Effects of an exercise intervention using Dance Dance Revolution on endothelial function and other risk factors in overweight children.

OBJECTIVE: To determine whether an exercise intervention using an active video game (Dance Dance Revolution [DDR]) is effective in improving endothelial dysfunction (EDF) and other risk factors in overweight children. DESIGN: Thirty-five children (Body mass index > or = 85(th) percentile, mean age 10.21+/-1.67 years, 17 females) with EDF were assessed for flow-mediated dilation (FMD), lipids, insulin, glucose, NO(2)+NO(3), asymmetric dimethylarginine, symmetric dimethylarginine, l-arginine, height, weight, aerobic fitness, and blood pressure. In a subsample, tumor necrosis factor alpha, interleukin-6, C-reactive protein, and adiponectin were also assessed. Subjects were randomly assigned to 12-weeks of aerobic exercise (EX) using DDR or to a non-exercising delayed-treatment control group (DTC). RESULTS: EX had significant improvements in FMD ( 5.56+/-5.04% compared with 0.263+/-4.54%, p=0.008), exercise time on the graded exercise test (53.59+/-91.54 compared with -12.83+/-68.10 seconds, p=0.025), mean arterial pressure (MAP) (-5.62+/-7.03 compared with -1.44+/-2.16 mmHg, p=0.05), weight (0.91+/-1.53 compared with 2.43+/-1.80 kg, p=0.017) and peak VO(2) (2.38+/-3.91 compared with -1.23+/-3.18 mg/kg/min, p=0.005) compared with the DTC. Thirteen EX subjects achieved normal EDF while ten did not. These groups differed at baseline with regard to total cholesterol (TC) and low-density lipoprotein (LDL). CONCLUSION: Twelve weeks of DDR-use improved FMD, aerobic fitness, and MAP in overweight children. Improvements occurred without changes in inflammatory markers or nitric oxide production. The results document the need to explore relationships between obesity, endothelial function, inflammation, lipids, exercise intensity, and gender in a larger sample of overweight children.

Role of pendrin in iodide balance: going with the flow.

Pendrin is expressed in the apical regions of type B and non-A, non-B intercalated cells, where it mediates Cl(-) absorption and HCO3(-) secretion through apical Cl(-)/HCO3(-) exchange. Since pendrin is a robust I(-) transporter, we asked whether pendrin is upregulated with dietary I(-) restriction and whether it modulates I(-) balance. Thus I(-) balance was determined in pendrin null and in wild-type mice. Pendrin abundance was evaluated with immunoblots, immunohistochemistry, and immunogold cytochemistry with morphometric analysis. While pendrin abundance was unchanged when dietary I(-) intake was varied over the physiological range, I(-) balance differed in pendrin null and in wild-type mice. Serum I(-) was lower, while I(-) excretion was higher in pendrin null relative to wild-type mice, consistent with a role of pendrin in renal I(-) absorption. Increased H2O intake enhanced differences between wild-type and pendrin null mice in I(-) balance, suggesting that H2O intake modulates pendrin abundance. Raising water intake from approximately 4 to approximately 11 ml/day increased the ratio of B cell apical plasma membrane to cytoplasm pendrin label by 75%, although circulating renin, aldosterone, and serum osmolality were unchanged. Further studies asked whether H2O intake modulates pendrin through the action of AVP. We observed that H2O intake modulated pendrin abundance even when circulating vasopressin levels were clamped. We conclude that H2O intake modulates pendrin abundance, although not likely through a direct, type 2 vasopressin receptor-dependent mechanism. As water intake rises, pendrin becomes increasingly critical in the maintenance of Cl(-) and I(-) balance.

Nmda alters the development of hypoxic pulmonary vasoconstriction and nitric oxide synthetase activity in the isolated perfused rat lung.

Using an isolated salt-perfused rat lung model, the authors investigated whether N-methyl-D-aspartate (NMDA) (1 mM) in the pulmonary circulation effects the pulmonary vascular responses to an acute stimulus of hypoxic insult under baseline, nitric oxide synthetase (NOS)-blocked conditions (N-omega-nitro-L arginine methyl ester; L-NAME, 2 mM), and with an NMDA receptor blocker, MK-801 (0.3 microM) added. NOS activity at baseline, and in response to hypoxia, NMDA, L-NAME, and a combination of these stimuli were also assessed. NMDA did not in itself alter hypoxic pulmonary vasoconstriction (HPV), but did significantly attenuate HPV during VOS blockade. This effect of NMDA was erased by MK-801. Assessment of NOS activity showed that hypoxia alone caused a doubling of NO production within the lung. This effect was erased by the addition of L-NAME. NMDA alone caused a significant, 3-fold increase in NOS activity, which was not further affected by hypoxic chalenge. L-NAME did not depress NOS activity in the hypoxia + NMDA group. These data suggest that NMDA receptor activation results in increased NOS activity and presumably increased production of NO. The increased NOS activity induced by NMDA receptor stimulation is resistant to the blockade effect of L-NAME. The actions of NMDA receptor activation may represent a natural protective mechanism, at least within the pulmonary vasculature, in face of acute, abnormal stimuli such as hypoxia.