Dietary nitrate reduces maximal oxygen consumption while maintaining work performance in maximal exercise

Larsen, Filip J.; Weitzberg, Eddie; Lundberg, Jon O.; Ekblom, Björn

doi:10.1016/j.freeradbiomed.2009.11.006

Cited by 270 publications

(276 citation statements)

References 46 publications

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“…In the severe exerciseintensity domain, the V O 2 at the point of volitional exhaustion would be expected to equal the maximum V O 2 (V O 2 max ) (11). Our results are therefore consistent with some (3, 37) but not all (5,25) previous studies that indicate that NO 3 Ϫ supplementation does not reduce V O 2 max . Interestingly, there was a disconnect between the effects of BR on steady-state V O 2 during moderate-intensity exercise (where the greatest reduction occurred at the highest dose of NO 3 Ϫ ) and the effects of BR on exercise tolerance (where the increased time-to-task failure was similar with 8.4 and 16.8 mmol NO 3 Ϫ ).…”

supporting

confidence: 94%

“…We assessed the acute response to three different doses of BR at 2.5 h postingestion, based on the significant dose-dependent elevation in plasma [NO 2 Ϫ ] observed at 2-3 h postingestion in S 1 (Fig. 1B) (37) but is smaller than the 6% reduction reported 1 h postingestion of 0.033 mmol/kg BM sodium nitrate (25). In contrast to acute ingestion, longer-term BR supplementation (3-6 days at approximately 5-7 mmol NO 3 Ϫ /day) resulted in an approximate 5-7% reduction in steady-state V O 2 during moderate-intensity cycling (3,26) and running (22).…”

Section: Dose Response: Moderate-intensity Exercisementioning

confidence: 99%

“…Previous studies have indicated that the lowering of submaximal exercise V O 2 , following dietary NO 3 Ϫ supplementation, may result from improved mitochondrial efficiency (25) and/or a reduction in the ATP cost of muscle force production (4). Alterations in protein expression have been proposed as the mechanistic basis for these effects (17,24); however, it is unlikely that these alterations occur quickly enough to explain the effects observed so soon (1-2.5 h) after NO 3 Ϫ ingestion (25,37).…”

Section: Dose Response: Moderate-intensity Exercisementioning

confidence: 99%

“…Alterations in protein expression have been proposed as the mechanistic basis for these effects (17,24); however, it is unlikely that these alterations occur quickly enough to explain the effects observed so soon (1-2.5 h) after NO 3 Ϫ ingestion (25,37). Alternatively, NO may acutely and reversibly impact protein function through post-translational protein modifications.…”

Section: Dose Response: Moderate-intensity Exercisementioning

confidence: 99%

“…It appears that these effects are related to NO 2 Ϫ or NO-mediated enhancements of muscle contractile function (2,17) and/or mitochondrial efficiency (24) and/or enhanced muscle blood flow, especially to type II fibers (14). Importantly, a reduction of the O 2 cost of exercise (25,37) and improved exercise performance (21) has also been reported as early as 2.5 h following a single dose of dietary NO 3 Ϫ , which is consistent with the time required for the peak plasma [NO 2 Ϫ ] to be attained (39). However, since all exercise-performance studies completed to date with BR have administered approximately 5-8 mmol NO 3 Ϫ , it is unclear whether a dose-response relationship exists between acute NO 3 Ϫ intake and the physiological responses to exercise.…”

mentioning

confidence: 99%

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Ϫ ] increased in a dose-dependent manner, with the peak changes occurring at approximately 2-3 h. Compared with PL, 70 ml BR did not alter the physiological responses to exercise. However, 140 and 280 ml BR reduced the steady-state oxygen (O2) uptake during moderateintensity exercise by 1.7% (P ϭ 0.06) and 3.0% (P Ͻ 0.05), whereas time-to-task failure was extended by 14% and 12% (both P Ͻ 0.05), respectively, compared with PL. The results indicate that whereas plasma [NO 2 Ϫ ] and the O2 cost of moderate-intensity exercise are altered dose dependently with NO 3 Ϫ -rich BR, there is no additional improvement in exercise tolerance after ingesting BR containing 16.8 compared with 8.4 mmol NO 3 Ϫ . These findings have important implications for the use of BR to enhance cardiovascular health and exercise performance in young adults.nitrate; nitrite; nitric oxide; blood pressure; exercise economy; O2 uptake; exercise tolerance NITRIC OXIDE (NO) IS A GASEOUS signaling molecule that modulates human physiological function via its role in, for example, the regulation of blood flow, neurotransmission, immune function, glucose and calcium homeostasis, muscle contractility, and mitochondrial respiration (9, 36). 1 NO is generated through the oxidation of the amino acid L-arginine Ϫ ] peaked 3 h postingestion, remained close to peak values until 5 h postingestion, and returned to baseline after 24 h (39). The systolic and diastolic BP and the mean arterial pressure (MAP) were reduced significantly, by ϳ10, ϳ8, and ϳ8 mmHg, respectively, at 2.5-3 h after BR intake. The same research group later reported a dose-dependent increase in plasma [ ] was accompanied by significant reductions in both systolic BP (of ϳ2, ϳ6, and ϳ9 mmHg, respectively) and diastolic BP (of ϳ4, ϳ4, and ϳ6 mmHg, respectively). However, since BR contains polyphenols and antioxidants, which can facilitate the synthesis of NO from NO 2 Ϫ in the stomach (30), it is unclear whether BP is similarly impacted when different doses of BR are ingested compared with equivalent doses of NO 3 Ϫ salts. Given the growing interest in dietary NO 3 Ϫ supplementation in the form of BR amongst athletes and the general population, it is important to determine the pharmacokinetic-pharmacodynamic relationship between different volumes of BR consumption and changes in plasma [NO 2 Ϫ ] and BP to establish an optimal dose for beneficial effects.Recent investigations suggest that dietary NO 3 Ϫ supplementation has the potential to influence human physiology beyond 1 This article is the topic of an Invited Editorial by L. Burke (5a).

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confidence: 94%