Moderate-intensity aerobic training reduces cardiac damage attributable to experimental iron overload in rats.

NEW FINDINGS: What is the central question of this study? The current literature indicates that oxidative stress plays a major role in iron overload. Although exercise is a well-established approach to treat/prevent cardiovascular diseases, its effects on iron overload are not known. What is the main finding and its importance? Moderate-intensity aerobic training had benefits in a rodent model of iron-overload cardiomyopathy by improving the antioxidant capacity of the heart. After further confirmation by translational and clinical studies, we should consider using this non-pharmacological, highly accessible and easily executable adjuvant approach allied to other therapies to improve the quality of life of iron-overloaded patients. ABSTRACT: Iron is an essential micronutrient for several life processes, but its excess can damage organs owing to oxidative stress, with cardiomyopathy being the leading cause of death in iron-overloaded patients. Although exercise has long been considered as a cardioprotective tool, its effects on iron overload are not known. This study was designed to investigate the effects of moderate-intensity aerobic training in rats previously submitted to chronic iron overload. Wistar rats received i.p. injections of iron dextran (100 mg/kg, 5 days/week for 4 weeks); thereafter, the rats were kept sedentary or exercised (60 min/day, progressive aerobic training, 60-70% of maximal speed, 5 days/week on a treadmill) for 8 weeks. At the end of the experimental period, haemodynamics were recorded and blood samples, livers and hearts harvested. Myocardial mechanics of papillary muscles were assessed in vitro, and cardiac remodelling was evaluated by histology and immunoblotting. Iron overload led to liver iron deposition, liver fibrosis and increased serum alanine aminotransferase and aspartate aminotransferase. Moreover, cardiac iron accumulation was accompanied by impaired myocardial mechanics, increased cardiac collagen type I and lipid peroxidation (TBARS), and release of creatine phosphokinase-MB to the serum. Although exercise did not influence iron levels, tissue injury markers were significantly reduced. Likewise, myocardial contractility and inotropic responsiveness were improved in exercised rats, in association with an increase in the endogenous antioxidant enzyme catalase. In conclusion, moderate-intensity aerobic exercise was associated with attenuated oxidative stress and cardiac damage in a rodent model of iron overload, thereby suggesting its potential role as a non-pharmacological adjuvant therapy for iron-overload cardiomyopathy.

Chronic Iron Overload Restrains the Benefits of Aerobic Exercise to the Vasculature.

Physical exercise is a well-recognized effective non-pharmacological therapy for cardiovascular diseases. However, because iron is essential element in many physiological processes including hemoglobin and myoglobin synthesis, thereby playing a role on oxygen transport, many athletes use iron supplement to improve physical performance. Regarding this, iron overload is associated with oxidative stress and damage to various systems, including cardiovascular. Thus, we aimed to identify the vascular effects of aerobic exercise in a rat model of iron overload. Male Wistar rats were treated with 100 mg/kg/day iron-dextran, i.p., 5 days a week for 4 weeks, and then underwent aerobic exercise protocol on a treadmill at moderate intensity, 60 min/day, 5 days a week for 8 weeks. Exercise reduced vasoconstrictor response of isolated aortic rings by increasing participation of nitric oxide (NO) and reducing oxidative stress, but these benefits to the vasculature were not observed in rats previously subjected to iron overload. The reduced vasoconstriction in the exercised group was reversed by incubation with superoxide dismutase (SOD) inhibitor, suggesting that increased SOD activity by exercise was lost in iron overload rats. Iron overload groups increased serum levels of iron, transferrin saturation, and iron deposition in the liver, gastrocnemius muscle, and aorta, and the catalase was overexpressed in the aorta probably as a compensatory mechanism to the increased oxidative stress. In conclusion, despite the known beneficial effects of aerobic exercise on vasculature, our results indicate that previous iron overload impeded the anticontractile effect mediated by increased NO bioavailability and endogenous antioxidant response due to exercise protocol.

Equidade na promoção das práticas corporais e atividades físicas no SUS: reflexões a partir do serviço de orientação ao exercício / Equity in the promotion of body practices and physical activities in SUS: reflections from the exercise guidance service / Equidad en la promoción de prácticas corporales y actividades físicas en SUS: reflexiones desde el servicio de orientación en ejercicio

A equidade é um dos princípios constitucionais e dou-trinários do Sistema Único de Saúde (SUS), assim como da Política Nacional de Promoção da Saúde, principal marco das Práticas Corporais e Atividades Físicas (PCAF) no referido sistema. Considerando as desigualdades sociais gerais e as iniquidades em saúde, a equidade deve ser prioritária. Assim, o trabalho, de caráter ensaístico, teve como objetivo apresentar a experiência do Serviço de Orientação ao Exercício na operacionalização des-te princípio. Foram abordados aspectos relacionados ao acesso, recursos, resultados e desafios para indicar possibilidades e ca-minhos para a efetivação da equidade na promoção das PCAF no SUS, visando o seu fortalecimento e qualificação como sistema de saúde universal, integral e equânime.

Equity is one of the constitutional and doctrinal principles of the Unified Health System (SUS), as well as of the National Health Promotion Policy, the main framework for Body Practices and Physical Activities (PCAF) in this system. Considering the general social inequalities and inequities in health, equity must be a priority. The aim of this essay was to present the experience of the Exercise Guidance Service in operationalizing this principle. Aspects related to access, resources, results and challenges were addressed in order to indicate possibilities and paths towards the realization of equity in the promotion of PCAF in the SUS, with a view to strengthening and qualifying it as a universal, comprehensive and equitable health system.

La equidad es uno de los principios constitucionales y doctrinales del Sistema Único de Salud (SUS), así como de la Política Nacional de Promoción de la Salud, marco principal de las Prácticas Corporales y Actividades Físicas (PCAF) de este sistema. Considerando las desigualdades sociales generales y las inequidades en salud, la equidad debe ser priorizada. El objetivo de este ensayo era, por tanto, presentar la experiencia del Servicio de Orientación para el Ejercicio en la puesta en práctica de este principio. Se analizaron aspectos relacionados con el acceso, los recursos, los resultados y los desafíos, a fin de indicar posibilidades y formas de hacer realidad la equidad en la promoción del PCAF en el SUS, con miras a fortalecerlo y calificarlo como sistema de salud universal, integral y equitativo.

Chronic iron overload induces vascular dysfunction in resistance pulmonary arteries associated with right ventricular remodeling in rats.

Although iron excess is toxic to the vasculature and even that pulmonary hypertension has been reported in this scenario, the role of iron overload per se remains to be clarified. This study aimed to test the effects of chronic iron-overload in rats on the morphophysiology of resistance pulmonary arteries (RPA) and right ventricle (RV) remodeling. Rats were injected with saline or iron-dextran (10, 100 and 200 mg/kg/day i.p.) for 28 days. Our results indicated increased circulating iron with significant lung deposits. Moreover, rats treated with the highest dose exhibited RV dysfunction and hypertrophy; inward remodeling and increased vasoconstriction of the RPA. Vascular hyperreactivity was accompanied by reduced nitric oxide (NO), and was reversed by incubation with Dimethylsulfoxide, Catalase and Tempol. The NADPH oxidase subunit gp91phox was increased due to iron-overload, and incubation with angiotensin II type-1 receptor (AT1) antagonist losartan not only reduced oxidative stress but also restored vascular function. Thus, we concluded that AT1 pathway plays a role in pulmonary vascular dysfunction by increasing oxidative stress and reducing NO bioavailability, thereby contributing to vascular remodeling and pulmonary hypertension of iron-overload. This finding should instigate future studies on the beneficial impacts of in vivo blockade of AT1 receptor under iron overload.

Post-exercise hypotension and heart rate variability response after water- and land-ergometry exercise in hypertensive patients.

BACKGROUND: systemic arterial hypertension is the most prevalent cardiovascular disease; physical activity for hypertensive patients is related to several beneficial cardiovascular adaptations. This paper evaluated the effect of water- and land-ergometry exercise sessions on post-exercise hypotension (PEH) of healthy normotensive subjects versus treated or untreated hypertensive patients. METHODS: Forty-five older women composed three experimental groups: normotensive (N, n = 10), treated hypertensive (TH, n = 15) and untreated hypertensive (UH, n = 20). The physical exercise acute session protocol was performed at 75% of maximum oxygen consumption (VO2max) for 45 minutes; systolic (SBP), diastolic (DBP) and mean (MBP) blood pressure were evaluated at rest, peak and at 15, 30, 45, 60, 75 and 90 minutes after exercise cessation. Additionally, the heart rate variability (HRV) was analyzed by R-R intervals in the frequency domain for the assessment of cardiac autonomic function. RESULTS: In both exercise modalities, equivalent increases in SBP were observed from rest to peak exercise for all groups, and during recovery, significant PEH was noted. At 90 minutes after the exercise session, the prevalence of hypotension was significantly higher in water- than in the land-based protocol. Moreover, more pronounced reductions in SBP and DBP were observed in the UH patients compared to TH and N subjects. Finally, exercise in the water was more effective in restoring HRV during recovery, with greater effects in the untreated hypertensive group. CONCLUSION: Our data demonstrated that water-ergometry exercise was able to induce expressive PEH and improve cardiac autonomic modulation in older normotensive, hypertensive treated or hypertensive untreated subjects when compared to conventional land-ergometry.