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Träfflista för sökning "WFRF:(Lundberg JO) srt2:(2010-2014)"

Sökning: WFRF:(Lundberg JO) > (2010-2014)

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  • Cermak, NM, et al. (författare)
  • No improvement in endurance performance after a single dose of beetroot juice
  • 2012
  • Ingår i: International journal of sport nutrition and exercise metabolism. - : Human Kinetics. - 1543-2742 .- 1526-484X. ; 22:6, s. 470-478
  • Tidskriftsartikel (refereegranskat)abstract
    • Dietary nitrate supplementation has received much attention in the literature due to its proposed ergogenic properties. Recently, the ingestion of a single bolus of nitrate-rich beetroot juice (500 ml, ~6.2 mmol NO3−) was reported to improve subsequent time-trial performance. However, this large volume of ingested beetroot juice does not represent a realistic dietary strategy for athletes to follow in a practical, performancebased setting. Therefore, we investigated the impact of ingesting a single bolus of concentrated nitrate-rich beetroot juice (140 ml, ~8.7 mmol NO3−) on subsequent 1-hr time-trial performance in well-trained cyclists.Methods:Using a double-blind, repeated-measures crossover design (1-wk washout period), 20 trained male cyclists (26 ± 1 yr, VO2peak 60 ± 1 ml · kg−1 · min−1, Wmax 398 ± 7.7 W) ingested 140 ml of concentrated beetroot juice (8.7 mmol NO3−; BEET) or a placebo (nitrate-depleted beetroot juice; PLAC) with breakfast 2.5 hr before an ~1-hr cycling time trial (1,073 ± 21 kJ). Resting blood samples were collected every 30 min after BEET or PLAC ingestion and immediately after the time trial.Results:Plasma nitrite concentration was higher in BEET than PLAC before the onset of the time trial (532 ± 32 vs. 271 ± 13 nM, respectively; p < .001), but subsequent time-trial performance (65.5 ± 1.1 vs. 65 ± 1.1 s), power output (275 ± 7 vs. 278 ± 7 W), and heart rate (170 ± 2 vs. 170 ± 2 beats/min) did not differ between BEET and PLAC treatments (all p > .05).Conclusion:Ingestion of a single bolus of concentrated (140 ml) beetroot juice (8.7 mmol NO3−) does not improve subsequent 1-hr time-trial performance in well-trained cyclists.
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  • Crespo, AS, et al. (författare)
  • Nasal nitric oxide and regulation of human pulmonary blood flow in the upright position
  • 2010
  • Ingår i: Journal of applied physiology (Bethesda, Md. : 1985). - : American Physiological Society. - 1522-1601 .- 8750-7587. ; 108:1, s. 181-188
  • Tidskriftsartikel (refereegranskat)abstract
    • There are a number of evidences suggesting that lung perfusion distribution is under active regulation and determined by several factors in addition to gravity. In this work, we hypothesised that autoinhalation of nitric oxide (NO), produced in the human nasal airways, may be one important factor regulating human lung perfusion distribution in the upright position. In 15 healthy volunteers, we used single-photon emission computed tomography technique and two tracers (99mTc and 113mIn) labeled with human macroaggregated albumin to assess pulmonary blood flow distribution. In the sitting upright position, subjects first breathed NO free air through the mouth followed by the administration of the first tracer. Subjects then switched to either nasal breathing or oral breathing with the addition of exogenous NO-enriched air followed by the administration of the second tracer. Compared with oral breathing, nasal breathing induced a blood flow redistribution of ∼4% of the total perfusion in the caudal to cranial and dorsal to ventral directions. For low perfused lung regions like the apical region, this represents a net increase of 24% in blood flow. Similar effects were obtained with the addition of exogenous NO during oral breathing, indicating that NO and not the breathing condition was responsible for the blood flow redistribution. In conclusion, these results provide evidence that autoinhalation of endogenous NO from the nasal airways may ameliorate the influence of gravity on pulmonary blood flow distribution in the upright position. The presence of nasal NO only in humans and higher primates suggest that it may be an important part of the adaptation to bipedalism.
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  • Feelisch, M, et al. (författare)
  • Is sunlight good for our heart?
  • 2010
  • Ingår i: European heart journal. - : Oxford University Press (OUP). - 1522-9645 .- 0195-668X. ; 31:9, s. 1041-1045
  • Tidskriftsartikel (refereegranskat)
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  • Gronros, J, et al. (författare)
  • Arginase inhibition restores in vivo coronary microvascular function in type 2 diabetic rats
  • 2011
  • Ingår i: American journal of physiology. Heart and circulatory physiology. - : American Physiological Society. - 1522-1539 .- 0363-6135. ; 300:4, s. H1174-H1181
  • Tidskriftsartikel (refereegranskat)abstract
    • Nitric oxide (NO) is crucial for maintaining normal endothelial function and vascular integrity. Increased arginase activity in diabetes might compete with NO synthase (NOS) for their common substrate arginine, resulting in diminished production of NO. The aim of this study was to evaluate coronary microvascular function in type 2 diabetic Goto-Kakizaki (GK) rats using in vivo coronary flow velocity reserve (CFVR) and the effect of arginase inhibition to restore vascular function. Different groups of GK and Wistar rats were given vehicle, the arginase inhibitor Nω-hydroxy-nor-l-arginine (nor-NOHA), l-arginine, and the NOS inhibitor NG-monomethyl -l-arginine (l-NMMA). GK rats had impaired CFVR compared with Wistar rats (1.31 ± 0.09 vs. 1.87 ± 0.05, P < 0.001). CFVR was restored by nor-NOHA treatment compared with vehicle in GK rats (1.71 ± 0.13 vs. 1.23 ± 0.12, P < 0.05) but remained unchanged in Wistar rats (1.88 ± 0.10 vs. 1.79 ± 0.16). The beneficial effect of nor-NOHA in GK rats was abolished after NOS inhibition. CFVR was not affected by arginine compared with vehicle. Arginase II expression was increased in the aorta and myocardium from GK rats compared with Wistar rats. Citrulline-to-ornithine and citrulline-to-arginine ratios measured in plasma increased significantly more in GK rats than in Wistar rats after nor-NOHA treatment, suggesting a shift of arginine utilization from arginase to NOS. In conclusion, coronary artery microvascular function is impaired in the type 2 diabetic GK rat. Treatment with nor-NOHA restores the microvascular function by a mechanism related to increased utilization of arginine by NOS and increased NO availability.
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  • Larsen, Filip, 1977-, et al. (författare)
  • Dietary inorganic nitrate improves mitochondrial efficiency in humans.
  • 2011
  • Ingår i: Cell Metabolism. - : Elsevier BV. - 1550-4131 .- 1932-7420. ; 13:2, s. 149-159
  • Tidskriftsartikel (refereegranskat)abstract
    • Nitrate, an inorganic anion abundant in vegetables, is converted in vivo to bioactive nitrogen oxides including NO. We recently demonstrated that dietary nitrate reduces oxygen cost during physical exercise, but the mechanism remains unknown. In a double-blind crossover trial we studied the effects of a dietary intervention with inorganic nitrate on basal mitochondrial function and whole-body oxygen consumption in healthy volunteers. Skeletal muscle mitochondria harvested after nitrate supplementation displayed an improvement in oxidative phosphorylation efficiency (P/O ratio) and a decrease in state 4 respiration with and without atractyloside and respiration without adenylates. The improved mitochondrial P/O ratio correlated to the reduction in oxygen cost during exercise. Mechanistically, nitrate reduced the expression of ATP/ADP translocase, a protein involved in proton conductance. We conclude that dietary nitrate has profound effects on basal mitochondrial function. These findings may have implications for exercise physiology- and lifestyle-related disorders that involve dysfunctional mitochondria.
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  • Larsen, Filip, et al. (författare)
  • Mitochondrial oxygen affinity predicts basal metabolic rate in humans
  • 2011
  • Ingår i: The FASEB Journal. - : Wiley. - 0892-6638 .- 1530-6860. ; 25:8, s. 2843-52
  • Tidskriftsartikel (refereegranskat)abstract
    • The basal metabolic rate (BMR) is referred to as the minimal rate of metabolism required to support basic body functions. It is well known that individual BMR varies greatly, even when correcting for body weight, fat content, and thyroid hormone levels, but the mechanistic determinants of this phenomenon remain unknown. Here, we show in humans that mass-related BMR correlates strongly to the mitochondrial oxygen affinity (p50(mito); R(2)=0.66, P=0.0004) measured in isolated skeletal muscle mitochondria. A similar relationship was found for oxygen affinity and efficiency during constant-load submaximal exercise (R(2)=0.46, P=0.007). In contrast, BMR did not correlate to overall mitochondrial density or to proton leak. Mechanistically, part of the p50(mito) seems to be controlled by the excess of cytochrome c oxidase (COX) protein and activity relative to other mitochondrial proteins. This is illustrated by the 5-fold increase in p50(mito) after partial cyanide inhibition of COX at doses that do not affect maximal mitochondrial electron flux through the ETS. These data suggest that the interindividual variation in BMR in humans is primarily explained by differences in mitochondrial oxygen affinity. The implications of these findings are discussed in terms of a trade-off between aerobic efficiency and power.
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  • Lundberg, JO, et al. (författare)
  • NO-synthase independent NO generation in mammals
  • 2010
  • Ingår i: Biochemical and biophysical research communications. - : Elsevier BV. - 1090-2104 .- 0006-291X. ; 396:1, s. 39-45
  • Tidskriftsartikel (refereegranskat)
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  • Nijs, Jo, et al. (författare)
  • Fear of movement and avoidance behaviour toward physical activity in chronic-fatigue syndrome and fibromyalgia: state of the art and implications for clinical practice.
  • 2013
  • Ingår i: Clinical Rheumatology. - : Springer Science and Business Media LLC. - 0770-3198 .- 1434-9949. ; 32:8, s. 1121-9
  • Tidskriftsartikel (refereegranskat)abstract
    • Severe exacerbation of symptoms following physical activity is characteristic for chronic-fatigue syndrome (CFS) and fibromyalgia (FM). These exacerbations make it understandable for people with CFS and FM to develop fear of performing body movement or physical activity and consequently avoidance behaviour toward physical activity. The aims of this article were to review what measures are available for measuring fear of movement and avoidance behaviour, the prevalence fear of movement and avoidance behaviour toward physical activity and the therapeutic options with fear of movement and avoidance behaviour toward physical activity in patients with CFS and FM. The review revealed that fear of movement and avoidance behaviour toward physical activity is highly prevalent in both the CFS and FM population, and it is related to various clinical characteristics of CFS and FM, including symptom severity and self-reported quality of life and disability. It appears to be crucial for treatment (success) to identify CFS and FM patients displaying fear of movement and avoidance behaviour toward physical activity. Individually tailored cognitive behavioural therapy plus exercise training, depending on the patient's classification as avoiding or persisting, appears to be the most promising strategy for treating fear of movement and avoidance behaviour toward physical activity in patients with CFS and FM.
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