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Dietary nitrate reduces maximal oxygen consumption while maintaining work performance in maximal exercise.
Gymnastik- och idrottshögskolan, GIH, Institutionen för idrotts- och hälsovetenskap, Björn Ekbloms forskningsgrupp.ORCID-id: 0000-0002-1343-8656
Gymnastik- och idrottshögskolan, GIH, Institutionen för idrotts- och hälsovetenskap, Björn Ekbloms forskningsgrupp.ORCID-id: 0000-0002-4030-5437
2010 (engelsk)Inngår i: Free Radical Biology & Medicine, ISSN 0891-5849, E-ISSN 1873-4596, Vol. 48, nr 2, s. 342-7Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

The anion nitrate-abundant in our diet-has recently emerged as a major pool of nitric oxide (NO) synthase-independent NO production. Nitrate is reduced stepwise in vivo to nitrite and then NO and possibly other bioactive nitrogen oxides. This reductive pathway is enhanced during low oxygen tension and acidosis. A recent study shows a reduction in oxygen consumption during submaximal exercise attributable to dietary nitrate. We went on to study the effects of dietary nitrate on various physiological and biochemical parameters during maximal exercise. Nine healthy, nonsmoking volunteers (age 30+/-2.3 years, VO(2max) 3.72+/-0.33 L/min) participated in this study, which had a randomized, double-blind crossover design. Subjects received dietary supplementation with sodium nitrate (0.1 mmol/kg/day) or placebo (NaCl) for 2 days before the test. This dose corresponds to the amount found in 100-300 g of a nitrate-rich vegetable such as spinach or beetroot. The maximal exercise tests consisted of an incremental exercise to exhaustion with combined arm and leg cranking on two separate ergometers. Dietary nitrate reduced VO(2max) from 3.72+/-0.33 to 3.62+/-0.31 L/min, P<0.05. Despite the reduction in VO(2max) the time to exhaustion trended to an increase after nitrate supplementation (524+/-31 vs 563+/-30 s, P=0.13). There was a correlation between the change in time to exhaustion and the change in VO(2max) (R(2)=0.47, P=0.04). A moderate dietary dose of nitrate significantly reduces VO(2max) during maximal exercise using a large active muscle mass. This reduction occurred with a trend toward increased time to exhaustion implying that two separate mechanisms are involved: one that reduces VO(2max) and another that improves the energetic function of the working muscles.

sted, utgiver, år, opplag, sider
2010. Vol. 48, nr 2, s. 342-7
HSV kategori
Forskningsprogram
Medicin/Teknik
Identifikatorer
URN: urn:nbn:se:gih:diva-1429DOI: 10.1016/j.freeradbiomed.2009.11.006PubMedID: 19913611OAI: oai:DiVA.org:gih-1429DiVA, id: diva2:360155
Tilgjengelig fra: 2010-11-02 Laget: 2010-11-02 Sist oppdatert: 2018-01-12bibliografisk kontrollert
Inngår i avhandling
1. Dietary inorganic nitrate: role in exercise physiology, cardiovascular and metabolic regulation
Åpne denne publikasjonen i ny fane eller vindu >>Dietary inorganic nitrate: role in exercise physiology, cardiovascular and metabolic regulation
2011 (engelsk)Doktoravhandling, med artikler (Annet vitenskapelig)
Abstract [en]

Nitric oxide (NO) is a ubiquitous signaling molecule with a vast number of tasks in the body, including regulation of cardiovascular and metabolic function. A decreased bioavailability of NO is a central event in disorders such as hypertension and metabolic syndrome. NO is also important in the regulation of blood flow and metabolism during exercise. The production of NO has previously been thought to be under the exclusive control of the nitric oxide synthases (NOS) but this view is now being seriously challenged. Recent lines of research suggest the existence of an NO-synthase independent pathway in which the supposedly inert NO oxidation products nitrate (NO3-) and nitrite (NO2-) can be reduced back to NO in blood and tissues. An important additional source of nitrate is our everyday diet and certain vegetables are particularly rich in this anion. In this thesis the possibility that dietary derived nitrate is metabolized in vivo to form reactive nitrogen oxides with NO-like bioactivity has been explored. It is shown that nitrate in amounts easily achieved via the diet, increases the systemic levels of nitrite and reduces blood pressure in healthy humans. Moreover, nitrate reduces whole body oxygen cost during submaximal and maximal exercise; a surprising effect involving improvement in mitochondrial efficiency and reduced expression of specific mitochondrial proteins regulating proton conductance. Alterations in the mitochondrial affinity for oxygen can explain this reduction in both submaximal and maximal oxygen consumption and predicts basal metabolic rate in humans. Finally, in mice lacking endothelial NO synthase, dietary supplementation with nitrate could reverse several features of the metabolic syndrome that develop in these animals. These studies demonstrate that dietary nitrate can fuel a nitrate-nitrite-NO pathway with important implications for cardiovascular and metabolic functions in health and disease.

sted, utgiver, år, opplag, sider
Solna: Karolinska Institutet, 2011
HSV kategori
Forskningsprogram
Medicin/Teknik
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urn:nbn:se:gih:diva-2079 (URN)978-91-7457-397-8 (ISBN)
Disputas
2011-06-17, Aulan Farmakologen, Nanna Svartz väg 2, Solna, 09:00 (engelsk)
Opponent
Veileder
Merknad
Avhandling vid Karolinska Institutet och Gymnastik- och idrottshögskolan, GIHTilgjengelig fra: 2012-01-09 Laget: 2012-01-09 Sist oppdatert: 2016-08-08bibliografisk kontrollert

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