Effects of nitrate supplementation in trained and untrained muscle are modest with initial high plasma nitrite levels.

Nitrate (NO3-) supplementation resulting in higher plasma nitrite (NO2-) is reported to lower resting mean arterial blood pressure (MAP) and oxygen uptake (VO2 ) during submaximal exercise in non-athletic populations, whereas effects in general are absent in endurance-trained individuals. To test whether physiologic effects of NO3- supplementation depend on local muscular training status or cardiovascular fitness, male endurance-trained cyclists (CYC, n=9, VO2 -max: 64±3 mL/min/kg; mean±SD) and recreational active subjects serving as a control group (CON, n=8, 46±3 mL/min/kg), acutely consumed nitrate-rich beetroot juice ([NO3-] ~9 mmol) (NIT) or placebo (PLA) with assessment of resting MAP and energy expenditure during moderate intensity (~50% VO2 -max) and incremental leg cycling (LEG-ex) and arm-cranking exercise (ARM-ex). NIT increased (P<.001) resting plasma NO3- by ~1200% relative to PLA. Plasma NO2- increased ~25% (P<.01) with a significant change only in CYC. LEG-ex VO2 (~2.60 L/min), ARM-ex VO2 (~1.14 L/min), and resting MAP (~87 mm Hg) remained unchanged for CYC, and similarly for CON, no changes were observed for LEG-ex VO2 (~2.03 L/min), ARM-ex VO2 (~1.06 L/min), or resting MAP (~85 mm Hg). VO2 -max was not affected by supplementation, but incremental test peak power was higher (P<.05) in LEG-ex for CYC in NIT relative to PLA (418±47 vs 407±46 W). In both CYC and CON, high initial baseline values and small increases in plasma NO2- after NIT may have lowered the effect of the intervention implying that muscular and cardiovascular training status is likely not the only factors that influence the physiologic effects of NO3- supplementation.

Effect of whey protein- and carbohydrate-enriched diet on glycogen resynthesis during the first 48 h after a soccer game.

The effect of a whey protein- and carbohydrate (CHO)-enriched diet on the rate of muscle glycogen resynthesis after a soccer match was examined. Sixteen elite soccer players were randomly assigned to a group ingesting a diet rich in carbohydrates and whey protein [CHO, protein, and fat content was 71, 21, and 8E%, respectively; high content of carbohydrates and whey protein (HCP), n = 9] or a group ingesting a normal diet (55, 18, and 26E%; control [CON], n = 7) during a 48-h recovery period after a soccer match. CON and three additional players carried out a 90- and 60-min simulated match without body contacts (SIM90 and SIM60). Muscle glycogen was lowered (P < 0.05) by 54, 48, 53, and 38% after the matches in CON, HCP, SIM90, and SIM60, respectively. Glycogen resynthesis during the first 48 h after the match was not different between CON and HCP, whereas glycogen resynthesis was slower (P < 0.05) during the first 24 h after SIM60 than SIM90 (2.88 ± 0.84 vs 4.32 ± 0.54 mmol/kg dw/h). In HCP, glycogen content in type II muscle fibers was still lowered 48 h after the match. In conclusion, glycogen resynthesis 48 h after a soccer match is not elevated by ingestion of a HCP diet. Furthermore, glycogen resynthesis does not appear to be impaired by body contacts during a match.

Influence of nitrate supplementation on VO2 kinetics and endurance of elite cyclists.

The present study examined if an elevated nitrate intake would improve VO(2) kinetics, endurance, and repeated sprint capacity in elite endurance athletes. Ten highly trained cyclists (72 ± 4 mL O(2) /kg/min, mean ± standard deviation) underwent testing for VO(2) kinetics (3 × 6 min at 298 ± 28 W), endurance (120 min preload followed by a 400-kcal time trial), and repeated sprint capacity (6 × 20 s sprints, recovery 100 s) during two 6-day periods in randomized order with a daily ingestion of either 0.5 L beetroot (BR) juice to increase nitrate levels or a 0.5 L placebo (PLA) drink with blackcurrant juice. Plasma NOx (nitrate + nitrite) levels were higher (P < 0.01) in BR (147 ± 102 and 159 ± 103 µM after 4 and 6 days of beverage intake, respectively) compared with PLA (41 ± 10 and 40 ± 7 µM). VO(2) kinetics and exercise economy were the same in BR and PLA. Time-trial performance was similar with an average completion time of 18:20 and 18:37 min:s in BR and PLA, respectively, with average power outputs of 290 ± 43 W in BR and 285 ± 44 W in PLA. Peak and mean power during repeated sprinting were similar in BR and PLA. In contrast to observations in moderately trained subjects intake of BR juice had no effect on VO(2) kinetics and performance in elite cyclists.

[Evaluation of ear temperature measurements in a geriatric department]. / Evaluering af øretemperaturmåling på en geriatrisk afdeling.

We evaluated an infrared tympanic thermometer (Genius 3000A) by comparing it with parallel measurements with an electronic rectal thermometer (Philips HP 5316) on 121 patients admitted to a geriatric department. Rectal temperature was on average 0.14 degree C +/- (ISD) above the ear temperature. 95% of the differences are within the interval from -1.18 degrees C to 1.46 degrees C. The coefficient of determination was only 0.30. The tympanic thermometer, Genius 3000A, cannot be recommended for daily use on a geriatric ward.

The sparteine/debrisoquine (CYP2D6) oxidation polymorphism and the risk of Parkinson's disease: a meta-analysis.

The association between the sparteine/debrisoquine (CYP2D6) oxidation polymorphism and the risk of Parkinson's disease was examined in a meta-analysis of case-control studies. The odds ratio was calculated for the risk of Parkinson's disease among poor metabolisers compared with extensive metabolisers. Twenty-one studies were identified of which six were excluded because they were not reported as full papers (n = 3), used incomplete genotype analysis (n = 2) or used Parkinson patients as both control individuals and cases (n = 1). The overall odds ratio was 1.48 (95% confidence interval 1.10-1.99). The odds ratio was 1.05 (95% confidence interval 0.63-1.77) in studies discriminating extensive and poor metabolisers by phenotyping (n = 8) and 1.67 (95% confidence interval 1.11-2.50) in studies using genotyping (n = 7). This difference was caused by a single large study using genotyping. We conclude that there is no convincing evidence of an association between the debrisoquine/sparteine polymorphism and Parkinson's disease. However, it could prove worthwhile to perform another large study using genotyping.

The sparteine/debrisoquine (CYP2D6) oxidation polymorphism and the risk of lung cancer: a meta-analysis.

OBJECTIVE: To examine the association between the sparteine/debrisoquine (CYP2D6) oxidation polymorphism and the risk of lung cancer. METHOD: Meta-analysis of case-control studies using a random effects model. The "Main outcome measure" was the odds ratio for the risk of lung cancer, using extensive metabolisers as the reference group. RESULTS: Thirteen studies were identified. The studies were too heterogeneous to be pooled the size of the odds ratio increased with the sample size. When the analysis was restricted to the largest studies, there was no difference in risk between poor and extensive metabolisers (odds ratio 0.95, 95% confidence interval 0.68-1.33). CONCLUSION: No association was found between the CYP2D6 oxidation polymorphism and lung cancer risk when sample size bias was taken into account.

Recombinant human extrinsic pathway inhibitor. Production, isolation, and characterization of its inhibitory activity on tissue factor-initiated coagulation reactions.

Previous studies have shown that extrinsic pathway inhibitor (EPI) is an effective inhibitor of factor Xa alone or factor VIIa-tissue factor complex in the presence of factor Xa. Since tissue factor exposure is implicated in thrombogenesis, we hypothesized that EPI may be valuable in the treatment of some thromboembolic episodes. Furthermore, EPI may be an important factor in bleeding complications in hemophiliacs. In the present study, human EPI was expressed in baby hamster kidney cells using a mammalian expression vector. Transfected cells expressed 1-2 micrograms/ml of recombinant EPI (rEPI) which was purified to homogeneity by heparin-Sepharose chromatography, ion-exchange chromatography, and reverse phase high performance liquid chromatography. Purified rEPI exhibited a specific activity of 30,000 units/mg and migrated as a single band in sodium dodecyl sulfate-polyacrylamide gel electrophoresis with an apparent molecular weight of 42,000. In addition, the NH2-terminal sequence of rEPI was identical to that of HepG2 EPI and HeLa EPI. The ability of rEPI to inhibit factor X activation by a complex of factor VIIa-tissue factor was then examined in the presence and absence of plasma concentrations of human factors VIII and IX. Using relipidated human brain tissue factor apoprotein, rEPI inhibited the factor VIIa-mediated activation of factor X half-maximally at 2.5 and 1 nM in the presence and absence of factors VIII and IX, respectively. Using monolayers of a human bladder carcinoma cell line (J82) as the source of tissue factor, the activation of factor X by cell-bound factor VIIa was inhibited half-maximally by 5 nM rEPI in the presence of factors VIII and IX. The proteolytic activity of J82 cell-bound factor Xa toward prothrombin was inhibited half-maximally at approximately 5 nM rEPI, while the amidolytic activity of factor Xa in solution was inhibited by rEPI with a Ki of 130 pM. Recombinant EPI also inhibited the amidolytic activity of factor VIIa half-maximally at 10 nM rEPI in the presence of relipidated tissue factor apoprotein and calcium. These results indicate that, in the presence of plasma concentrations of factors VIII and IX, at least 10 times the plasma concentration of EPI is required to reduce factor VIIa-dependent factor X activation one order of magnitude in vitro. In the absence of functional factor VIII and IX, rEPI at plasma levels was a potent inhibitor of factor VIIa-mediated factor X activation, and this activity presumably accounts for the inability of hemophiliacs to initiate hemostasis via the extrinsic pathway.

Changing the insulin receptor to possess insulin-like growth factor I ligand specificity.

To examine the role of the N-terminal part of the insulin-like growth factor I (IGF-I) receptor and insulin receptor in determining ligand specificity, we prepared an expression vector encoding a hybrid receptor where exon 1 (encoding the signal peptide and seven amino acids of the alpha-subunit), exon 2, and exon 3 of the insulin receptor were replaced with the corresponding IGF-I receptor cDNA (938 nucleotides). To allow direct quantitative comparison of the binding capabilities of this hybrid receptor with those of the human IGF-I receptor and the insulin receptor, all three receptors were expressed in baby hamster kidney (BHK) cells as soluble molecules and partially purified before characterization. The hybrid IGF-I/insulin receptor bound IGF-I with an affinity comparable to that of the wild-type IGF-I receptor. In contrast, the hybrid receptor no longer displayed high-affinity binding of insulin. These results directly demonstrate that it is possible to change the specificity of the insulin receptor to that of the IGF-I receptor and, furthermore, that the binding specificity for IGF-I is encoded within the nucleotide sequence from 135 to 938 of the IGF-I receptor cDNA. Since the hybrid receptor only bound insulin with low affinity, the insulin binding region is likely to be located within exons 2 and 3 of the insulin receptor.