Ϫ ]), oxygen uptake (V O2) kinetics, and exercise tolerance in normoxia (N) and hypoxia (H). In a doubleblind, crossover study, 12 healthy subjects completed cycle exercise tests, twice in N (20.9% O2) and twice in H (13.1% O2). Subjects ingested either 140 ml/day of NO 3 Ϫ -rich beetroot juice (8.4 mmol NO3; BR) or NO 3 Ϫ -depleted beetroot juice (PL) for 3 days prior to moderate-intensity and severe-intensity exercise tests in H and N. Preexercise plasma [NO 2 Ϫ ] was significantly elevated in H-BR and N-BR compared with H-PL (P Ͻ 0.01) and N-PL (P Ͻ 0.01). The rate of decline in plasma [NO 2 Ϫ ] was greater during severe-intensity exercise in H-BR [Ϫ30 Ϯ 22 nM/min, 95% confidence interval (CI); Ϫ44, Ϫ16] compared with H-PL (Ϫ7 Ϯ 10 nM/min, 95% CI; Ϫ13, Ϫ1; P Ͻ 0.01) and in N-BR (Ϫ26 Ϯ 19 nM/min, 95% CI; Ϫ38, Ϫ14) compared with N-PL (Ϫ1 Ϯ 6 nM/min, 95% CI; Ϫ5, 2; P Ͻ 0.01). During moderate-intensity exercise, steady-state pulmonary V O2 was lower in H-BR (1.91 Ϯ 0.28 l/min, 95% CI; 1.77, 2.13) compared with H-PL (2.05 Ϯ 0.25 l/min, 95% CI; 1.93, 2.26; P ϭ 0.02), and V O2 kinetics was faster in H-BR (: 24 Ϯ 13 s, 95% CI; 15, 32) compared with H-PL (31 Ϯ 11 s, 95% CI; 23, 38; P ϭ 0.04). NO 3 Ϫ supplementation had no significant effect on V O2 kinetics during severe-intensity exercise in hypoxia, or during moderate-intensity or severe-intensity exercise in normoxia. Tolerance to severe-intensity exercise was improved by NO 3 Ϫ in hypoxia (H-PL: 197 Ϯ 28; 95% CI; 173, 220 vs. H-BR: 214 Ϯ 43 s, 95% CI; 177, 249; P ϭ 0.04) but not normoxia. The metabolism of NO 2 Ϫ during exercise is altered by NO 3 Ϫ supplementation, exercise, and to a lesser extent, hypoxia. In hypoxia, NO 3 Ϫ supplementation enhances V O 2 kinetics during moderate-intensity exercise and improves severe-intensity exercise tolerance. These findings may have important implications for individuals exercising at altitude. hypoxia; beetroot juice; nitric oxide; efficiency; performance NITRIC OXIDE (NO) IS A UBIQUITOUS, water-soluble, free radical gas that plays a crucial role in many biological processes. Effective NO production is important in normal physiological functioning, from the regulation of blood flow, muscle contractility, and mitochondrial respiration to host defense, neurotransmission, and glucose and calcium homeostasis (11,17,60). NO production via the oxidation of L-arginine, in a process catalyzed by nitric oxide synthase (NOS), may be blunted in conditions of reduced O 2 availability (52). It is now widely accepted that NO can also be generated via an alternative pathway, whereby inorganic nitrate (NO 3 Ϫ ) is reduced to nitrite (NO 2 Ϫ ) and further to NO. This NOS-and O 2 -independent NO 3 Ϫ -NO 2 Ϫ -NO pathway represents a complementary system for NO synthesis spanning a broad range of redox states (49). In addition to being produced endogenously, the body's NO 3 Ϫ stores can be increased via the diet, with green leafy vegetables and beetroot being particularly rich in NO 3 Ϫ . Upon ingestion, inorganic NO 3 Ϫ is absorbed from the ...

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The interaction of serum albumin with a model epithelial mucin from pig stomach was explored by rotary viscometry. During 30 min of incubation of human serum albumin(20mg/ml) and pig gastric mucin (8mg/ml) in iso-osmotic buffers at 37 degrees C, the solution became markedly viscous. Viscosity enhancement was proportional to albumin concentration (2-40mg/ml), was most pronounced under conditions of low shear rate (less than 45S-1), and was considerably greater than the additive or multiplicative viscosity values calculated from albumin or mucin solutions measured separately. The viscous mucin-albumin complex was destroyed by high shear rates (greater than 90S-1), but slowly re-formed under zero shear conditions. Elevation of pH (7 to 9), ionic strength (0.1 to 1.0), and addition of disodium EDTA (5mM) did not cause marked or specific alterations in the viscosity of the mixture, suggesting that electrostatic interactions probably do not stabilize mucin-albumin complexes. Urea (7M) and heating (35 to 55 degrees C) caused a major increase in the viscosity of mucin and mucin-albumin mixtures, suggesting that rupture of hydrogen bonds, unfolding and partial denaturation of mucin promotes greater intertangling (possibly hydrophobic interactions) between mucin and albumin molecules. The implications of mucin-albumin interaction in diseases associated with mucus obstruction are briefly discussed.

A procedure was developed to identify receptors for dopamine and serotonin separately and selectively by means of [3H]spiperone and to measure the density of each receptor in different regions of the rat brain. In the striatum, the binding of [3H]spiperone to dopamine receptors was inhibited by sulpiride but not by quinazolinedone R43448 (R43448); in the frontal cortex, however, the binding of [3H]spiperone to serotonin receptors was inhibited by R43448 but not by sulpiride. Thus, the density of dopamine receptors (D2 sites) was measured by [3H]spiperone binding in the presence of 0.1 microM R43448 (to preclude the attachment of the 3H-labeled ligand to serotonin sites), while the density of serotonin receptors (S2 sites) was measured by [3H]spiperone binding in the presence of 10 microM sulpiride (to preclude the attachment of the 3H-labeled ligand to dopamine sites). The density of D2 sites was highest in the striatum, followed by the olfactory tubercle, hypothalamus, substantia nigra, and the lower pons--medulla region. All five regions had similar dissociation constants (Kd values) of 0.05--0.15 nM. The density of S2 sites was highest in the frontal cortex, followed by the posterior cortex, olfactory tubercle, striatum, hypothalamus, and thalamus, and all regions had Kd values in the range 0.6--2.3 nM. Thus, because the Kd values were similar for all regions, and because Scatchard analyses revealed a single set of sites for either D2 or S2 (where detected), the main criteria for resolving the dopamine and serotonin components of [3H]spiperone binding were considered fulfilled.

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