepinephrine levels and prevented reduction in cardiac nitrate levels and reduced: oxidized glutathione ratio. Exercise training and/or caloric restriction prevented reduction in left ventricular fractional shortening and in phosphorylation of the Ser(2808)-ryanodine receptor and Thr(17)-phospholamban. These findings show that exercise training and/or caloric restriction prevent cardiac dysfunction in high-fat and sucrose diet rats, which seems to be attributed to decreased circulating neurohormone levels. In addition, this nonpharmacological paradigm prevents a reduction in the Ser(2808)-ryanodine receptor and Thr(17-)phospholamban phosphorylation and redox status. (Hypertension. 2010;56:629-635.)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP