ABSTRACT
The search for the causes of obesity has involved genetic abnormalities and endocrine and neural lesions. Although evidence suggests that genetics plays an important role in body weight regulation, rapid increases in obesity rates do not seem to be caused by significant genetic changes within populations. Total energy expenditure and total energy intake are not the only factors that regulate body fat. Nitrogen and carbohydrate balances are eased by the capacity of the organism for adjusting amino acids and glucose oxidation rates, respectively. Regarding fat, this mechanism is considerably less precise; a fat intake increase does not stimulate its oxidation on the same basis. In addition, dietary fat is stored very efficiently as body fat. Elevated carbohydrate ingestion enhances glycogen reserves, which usually are much smaller than the maximum capacity of storage and enlargement of these stores, thus stimulating this nutrient's oxidation. These data point to a very well controlled carbohydrate balance in the body. Various studies show lack of efficiency of the hyperlipidic diet in stimulating satiety. Signals arising from the gastrointestinal tract play a fundamental role in regulation of appetite and energy intake, and evidence indicates that the gastrointestinal and hormonal mechanisms involved in the suppression of appetite and in energy intake are compromised in obesity. A high-fat diet is important in its origin. Additional studies are necessary to explain the mechanisms that lead to adipose tissue retention resulting in a fat-rich diet.
Subject(s)
Adipose Tissue/metabolism , Appetite Regulation/physiology , Dietary Carbohydrates/metabolism , Dietary Fats/metabolism , Energy Metabolism , Obesity/physiopathology , Dietary Fats/pharmacology , Energy Intake/drug effects , Gastrointestinal Hormones/metabolism , Glycogen/metabolism , Humans , Obesity/etiology , Obesity/metabolism , Oxidation-Reduction , Satiation/drug effectsABSTRACT
The aim of the present study was to investigate whether preexercise sodium-bicarbonate ingestion improves judo-related performance. The study used 2 different protocols to evaluate performance: 3 bouts of a specific judo test (n = 9) and 4 bouts of the Wingate test for upper limbs (n = 14). In both protocols athletes ingested 0.3 g/kg of sodium bicarbonate or placebo 2 h before the tests. Blood samples were collected to determine lactate level, and levels of perceived exertion were measured throughout the trials. The study used a double-blind, counterbalanced, crossover design. Ingestion of sodium bicarbonate improved performance in Bouts 2 and 3 of Protocol 1 (P < 0.05), mean power in Bouts 3 and 4 of Protocol 2 (P < 0.05), and peak power in Bout 4 of Protocol 2 (P < 0.05). Ingestion of bicarbonate increased lactate concentration in Protocol 1 (P < 0.05) but not in Protocol 2. Ratings of perceived exertion did not differ between treatments. In conclusion, sodium bicarbonate improves judo-related performance and increases blood lactate concentration but has no effect on perceived exertion.
Subject(s)
Acid-Base Equilibrium/drug effects , Lactates/blood , Martial Arts/physiology , Sodium Bicarbonate/administration & dosage , Adult , Alkalosis/prevention & control , Cross-Over Studies , Double-Blind Method , Humans , Time FactorsABSTRACT
O objetivo deste estudo foi investigar o efeito da ingestão de NaHCO3 sobre o desempenho no judô. Seis atletas do sexo masculino ingeriram 0,3g x kg¹ de peso corporal de NaHCO3 ou CaCO3 (placebo) 2h antes de três lutas de 5 min, intercaladas por 15 min de recuperação. Imediatamente após e 15 min após cada luta, os atletas relataram a percepção subjetiva de esforço. A concentração sanguínea de lactato foi verificada em repouso, após o aquecimento, 0, 3, 5, 7, 10 e 15 min após cada luta. O mesmo protocolo experimental foi repetido duas vezes por cada atleta, com exceção da substância ingerida. O estudo adotou o modelo duplo-cego contrabalançado. Não houve diferença significativa para as variáveis de desempenho. A percepção subjetiva de esforço não diferiu entre os tratamentos e a concentração sanguínea de lactato foi significativamente maior (p < 0,05) após a ingestão de NaHCO3, especialmente nos primeiros momentos da coleta. Concluindo, os efeitos ergogênicos do NaHCO3 não parecem ser suficientes para contribuir para a melhora da performance em lutas de judô. Contudo, as limitações do modelo utilizado devem ser consideradas quando da generalização dos resultados. Estudos futuros devem utilizar outras ferramentas para avaliar o desempenho no judô.
The objective of this study was to investigate the effect of the NaHCO3 ingestion on the judo performance. Six male athletes ingested 0.3 g x kg¹ body weight of NaHCO3 or CaCO3 (placebo) 2 h before 3 fights of 5 min, with 15 min recovery. Immediately afterwards, and 15 min after each fight, the athletes related their perceived exertion. The blood lactate concentration was verified in rest, after warming up, 0, 3, 5, 7, 10 and 15 min after each fight. The same experimental protocol was repeated twice by each athlete, except for the ingested substance. The study adopted the counterbalanced double-blind model. There was no significant difference for the performance variables. The perceived exertion did not differ among the treatments, and the blood lactate concentration was significantly greater (p < 0.05) after NaHCO3 ingestion in the first moments of the protocol. In conclusion, the ergogenic effects of NaHCO3 are not enough to contribute to the improvement of the performance in judo fights. However, the model limitations must be considered when generalizing these results. Future studies should use other tools to evaluate the performance in judo.
El objetivo de este trabajo ha sido el de investigar el efecto sobre el desempeño en judo al ingerir NaHCO3. Seis deportistas del sexo masculino ingirieron 0,3 g x kg-1 de peso corporal de NaHCO3 o CaCO3 (placebo) 2 h antes de 3 luchas de 5 min, intercaladas por 15 min de recuperación. Inmediatamente después, y 15 min después de cada lucha, los deportistas relataron la percepción subjetiva del esfuerzo. La concentración sanguínea de lactato fue verificada en reposo, después del precalentamiento, 0, 3, 5, 7, 10 y 15 min después de cada lucha. El mismo protocolo experimental fue repetido dos veces en cada deportista, con excepción de la sustancia ingerida. El estudio adoptó el modelo doble-ciego contrabalanceado. No hubo diferencia significativa para las variables de desempeño. La percepción subjetiva del esfuerzo no difirió entre los tratamientos, y la concentración sanguínea de lactato fue significativamente mayor (p < 0.05) después de ingerir NaHCO3, especialmente en los primeros momentos de colecta. En conclusión, los efectos ergogénicos de NaHCO3 no parecen ser suficientes para contribuir en la mejoría del desempeño en las luchas de judo. A pesar de eso, las limitaciones del modelo utilizado deben ser consideradas al intentar generalizar resultados. Estudios futuros deben utilizar otras herramientas para evaluar el desempeño en el judo.
