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Abstract Fluid volume and hemodynamic management in hemodialysis patients is an essential component of dialysis adequacy. Restoring salt and water homeostasis in hemodialysis patients has been a permanent quest by nephrologists summarized by the 'dry weight' probing approach. Although this clinical approach has been associated with benefits on cardiovascular outcome, it is now challenged by recent studies showing that intensity or aggressiveness to remove fluid during intermittent dialysis is associated with cardiovascular stress and potential organ damage. A more precise approach is required to improve cardiovascular outcome in this high-risk population. Fluid status assessment and monitoring rely on four components: clinical assessment, non-invasive instrumental tools (e.g., US, bioimpedance, blood volume monitoring), cardiac biomarkers (e.g. natriuretic peptides), and algorithm and sodium modeling to estimate mass transfer. Optimal management of fluid and sodium imbalance in dialysis patients consist in adjusting salt and fluid removal by dialysis (ultrafiltration, dialysate sodium) and by restricting salt intake and fluid gain between dialysis sessions. Modern technology using biosensors and feedback control tools embarked on dialysis machine, with sophisticated analytics will provide direct handling of sodium and water in a more precise and personalized way. It is envisaged in the near future that these tools will support physician decision making with high potential of improving cardiovascular outcome.

Resumo O volume de fluidos e o controle hemodinâmico em pacientes em hemodiálise é um componente essencial da adequação da diálise. A restauração da homeostase do sal e da água em pacientes em hemodiálise tem sido uma busca constante por parte dos nefrologistas, no que condiz à abordagem do "peso seco. Embora essa abordagem clínica tenha sido associada a benefícios no desfecho cardiovascular, recentemente tem sido questionada por estudos que mostram que a intensidade ou agressividade para remover fluidos durante a diálise intermitente está associada a estresse cardiovascular e dano potencial a órgãos.para remover fluidos durante a diálise intermitente está associada a estresse cardiovascular e dano potencial a órgãos. Uma abordagem mais precisa é necessária para melhorar o desfecho cardiovascular nessa população de alto risco. A avaliação e monitorização do estado hídrico baseiam-se em quatro componentes: avaliação clínica, ferramentas instrumentais não invasivas (por exemplo, US, bioimpedância, monitorização do volume sanguíneo), biomarcadores cardíacos (e.g. peptídeos natriuréticos), algoritmos e modelagem de sódio para estimar a transferência de massa. O manejo otimizado do desequilíbrio hídrico e de sódio em pacientes dialíticos consiste em ajustar a remoção de sal e líquido por diálise (ultrafiltração, dialisato de sódio), e restringir a ingestão de sal e o ganho de líquido entre as sessões de diálise. Tecnologia moderna que utiliza biosensores e ferramentas de controle de feedback, hoje parte da máquina de diálise, com análises sofisticadas, proporcionam o manejo direto sobre o sódio e a água de uma maneira mais precisa e personalizada. Prevê-se no futuro próximo que essas ferramentas poderão auxiliar na tomada de decisão do médico, com alto potencial para melhorar o resultado cardiovascular.

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Fluid volume and hemodynamic management in hemodialysis patients is an essential component of dialysis adequacy. Restoring salt and water homeostasis in hemodialysis patients has been a permanent quest by nephrologists summarized by the 'dry weight' probing approach. Although this clinical approach has been associated with benefits on cardiovascular outcome, it is now challenged by recent studies showing that intensity or aggressiveness to remove fluid during intermittent dialysis is associated with cardiovascular stress and potential organ damage. A more precise approach is required to improve cardiovascular outcome in this high-risk population. Fluid status assessment and monitoring rely on four components: clinical assessment, non-invasive instrumental tools (e.g., US, bioimpedance, blood volume monitoring), cardiac biomarkers (e.g. natriuretic peptides), and algorithm and sodium modeling to estimate mass transfer. Optimal management of fluid and sodium imbalance in dialysis patients consist in adjusting salt and fluid removal by dialysis (ultrafiltration, dialysate sodium) and by restricting salt intake and fluid gain between dialysis sessions. Modern technology using biosensors and feedback control tools embarked on dialysis machine, with sophisticated analytics will provide direct handling of sodium and water in a more precise and personalized way. It is envisaged in the near future that these tools will support physician decision making with high potential of improving cardiovascular outcome.

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BACKGROUND: Breast cancer is one of the leading causes of death worldwide. Heart rate variability (HRV) has attracted scientific community attention in different pathologies, becoming thus an ultimate importance tool in both clinical and research setting, being a good predictor of cardiac events and mortality risk and also used in physical exercise and sports in general. The aim of the present study was to evaluate 12 weeks of exercise training and six weeks of detraining in cardiorespiratory capacity, and autonomic modulation in breast cancer patients. METHODS: The sample was composed of 18 females (9 controls and 9 exercised), (aged 30-60 years). The HRV in the time and frequency domain was performed using an electrocardiogram before, after 12 weeks of the session of exercise training and after six weeks of detraining. Shapiro-Wilk and Mann-Whitney tests were made. RESULTS: No significant changes in time domain were found. In the frequency domain, 12 weeks of exercise training promote a decrease in LF (nu) and decrease in HF (nu) Index. The exercise training period promoted a decrease in LF/HF. The autonomic data returned to baseline levels after the detraining period. However, cardiorespiratory capacity remained increased after the detraining period. CONCLUSIONS: These data demonstrated that exercise training can be used to prevent autonomic dysfunction in breast cancer patients, but detraining promotes loss of all autonomic benefits.

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INTRODUCTION: Detraining is the loss of improvements obtained through the participation in physical exercise/training after training cessation, an aspect that has been poorly studied in obese child population. Therefore, the purpose of this study was to assess the effects of detraining on the lipid profile (HDL, LDL, total cholesterol and triglycerides) of obese children. POPULATION AND METHODS: Studies were collected through a search across seven databases. The search was limited to physical exercise programs that lasted, at least, eight weeks and the corresponding detraining, with an assessment of obese children lipid profile. Effect size (ES), 95% confidence intervals and study heterogeneity were estimated using Cochran's Q test (random effects model). RESULTS: Five studies complied with the inclusion criteria and were selected for review (n= 330). In general, intra-group results (posttest versus detraining) indicated that, following detraining, blood levels of HDL cholesterol (ES= 0.12) and total cholesterol (ES= 1.41) were increased. Likewise, inter-group results (experimental group versus control group) confirmed the increase of HDL cholesterol following detraining (ES= 0.49). CONCLUSIONS: The results of this systematic review suggest that detraining after a physical exercise program does not lead to a significant loss of the benefits gained in relation to the lipid profile of obese children. However, given the number of analyzed studies and the heterogeneity observed in the analyses and the period defined as detraining (12 to 48 weeks), a higher number of well designed studies is required to obtain more conclusive results.

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Despite the advances in the treatment and prevention, myocardial infarction (MI) remains the leading causeof morbidity and mortality worldwide. Different degrees of ventricular dysfunction, changes in hemodynamicand molecular mechanisms, as well as neurohumoral derangements, are substantially associated with increasedmortality rate in MI patients. Cardiovascular, metabolic and autonomic benefits of acute and chronic exercise training (ET) have led many researchers to suggest ET as an important tool in the management of coronary artery disease and after MI. Regarding cardiovascular rehabilitation, several factors, such as illness, injury, travel, vacation or even rehabilitation program discharge may often interfere with the ET process, leading toa disruption in physical activity patterns by either decreasing training level or frequency or interrupting thetraining program altogether. Thus, it is necessary to identify the impact of ET after MI, as well as the possibleconsequences of such disruption in infarcted individuals.

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We determined the effects of exercise training and detraining on the morphological and mechanical properties of left ventricular myocytes in 4-month-old spontaneously hypertensive rats (SHR) randomly divided into the following groups: sedentary for 8 weeks (SED-8), sedentary for 12 weeks (SED-12), treadmill-running trained for 8 weeks (TRA, 16 m/min, 60 min/day, 5 days/week), and treadmill-running trained for 8 weeks followed by 4 weeks of detraining (DET). At sacrifice, left ventricular myocytes were isolated enzymatically, and resting cell length, width, and cell shortening after stimulation at a frequency of 1 Hz (~25°C) were measured. Cell length was greater in TRA than in SED-8 (161.30 ± 1.01 vs 156.10 ± 1.02 µm, P < 0.05, 667 vs 618 cells, respectively) and remained larger after detraining. Cell width and volume were unaffected by either exercise training or detraining. Cell length to width ratio was higher in TRA than in SED-8 (8.50 ± 0.08 vs 8.22 ± 0.10, P < 0.05) and was maintained after detraining. Exercise training did not affect cell shortening, which was unchanged with detraining. TRA cells exhibited higher maximum velocity of shortening than SED-8 (102.01 ± 4.50 vs 82.01 ± 5.30 µm/s, P < 0.05, 70 cells per group), with almost complete regression after detraining. The maximum velocity of relengthening was higher in TRA cells than in SED-8 (88.20 ± 4.01 vs70.01 ± 4.80 µm/s, P < 0.05), returning to sedentary values with detraining. Therefore, exercise training affected left ventricle remodeling in SHR towards eccentric hypertrophy, which remained after detraining. It also improved single left ventricular myocyte contractile function, which was reversed by detraining.

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We determined the effects of exercise training and detraining on the morphological and mechanical properties of left ventricular myocytes in 4-month-old spontaneously hypertensive rats (SHR) randomly divided into the following groups: sedentary for 8 weeks (SED-8), sedentary for 12 weeks (SED-12), treadmill-running trained for 8 weeks (TRA, 16 m/min, 60 min/day, 5 days/week), and treadmill-running trained for 8 weeks followed by 4 weeks of detraining (DET). At sacrifice, left ventricular myocytes were isolated enzymatically, and resting cell length, width, and cell shortening after stimulation at a frequency of 1 Hz (~25°C) were measured. Cell length was greater in TRA than in SED-8 (161.30 ± 1.01 vs 156.10 ± 1.02 μm, P < 0.05, 667 vs 618 cells, respectively) and remained larger after detraining. Cell width and volume were unaffected by either exercise training or detraining. Cell length to width ratio was higher in TRA than in SED-8 (8.50 ± 0.08 vs 8.22 ± 0.10, P < 0.05) and was maintained after detraining. Exercise training did not affect cell shortening, which was unchanged with detraining. TRA cells exhibited higher maximum velocity of shortening than SED-8 (102.01 ± 4.50 vs 82.01 ± 5.30 μm/s, P < 0.05, 70 cells per group), with almost complete regression after detraining. The maximum velocity of relengthening was higher in TRA cells than in SED-8 (88.20 ± 4.01 vs70.01 ± 4.80 μm/s, P < 0.05), returning to sedentary values with detraining. Therefore, exercise training affected left ventricle remodeling in SHR towards eccentric hypertrophy, which remained after detraining. It also improved single left ventricular myocyte contractile function, which was reversed by detraining.

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Exercise training is assumed to improve myocardial function; however, the role of detraining and its effect on myocardial parameters are still unclear. The aim of the present study was to evaluate the effect of detraining on ventricular remodeling and myocardial mechanical parameters after an 8 week (5 days/week, 60 min/day) swimming training period. Forty-three female Wistar rats were distributed into six groups: trained (T, n = 9), detrained 2 weeks (D2, n = 8), detrained 4 weeks (D4, n = 8) and their respective controls: untrained (U, n = 5), untrained 2 weeks (U2, n = 5) and untrained 4 weeks (U4, n = 5). Detrained rats underwent training and then remained sedentary (i.e., "detraining") for 2 or 4 weeks. After training, the T group demonstrated increased physical capacity, left ventricular (LV) posterior wall thickness, and LV end-diastolic diameter, along with decreased heart rate, as evaluated by echocardiogram. In addition, the inotropism and lusitropism parameters studied on papillary muscles showed improvement in the T group (P < 0.05). However, after just 2 weeks of detraining, all parameters regressed back to values which were similar to those of the untrained groups. In conclusion, our results confirmed that exercise training is capable of inducing myocardial remodeling and improving contractile performance; however, these changes are completely lost after a short period of detraining.

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OBJECTIVE: To determine the extent and severity of obesity-related cardiorespiratory morbidity in children with body mass index (BMI) >or=40 kg/m(2). STUDY DESIGN: Cross-sectional analysis of a cohort comprised of 48 boys and girls aged 8 to 17 years with BMI >or=40 kg/m(2). Cardiorespiratory fitness (graded cycle exercise test), left ventricular (LV) mass (echocardiography), blood pressure, fasting lipid profile, fasting insulin, fasting glucose, HbA1c, and pulmonary function (spirometry and sleep studies) were measured. RESULTS: The cohort averaged 14.2 +/- 2 years of age with mean BMI of 45.5 kg/m(2). Only 2 patients had normal fitness; 37 of 48 had peak oxygen consumption <20 mL O(2)/minute. Hypertension was present in 10 of 48 patients. Mean lipid values were: triglycerides 103 +/- 48 mg/dL, HDL cholesterol 41 +/- 10 mg/dL, and LDL cholesterol 108 +/- 26 mg/dL. Type II diabetes mellitus was diagnosed in 6 patients. Mean fasting insulin was 31 +/- 19 microU/mL. Asthma treatment, small airways disease by pulmonary function testing, or both were present in 35 of 48 patients; upper airway obstruction was present in 7 patients. LV hypertrophy was present in 8 patients, with a mean LV mass of 43 +/- 11 g/m(2.7). CONCLUSIONS: Children and adolescents with BMI >or=40 kg/m(2) have substantial cardiorespiratory morbidity including severe physical deconditioning.

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As adaptaçöes cardiovasculares e metabólicas adquiridas com o treinamento físico de "endurance" podem ser revertidas quando o atleta é submetido a um período de inatividade física, devido ao reajuste dos sistemas corporais às alteraçöes dos estímulos fisiológicos induzidos pelo treinamento físico. Reduçöes significantes do consumo máximo de oxigênio (VO2max) parecem ocorrer dentro de duas a quatro semanas de destreinamento físico, provocando um grande declínio da "performance" do atleta em esportes de "endurance". A queda inicial do VO2max está associada à reduçäo do débito cardíaco consequente da reduçäo significante da diferença artério-venosa máxima de oxigênio contribuindo também para a reduçäo do VO2max. Se a condiçäo física elevada de um atleta pode ser obtida após alguns anos seguidos de eventualidades que impeçam a continuidade da preparaçäo física do atleta näo resultem em prejuízos na sua "performance". Sendo assim, esta revisäo tem como objetivo descrever o curso temporal e a magnitude de perda das adaptaçöes fisiológicas adquiridas com o treinamento físico, bem como os mecanismos envolvidos nas mesmas

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Unlike the type 1, type 2 diabetes benefits from an improvement in glycaemic control, because of the effect of exercise on insulin sensitivity. The level of improvement is comparable to that achieved with pharmacological agents. This is significant where cost is a major consideration. These positive effects of exercise are maintained only if exercise is sustained. The effect of a single bout of exercise lasts from 12-48 hours, so exercise should be performed at least every other day or preferably every day. Improvement in glycaemic control with exercise is not related to level of fitness so everyone can benefit, as long as glycogen depletion is achieved, with results from moderately intense exercise for a reasonable duration of time. Even more important than glycaemic control is the benefit of reducing the risk of developing coronary events. Cardiovascular abnormalities are commonly seen in diabetes especially in those persons with type 2 and this is all related to the state of insulin resistance. Exercise also reduces the progression of metabolic abnormalities from mild to more severe forms of diabetes mellitus. The exercise prescription must consider socioeconomic and personal factors in addition to scientific criteria of exercise intensity. The current trend is to recommend a combination of modest, high-volume resistance training and aerobic training. Diabetes have a lower VO2max than normal individuals and so should not be placed on the same programmes. Flexibility is advised. For example, although the exercise period may be an hour long, little rest periods at intervals will not undo the metabolic benefits.

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Unlike the type 1, type 2 diabetes benefits from an improvement in glycaemic control, because of the effect of exercise on insulin sensitivity. The level of improvement is comparable to that achieved with pharmacological agents. This is significant where cost is a major consideration. These positive effects of exercise are maintained only if exercise is sustained. The effect of a single bout of exercise lasts from 12-48 hours, so exercise should be performed at least every other day or preferably every day. Improvement in glycaemic control with exercise is not related to level of fitness so everyone can benefit, as long as glycogen depletion is achieved, with results from moderately intense exercise for a reasonable duration of time. Even more important than glycaemic control is the benefit of reducing the risk of developing coronary events. Cardiovascular abnormalities are commonly seen in diabetes especially in those persons with type 2 and this is all related to the state of insulin resistance. Exercise also reduces the progression of metabolic abnormalities from mild to more severe forms of diabetes mellitus. The exercise prescription must consider socioeconomic and personal factors in addition to scientific criteria of exercise intensity. The current trend is to recommend a combination of modest, high-volume resistance training and aerobic training. Diabetes have a lower VO2max than normal individuals and so should not be placed on the same programmes. Flexibility is advised. For example, although the exercise period may be an hour long, little rest periods at intervals will not undo the metabolic benefits.(AU)

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