Abstract Objective: To analyze the impact of I/D polymorphism of the angiotensin-converting enzyme gene on the responses of 24 h blood pressure, heart rate variability and nitric oxide after moderate aerobic exercise session. Method: Twenty seven hypertensive elderly were genotyped for the I/D polymorphism of the angiotensin-converting enzyme gene (D/D: n = 9; I/D: n = 9; I/I: n = 9) and performed a bout of aerobic exercise at 90% of anaerobic threshold. Measurements of mean blood pressure, heart rate variability and nitric oxide were performed before and during 24 h post-aerobic exercise session. Results: The D/D genotype showed impaired mean arterial pressure responses (elevation) in the nocturnal sleep (10:30 pm to 06:30 am) post-aerobic exercise when compared to rest (D/D = −4.2 ± 8.1 mmHg; p > 0.05, I/D = −9.2 ± 9.1 mmHg; p < 0.05 and I/I = −7.0 ± 6.9 mmHg; p < 0.05). Besides, in day time of 06:30 am to 10:30 am (next day) higher values of mean arterial pressure responses occur between D/D = 4.7 ± 4.6 mmHg vs. I/D = −2.0 ± 13.0 mmHg; p < 0.05. The carriers of the D allele, in addition to not release nitric oxide significantly post-aerobic exercise session (p > 0.05), showed reduced elevation of nitric oxide between genotypes immediately after aerobic exercise (D/D = 12.8 ± 135.3 μM and I/D = −8.7 ± 69.0 μM vs. I/I = 132.9 ± 188.7 μM; p < 0.05). Reduced elevation of heart rate variability post-aerobic exercise session occurred when compared to rest (D/D = 1 h: −0.08 ± 0.09 s; p < 0.05 and 24 h: −0.08 ± 0.11 s; p < 0.05). Conclusion: Elderly hypertensive individuals carrying the D/D genotype of the angiotensin converting enzyme gene showed impaired responses of blood pressure post-aerobic exercise, especially during sleep, and reduced heart rate variability during the 24 h post-aerobic exercise. Besides, to angiotensin converting enzyme genotypes with the presence of D allele (D/D and I/D) was impaired release of nitric oxide post-aerobic exercise session.

Resumo Objetivo: Analisar o impacto do polimorfismo I/D do gene da enzima conversora da angiotensina na pressão sanguínea, variabilidade da frequência cardíaca e óxido nítrico durante 24 h, em resposta a uma bateria moderada de exercícios aeróbicos. Método: Vinte e sete idosas hipertensas foram genotipadas para o polimorfismo I/D do gene da enzima conversora da angiotensina (D/D: n = 9; I/D: n = 9; I/I: n = 9) e realizaram uma sessão de exercício aeróbio à 90% do limiar anaeróbio. Medidas de pressão arterial média, variabilidade da frequência cardíaca e óxido nítrico foram coletadas antes e durante as 24 h seguintes, após a sessão de exercício aeróbio. Resultados: O genótipo D/D mostrou uma resposta inadequada da pressão arterial média (elevação) durante o sono após o exercício (22:30-06:30) em comparação ao repouso (D/D = -4.2 ± 8.1 mmHg; p > 0.05, I/D = -9.2 ± 9.1 mmHg; p < 0.05 e I/I = -7.0 ± 6.9 mmHg; p < 0.05). Além disso, durante o dia, de 06:30-10:30 da manhã (do dia seguinte), maiores valores de pressão arterial média ocorreram entre D/D = 4.7 ± 4.6 mmHg vs. I/D = -2.0 ± 13.0 mmHg; p < 0.05. O grupo carreador do alelo D, além de não revelar significância no óxido nítrico após a sessão de exercício, mostrou uma redução da elevação do óxido nítrico entre os genótipos logo após o exercício aeróbio (D/D = 12.8 ± 135.3 μM e I/D = -8.7 ± 69.0 μM vs. I/I = 132.9 ± 188.7 μM; p < 0.05). Ocorreu uma redução do R-Ri após os exercícios quando comparada com os valores do repouso (D/D = 1 h: -0.08 ± 0.09 s; p < 0.05 e 24 h: -0.08 ± 0.11 s; p < 0.05). Conclusão: Indivíduos idosos e hipertensos carreadores do genótipo D/D para o gene da enzima conversora da angiotensina mostraram resposta inadequada de pressão arterial pós-exercício aeróbio, especialmente durante o sono, e reduzida variabilidade da frequência cardíaca durante as 24 h seguintes pós-exercício. Além disso, o genótipo da enzima conversora da angiotensina com a presença do alelo D (D/D e I/D) teve sua liberação de óxido nítrico prejudicada nos momentos após a sessão de exercício aeróbio.

Resumen Objetivo: Analizar el impacto del polimorfismo I/D del gen de la enzima conversora de la angiotensina en la presión sanguínea, variación de la frecuencia cardíaca y óxido nítrico durante 24 h en respuesta a una batería moderada de ejercicios aeróbicos. Método: Veintisiete ancianas hipertensas fueron genotipadas para el polimorfismo I/D del gen de la enzima conversora de la angiotensina (D/D: n = 9; I/D: n = 9; I/I: n = 9) y realizaron una batería de ejercicios aeróbicos al 90% del umbral anaeróbico. Se realizaron medidas de la presión arterial media, variabilidad de la frecuencia cardíaca y óxido nítrico, antes y durante las 24 h siguientes después de una sesión de ejercicios aeróbicos. Resultados: El genotipo D/D presentó una respuesta inadecuada de la presión arterial media (aumento) durante el sueño nocturno después del ejercicio (22:30-06:30) en comparación con el reposo (D/D = -4.2 ± 8.1 mmHg; p > 0.05, I/D = -9.2 ± 9.1 mmHg; p < 0.05 and I/I = -7.0 ± 6.9 mmHg; p < 0.05). Por otro lado, durante el día, de 06:30 hasta las 10:30 de la mañana (del día siguinete) se registraron valores elevados del aumento de la presión arterial media en el genotipo D/D = 4.7 ± 4.6 mmHg vs. I/D = -2.0 ± 13.0 mmHg; p < 0.05. Las portadoras del alelo D, más allá de no mostrar significación en los niveles de óxido nítrico después de la sesión de ejercicio, mostraron una reducción del incremento de óxido nítrico entre los genotipos después del ejercicio aeróbico (D/D = 12.8 ± 135.3 μM y I/D = -8.7 ± 69.0 μM vs. I/I = 132.9 ± 188.7 μM; p < 0.05). Se observó una reducción del aumento de la variabilidad de la frecuencia cardíaca después de los ejercicios, cuando se compara con los valores de reposo (D/D = 1 h: -0.08 ± 0.09 s; p < 0.05 y 24 h: -0.08 ± 0.11 s; p < 0.05). Conclusión: Individuos ancianos e hipertensos portadores del genotipo D/D del gen de la enzima conversora de la angiotensina mostraron una respuesta inadecuada de la presión sanguínea postejercicio aeróbico, especialmente durante el sueño, y reducción de la variabilidad de la frecuencia cardíaca durante las 24 h siguientes tras el ejercicio. Además, el genotipo de la enzima conversora de la angiotensina, con presencia del alelo D (D/D e I/D), tiene la liberación de óxido nítrico alterada, después de la sesión de ejercicio aeróbico.

The aim of this study was to analyze the acute responses of bradykinin, insulin, and glycemia to exercise performed above and below lactate threshold (LT) in individuals with type 2 diabetes mellitus (T2D). Eleven participants with a diagnosis of T2D randomly underwent three experimental sessions 72 h apart: 1) 20 min of exercise performed at 120% of LT (120%LT), 2) 20 min of exercise performed at 80% of LT (80%LT), and 3) 20 min of control session. Blood glucose was analyzed before, during, and at 45 min post-exercise. Bradykinin and insulin were analyzed before and at 45 min post-exercise. Both exercise sessions elicited a parallel decrease in glucose level during exercise (P≤0.002), with a greater decrease being observed for 120%LT (P=0.005). Glucose decreased 22.7 mg/dL (95%CI=10.3 to 35, P=0.001) at the 45 min post-exercise recovery period for 80%LT and decreased 31.2 mg/dL (95%CI=18.1 to 44.4, P<0.001) for 120%LT (P=0.004). Insulin decreased at post-exercise for 80%LT (P=0.001) and control (P≤0.035). Bradykinin increased at 45 min post-exercise only for 80%LT (P=0.013), but was unrelated to the decrease in glucose (r=-0.16, P=0.642). In conclusion, exercise performed above and below LT reduced glycemia independently of insulin, but exercise above LT was more effective in individuals with T2D. However, these changes were unrelated to the increase in circulating bradykinin.

Introdução: A potência anaeróbia pode ser definida como o máximo de energia liberada por unidade de tempo por esse sistema, enquanto que a capacidade anaeróbia pode ser definida como a quantidade total de energia disponível nesse sistema. As características específicas da potência e capacidade anaeróbia em diferentes categorias do futebol ainda não foram elucidadas. Objetivo: Avaliar e comparar a potência e capacidade anaeróbia em atletas de futebol das categorias de base sub 15, sub 17 e sub 20, com atletas adultos de um clube de futebol profissional. Metodologia: A amostra foi composta por 197 indivíduos do sexo masculino, atletas de futebol, divididos pela categoria em que disputam os campeonatos: Grupo Sub 15 (n = 42); Grupo Sub 17 (n = 41); Grupo sub 20 (n = 86); Grupo Adulto (n = 28). Para determinação dos parâmetros de potência e capacidade anaeróbia os sujeitos realizaram o teste de Wingate. Conclusão: Os resultados nos permitem concluir que em jogadores de futebol a potência anaeróbia máxima é dependente da idade cronológica até a categoria adulta, já a capacidade anaeróbia mostrou-se dependente da idade até a categoria sub 20. A potência anaeróbia máxima relativa foi maior na categoria sub 20, porém houve um declínio dessa variável na categoria adulta.

Introduction: The anaerobic power can be defined as the maximum energy released per unit time for this system, while the anaerobic capacity can be defined as the full amount of energy available in the system. The characteristics of the development of anaerobic power and capacity in soccer players have not been elucidated. Objective: Evaluate and compare the power and anaerobic capacity in soccer players of the basic categories, sub15, sub 17, sub 20 and adult athletes that play in professional football club. Methodology: The sample consisted of 197 male soccer players, divided by category vying for championships: Group Sub 15 (n = 42), Group Sub 17 (n = 41), Group Sub 20 (n = 86); Group Adult (n = 28). To determine the parameters of power and capacity anaerobic subjects performed the Wingate Test. Results: the results allowed for the conclusion that in soccer players the maximum anaerobic power is dependent on the chronological age until the adult category, since the anaerobic capacity was dependent until the age of 20 sub category. The maximum relative anaerobic power was higher in the category under 20, but there was a decline of this variable in the adult category.

Rubinstein-Taybi syndrome (RTS) is a rare developmental disorder characterized by craniofacial dysmorphisms, broad thumbs and toes, mental and growth deficiency, and recurrent respiratory infections. RTS has been associated with CREBBP gene mutations, but EP300 gene mutations have recently been reported in 6 individuals. In the present study, the humoral immune response in 16 RTS patients with recurrent respiratory infections of possible bacterial etiology was evaluated. No significant differences between patients and 16 healthy controls were detected to explain the high susceptibility to respiratory infections: normal or elevated serum immunoglobulin levels, normal salivary IgA levels, and a good antibody response to both polysaccharide and protein antigens were observed. However, most patients presented high serum IgM levels, a high number of total B cell and B subsets, and also high percentiles of apoptosis, suggesting that they could present B dysregulation. The CREBBP/p300 family gene is extremely important for B-cell regulation, and RTS may represent an interesting human model for studying the molecular mechanisms involved in B-cell development.

We analyzed the genetic recombination pattern of the T-cell receptor beta-chain gene (TCR-beta) in order to identify clonal expansion of T-lymphocytes in 17 human T-lymphotropic virus type I (HTLV-I)-positive healthy carriers, 7 of them with abnormal features in the peripheral blood lymphocytes. Monoclonal or oligoclonal expansion of T-cells was detected in 5 of 7 HTLV-I-positive patients with abnormal lymphocytes and unconfirmed diagnosis by using PCR amplification of segments of TCR-beta gene, in a set of reactions that target 102 different variable (V) segments, covering all members of the 24 V families available in the gene bank, including the more recently identified segments of the Vbeta-5 and Vbeta-8 family and the two diversity beta segments. Southern blots, the gold standard method to detect T-lymphocyte clonality, were negative for all of these 7 patients, what highlights the low sensitivity of this method that requires a large amount of very high quality DNA. To evaluate the performance of PCR in the detection of clonality we also analyzed 18 leukemia patients, all of whom tested positive. Clonal expansion was not detected in any of the negative controls or healthy carriers without abnormal lymphocytes. In conclusion, PCR amplification of segments of rearranged TCR-beta is reliable and highly suitable for the detection of small populations of clonal T-cells in asymptomatic HTLV-I carriers who present abnormal peripheral blood lymphocytes providing an additional instrument for following up these patients with potentially higher risk of leukemia.