Introdução: Achados da literatura sugerem que oscilações dos hormônios sexuais femininos podem alterar o consumo máximo de oxigênio (VO2max).Objetivo: Comparar o VO2max entre ratos machos (M, n=8), fêmeas nas fases ovulatórias (OV, n=8) ou não-ovulatórias (NOV, n=8) do ciclo estral e ooforectomizadas (OS, n=8).Métodos: A avaliação do consumo de oxigênio foi realizada em esteira rolante com caixa metabólica acoplada.Resultados: Em repouso, o VO2 foi semelhante entre os grupos estudados. O grupo M apresentou maior VO2max em relação ao grupo NOV, mas valores semelhantes ao do grupo OV. O VO2max foi menor no grupo ooforectomizado (OS: 62±3 ml.kg-1.min-1) quando comparado aos demais grupos (M: 92±2; NOV: 77±4; OV: 87±3 ml.kg-1.min-1).Conclusões: Esses achados evidenciam que a variação hormonal decorrente das diferentes fases do ciclo estral e da privação dos hormônios ovarianos pode induzir alterações no consumo máximo de oxigênio em ratos.

Introduction: Literature findings suggest that fluctuations of female sex hormones may change the maximum oxygen consumption (VO2max).Objective:To compare the VO2max among male rats (M, n = 8), female rats on ovulatory (OV, n=8) or non-ovulatory (NOV, n=8) phases of the estrous cycle and ovariectomized (OS, n=8).Methods:The evaluation of oxygen consumption was performed on a treadmill coupled with metabolic box.Results: At rest VO2 was similar among groups. The M group had a higher VO2max compared to the NOV group, however showed similar values when compared to OV group. The VO2max was lower in the ovariectomized group (OS: 62±3 ml.kg-1.min-1) compared to other groups (M: 92±2; NOV: 77 ± 4; OV: 87 ± 3 ml.kg-1.min-1).Conclusions: These findings suggest that hormonal variation resulting from different phases of the estrous cycle and ovarian hormone deprivation can induce changes in maximal oxygen uptake in rats.

Introducción: Hallazgos de la literatura sugieren que oscilaciones de las hormonas sexuales femeninas pueden alterar el consumo máximo de oxígeno (VO2max).Objetivo: Comparar el VO2max entre ratas machos (M, n=8), hembras en las fases ovulatorias (OV, n=8) o no ovulatorias (NOV, n=8) del ciclo estral y ooforectomizadas (OS, n=8).Métodos: La evaluación del consumo de oxígeno fue realizada en cinta rodante con caja metabólica acoplada.Resultados: En reposo, el VO2 fue semejante entre los grupos estudiados. El grupo M presentó mayor VO2max en relación al grupo NOV, pero valores semejantes a los del grupo OV. El VO2max fue menor en el grupo ooforectomizado (OS: 62±3 ml.kg-1.min-1) cuando comparado a los demás grupos (MS: 92±2; NOV: 77±4; OV: 87±3 ml.kg-1.min-1).Conclusiones: Esos hallazgos evidencian que la variación hormonal proveniente de las diferentes fases del ciclo estral y de la privación de las hormonas ováricas puede inducir alteraciones en el consumo máximo de oxígeno en ratas.

OBJECTIVES: To investigate the effects of hyperglycemia on left ventricular dysfunction, morphometry, myocardial infarction area, hemodynamic parameters, oxidative stress profile, and mortality rate in rats that had undergone seven days of myocardial infarction. INTRODUCTION: Previous research has demonstrated that hyperglycemia may protect the heart against ischemic injury. METHODS: Male Wistar rats were divided into four groups: control-sham, diabetes-sham, myocardial infarction, and diabetes + myocardial infarction. Myocardial infarction was induced 14 days after diabetes induction. Ventricular function and morphometry, as well as oxidative stress and hemodynamic parameters, were evaluated after seven days of myocardial infarction. RESULTS: The myocardial infarction area, which was similar in the infarcted groups at the initial evaluation, was reduced in the diabetes + myocardial infarction animals (23 ± 3%) when compared with the myocardial infarction (42 ± 7%, p<0.001) animals at the final evaluation. The ejection fraction (22%, p = 0.003), velocity of circumferential fiber shortening (30%, p = 0.001), and left ventricular isovolumetric relaxation time (26%, p = 0.002) were increased in the diabetes + myocardial infarction group compared with the myocardial infarction group. The diabetes-sham and diabetes + myocardial infarction groups displayed increased catalase concentrations compared to the control-sham and myocardial infarction groups (diabetes-sham: 32± 3; diabetes + myocardial infarction: 35± 0.7; control-sham: 12 ± 2; myocardial infarction: 16 ± 0.1 pmol min-1 mg-1 protein). The levels of thiobarbituric acid-reactive substances were reduced in the diabetes-sham rats compared to the control-sham rats. These positive adaptations were reflected in a reduced mortality rate in the diabetes + myocardial infarction animals (18.5%) compared with the myocardial infarction animals (40.7%, p = 0.001). CONCLUSIONS: These data suggest that short-term hyperglycemia initiates compensatory mechanisms, as demonstrated by increased catalase levels, which culminate in improvements in the ventricular response, infarcted area, and mortality rate in diabetic rats exposed to ischemic injury.