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OBJECTIVES: Evidence suggests that ω-3 fatty acids (FA) may have an anabolic effect on skeletal muscle. However, questions about dosage, frequency, combined protein supplementation, or different physical exercises remain unanswered. The aim of this study was to quantify by stereology whether supplementation with high dosages of ω-3 FA combined with swimming has an anabolic effect on the skeletal musculature and on the lipid profile of rats. METHODS: Sixty male Wistar rats were divided into four groups: placebo sedentary (PS), ω-3 FA sedentary (ω-3 S), placebo exercise (PE), and ω-3 FA exercise (ω-3 E). The animals in the PE and ω-3 E groups were submitted to swimming 5 d/wk, with an overload of 15% of body weight. The animals received ω-3 FA or olive oil (placebo) by gavage. After sacrifice, blood samples and the gastrocnemius muscle were collected for analysis. RESULTS: Results from this study did not show a difference in the cross-sectional areas of the gastrocnemius muscle between groups. The administration of high doses of ω-3 FA reduced plasmatic concentrations of low-density lipoprotein. Additionally, an interaction effect was observed between physical exercise and supplementation with ω-3 on levels of high-density lipoprotein. Therefore, the association between these two treatments increased high-density lipoprotein levels. CONCLUSIONS: The administration of high doses of ω-3 associated with physical activity may be beneficial in the treatment of dyslipidemia. High doses of ω-3 FA do not cause muscle mass alteration.
Assuntos
Ácidos Graxos Ômega-3 , Animais , Suplementos Nutricionais , Ácidos Graxos Ômega-3/farmacologia , Lipídeos , Masculino , Músculo Esquelético , Ratos , Ratos Wistar , NataçãoRESUMO
Neurogenesis impairment is associated with the chronic phase of the epilepsy in humans and also observed in animal models. Recent studies with animal models have shown that physical exercise is capable of improving neurogenesis in adult subjects, alleviating cognitive impairment and depression. Here, we show that there is a reduction in the generation of newborn granule cells in the dentate gyrus of adult rats subjected to a chronic model of epilepsy during the postnatal period of brain development. We also show that the physical exercise was capable to restore the number of newborn granule cells in this animals to the level observed in the control group. Notably, a larger number of newborn granule cells exhibiting morphological characteristics indicative of correct targeting into the hippocampal circuitry and the absence of basal dendrite projections was also observed in the epileptic animals subjected to physical exercise compared to the epileptic animals. The results described here could represent a positive interference of the physical exercise on the neurogenesis process in subjects with chronic epilepsy. The results may also help to reinterpret the benefits of the physical exercise in alleviating symptoms of depression and cognitive dysfunction.
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Severe obesity affects metabolism with potential to influence the lactate and glycemic response to different exercise intensities in untrained and trained rats. Here we evaluated metabolic thresholds and maximal aerobic capacity in rats with severe obesity and lean counterparts at pre- and post-training. Zucker rats (obese: n = 10, lean: n = 10) were submitted to constant treadmill bouts, to determine the maximal lactate steady state, and an incremental treadmill test, to determine the lactate threshold, glycemic threshold and maximal velocity at pre and post 8 weeks of treadmill training. Velocities of the lactate threshold and glycemic threshold agreed with the maximal lactate steady state velocity on most comparisons. The maximal lactate steady state velocity occurred at higher percentage of the maximal velocity in Zucker rats at pre-training than the percentage commonly reported and used for training prescription for other rat strains (i.e., 60%) (obese = 78 ± 9% and lean = 68 ± 5%, P < 0.05 vs. 60%). The maximal lactate steady state velocity and maximal velocity were lower in the obese group at pre-training (P < 0.05 vs. lean), increased in both groups at post-training (P < 0.05 vs. pre), but were still lower in the obese group at post-training (P < 0.05 vs. lean). Training-induced increase in maximal lactate steady state, lactate threshold and glycemic threshold velocities was similar between groups (P > 0.05), whereas increase in maximal velocity was greater in the obese group (P < 0.05 vs. lean). In conclusion, lactate threshold, glycemic threshold and maximal lactate steady state occurred at similar exercise intensity in Zucker rats at pre- and post-training. Severe obesity shifted metabolic thresholds to higher exercise intensity at pre-training, but did not attenuate submaximal and maximal aerobic training adaptations.
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It is extremely difficult to estimate the occurrence of sudden unexpected death in epilepsy (SUDEP). On the other hand, discovering and carefully evaluating new risk factors that may contribute to the onset of cardiovascular abnormalities in people with refractory epilepsy may prevent fatal events in these individuals. In this context, we should not ignore that urban air pollution is a leading problem for environmental health and is able to cause serious cardiovascular dysfunctions that culminate in sudden death. In this regard, we aimed to determine whether environmental exposure to air pollution is an aggravating event for SUDEP.
Assuntos
Poluição do Ar/efeitos adversos , Morte Súbita/etiologia , Epilepsia/mortalidade , Anormalidades Cardiovasculares/mortalidade , Exposição Ambiental/efeitos adversos , Epilepsia/prevenção & controle , Ácidos Graxos Ômega-3/administração & dosagem , Humanos , Fatores de RiscoRESUMO
Clinical experience suggests that restless legs syndrome (RLS), periodic leg movement (PLM), and attention-deficit hyperactivity disorder (ADHD) may co-occur in both children and adults. The purpose of the present study was to provide an electrocorticography and electromyography evaluation of the spontaneously hypertensive rat (SHR) to investigate the potential of this rat strain as an animal model of RLS-PLM. Initial work focused on evaluating sleep patterns and limb movements during sleep in SHR, having normotensive Wistar rats (NWR) as control, followed by comparison of two treatments (pharmacological-dopaminergic agonist treatment and nonpharmacological-chronic physical exercise), known to be clinically beneficial for sleep-related movement disorders. The captured data strengthen the association between SHR and RLS-PLM, revealing a significant reduction on sleep efficiency and slow wave sleep and an increase on wakefulness and limb movements for the SHR group during the dark period, as compared to the NWR group, effects that have characteristics that are strikingly consistent with RLS-PLM. The pharmacological and nonpharmacological manipulations validated these results. The present findings suggest that the SHR may be a useful putative animal model to study sleep-related movement disorders mechanisms.
Assuntos
Benzotiazóis/farmacologia , Modelos Animais de Doenças , Agonistas de Dopamina/farmacologia , Síndrome das Pernas Inquietas/fisiopatologia , Vigília/fisiologia , Animais , Benzotiazóis/uso terapêutico , Agonistas de Dopamina/uso terapêutico , Eletroencefalografia , Eletromiografia , Feminino , Masculino , Pramipexol , Ratos , Ratos Endogâmicos SHR , Síndrome das Pernas Inquietas/tratamento farmacológico , Vigília/efeitos dos fármacosRESUMO
It is extremely difficult to estimate the occurrence of sudden unexpected death in epilepsy (SUDEP). On the other hand, discovering and carefully evaluating new risk factors that may contribute to the onset of cardiovascular abnormalities in people with refractory epilepsy may prevent fatal events in these individuals. In this context, we should not ignore that urban air pollution is a leading problem for environmental health and is able to cause serious cardiovascular dysfunctions that culminate in sudden death. In this regard, we aimed to determine whether environmental exposure to air pollution is an aggravating event for SUDEP.
É extremamente difícil estimar a ocorrência de morte súbita em epilepsia (SUDEP). Por outro lado, detectar e avaliar cuidadosamente novos factores de risco que podem contribuir para o aparecimento de alterações cardiovasculares em pessoas com epilepsia refratária poderá ser capaz de impedir a ocorrência de eventos fatais nestes indivíduos. Neste contexto, não devemos negligenciar hoje que a poluição do ar nas grandes cidades é um problema para a saúde ambiental, podendo causar graves disfunções cardiovasculares, que culminam em morte súbita. Neste sentido, propusemos nesse trabalho que a exposição ambiental a poluição do ar é um evento agravante para a ocorrência de SUDEP.
Assuntos
Humanos , Poluição do Ar/efeitos adversos , Morte Súbita/etiologia , Epilepsia/mortalidade , Anormalidades Cardiovasculares/mortalidade , Exposição Ambiental/efeitos adversos , Epilepsia/prevenção & controle , /administração & dosagem , Fatores de RiscoRESUMO
It is clear that sudden unexpected death in epilepsy (SUDEP) is mainly a problem for people with refractory epilepsy, but our understanding of the best way to its prevention is still incomplete. Although the pharmacological treatments available for epilepsies have expanded, some antiepileptic drugs are still limited in clinical efficacy. In the present paper, we described an experience with vagus nerve stimulation (VNS) treatment by opening space and providing the opportunity to implement effective preventative maps to reduce the incidence of SUDEP in children and adolescents with refractory epilepsy.
Está claro que a morte súbita e inesperada em epilepsias (SUDEP) é principalmente um problema para as pessoas com epilepsia refratária, mas o entendimento para estabelecer medidas preventivas ainda está incompleto. Embora os tratamentos farmacológicos disponíveis para epilepsias tenham sido expandidos, algumas drogas antiepilépticas ainda são limitadas em termos de eficácia clínica. No presente trabalho, foi descrita uma experiência com a estimulação do nervo vago (VNS), abrindo espaço e fornecendo a oportunidade de implementar eficazes mapas preventivoss para reduzir a incidência da SUDEP em crianças e adolescentes com epilepsia refratária.
Assuntos
Adolescente , Criança , Humanos , Morte Súbita/prevenção & controle , Epilepsia/terapia , Estimulação do Nervo Vago , Morte Súbita/etiologia , Epilepsia/complicaçõesRESUMO
Schizophrenia is a devastating mental disorder, affecting cognitive, emotional, and behavioral conditions, ability to work, social functioning, family stability and self-esteem of the patient. People with schizophrenia show a two to three-fold increased risk to die prematurely than those without schizophrenia. Understanding the mechanisms behind sudden cardiac death in individuals with schizophrenia is a key to prevention. Although different mechanisms may be related, there are clear indications that cardiac abnormalities play a potential role. Some antipsychotics may be associated with cardiovascular adverse events, e.g., QT interval prolongation, metabolic dysfunction, blood pressure and heart rate alterations. Magnesium (Mg) abnormalities may lead to various morphological and functional dysfunctions of the heart and low levels of serum Mg are considered to be at high risk for sudden cardiac death. As low serum Mg is associated with detrimental effects on the heart and that antipsychotic-treated schizophrenia patients frequently affect the heart rate, possibly, these factors together must change the normal functioning of the heart and consequently being able to culminate in a catastrophic event.