Acute dietary nitrate supplementation does not augment submaximal forearm exercise hyperemia in healthy young men

Kim, Jin-Kwang; Moore, David; Maurer, David; Kim‐Shapiro, Daniel B.; Basu, Swati; Flanagan, Michael; Skulas‐Ray, Ann C.; Kris-Etherton, Penny M.; Proctor, David N.

doi:10.1139/apnm-2014-0228

Cited by 41 publications

(35 citation statements)

References 40 publications

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“…Results from a meta‐analysis (Siervo, Lara, Ogbonmwan, & Mathers, ) showed that in healthy subjects, acute and chronic inorganic nitrate supplementation induces a 4.4 mmHg mean reduction in systolic blood pressure. Similar to the present study, however, several studies, especially including healthy young adults, reported no effect of NO precursor supplementation on resting blood pressure (Kim et al., ; Le Roux‐Mallouf et al., ; Wightman et al., ). There are several possible explanations for these contrasting results.…”

Section: Discussionsupporting

confidence: 85%

“…() have shown that acute beetroot juice consumption increased human muscle blood flow during moderate‐to high‐intensity handgrip exercise via local vasodilatation. Previous studies (Craig, Broxterman, Smith, Allen, & Barstow, ; Kim et al., ), measuring muscle oxygenation by NIRS in healthy humans during local exercise, have not found a positive effect of acute nitrate supplementation. There are several observations that merit discussion.…”

Section: Discussionmentioning

confidence: 86%

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Effects of acute nitric oxide precursor intake on peripheral and central fatigue during knee extensions in healthy men

Roux-Mallouf

Laurent

Besset

et al. 2019

Experimental Physiology

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New Findings What is the central question of this study?What is the effect of acute NO precursor intake on vascular function, muscle and cerebral oxygenation and peripheral and central neuromuscular fatigue during knee‐extension exercise? What is the main finding and its importance?Acute NO precursor ingestion increases the plasma concentrations of NO precursors (nitrate, arginine and citrulline) and enhances post‐ischaemic vasodilatation, but has no significant effect on muscle and cerebral oxygenation, peripheral and central mechanisms of neuromuscular fatigue and, consequently, does not improve exercise performance. Abstract Nitric oxide (NO) plays an important role in matching blood flow to oxygen demand in the brain and contracting muscles during exercise. Previous studies have shown that increasing NO bioavailability can improve muscle function. The aim of this study was to assess the effect of acute NO precursor intake on muscle and cerebral oxygenation and on peripheral and central neuromuscular fatigue during exercise. In four experimental sessions, 15 healthy men performed a thigh ischaemia–reperfusion test followed by submaximal isometric knee extensions (5 s on–4 s off; 45% of maximal voluntary contraction) until task failure. In each session, subjects drank a nitrate‐rich beetroot juice containing 520 mg nitrate (N), N and citrulline (6 g; N+C), N and arginine (6 g; N+A) or a placebo (PLA). Prefrontal cortex and quadriceps near‐infrared spectroscopy parameters were monitored continuously. Transcranial magnetic stimulation and femoral nerve electrical stimulation were used to assess central and peripheral determinants of fatigue. The post‐ischaemic increase in thigh blood total haemoglobin concentration was larger in N (10.1 ± 3.7 mmol) and N+C (10.9 ± 3.3 mmol) compared with PLA (8.2 ± 2.7 mmol; P < 0.05). Nitric oxide precursors had no significant effect on muscle and cerebral oxygenation or on peripheral and central mechanisms of neuromuscular fatigue during exercise. The total number of knee extensions did not differ between sessions (N, 71.9 ± 33.2; N+A, 73.3 ± 39.4; N+C, 74.6 ± 34.0; PLA, 71.8 ± 39.9; P > 0.05). In contrast to the post‐ischaemic hyperaemic response, NO bioavailability in healthy subjects might not be the limiting factor for tissue perfusion and oxygenation during submaximal knee extensions to task failure.

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Section: Discussionsupporting

confidence: 85%

Section: Discussionmentioning

confidence: 86%

Effects of acute nitric oxide precursor intake on peripheral and central fatigue during knee extensions in healthy men

Roux-Mallouf

Laurent

Besset

et al. 2019

Experimental Physiology

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“…We did not collect plasma samples for

{NO}_{3}^{-}

{NO}_{2}^{-}

from subjects who received the placebo shots since previous studies clearly indicate that there is no change in plasma concentrations of

{NO}_{3}^{-}

and

{NO}_{2}^{-}

following placebo (

{NO}_{3}^{-}

free) BR ingestion (Kim et al. ; Lansley et al. ; Wylie et al.…”

Section: Resultsmentioning

confidence: 99%

“…; Kim et al. ) using acute

{NO}_{3}^{-}

supplementation via BR have failed to replicate these findings in rats. Although it is unclear why these studies did not demonstrate an increase in exercising muscle blood flow, issues related to the magnitude of increase in plasma

{NO}_{2}^{-}

, as well as exercise intensity and/or exercise duration may have contributed.…”

Section: Introductionmentioning

confidence: 97%

Acute ingestion of dietary nitrate increases muscle blood flow via local vasodilation during handgrip exercise in young adults

et al. 2018

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Dietary nitrate (NO3−) is converted to nitrite (NO2−) and can be further reduced to the vasodilator nitric oxide (NO) amid a low O2 environment. Accordingly, dietary NO3− increases hind limb blood flow in rats during treadmill exercise; however, the evidence of such an effect in humans is unclear. We tested the hypothesis that acute dietary NO3− (via beetroot [BR] juice) increases forearm blood flow (FBF) via local vasodilation during handgrip exercise in young adults (n = 11; 25 ± 2 years). FBF (Doppler ultrasound) and blood pressure (Finapres) were measured at rest and during graded handgrip exercise at 5%, 15%, and 25% maximal voluntary contraction (MVC) lasting 4 min each. At the highest workload (25% MVC), systemic hypoxia (80% SaO2) was induced and exercise continued for three additional minutes. Subjects ingested concentrated BR (12.6 mmol nitrate (n = 5) or 16.8 mmol nitrate (n = 6) and repeated the exercise bout either 2 (12.6 mmol) or 3 h (16.8 mmol) postconsumption. Compared to control, BR significantly increased FBF at 15% MVC (184 ± 15 vs. 164 ± 15 mL/min), 25% MVC (323 ± 27 vs. 286 ± 28 mL/min), and 25% + hypoxia (373 ± 39 vs. 343 ± 32 mL/min) and this was due to increases in vascular conductance (i.e., vasodilation). The effect of BR on hemodynamics was not different between the two doses of BR ingested. Forearm VO2 was also elevated during exercise at 15% and 25% MVC. We conclude that acute increases in circulating NO3− and NO2− via BR increases muscle blood flow during moderate‐ to high‐intensity handgrip exercise via local vasodilation. These findings may have important implications for aging and diseased populations that demonstrate impaired muscle perfusion and exercise intolerance.

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“…A randomized cross-over double-blind study in 14 healthy volunteers demonstrated that, while an 8 mmol dose of KNO 3 improved PWV and reduced BP measured 3 h following ingestion, no change in the FMD response was evident [115]. More recently, Kim and coworkers in a study assessing the increase in flow and brachial artery diameter following hand-grip exercise in healthy volunteers, also demonstrated improved PWV but no effect on endothelial function with dietary NO 3 − administration [118]. These observations contrast with two other published studies.…”

Section: No 2 − /No 3 − and Vascular Functionmentioning

confidence: 99%

A ‘green’ diet‐based approach to cardiovascular health? Is inorganic nitrate the answer?

Rathod

Velmurugan

Ahluwalia

2015

Molecular Nutrition Food Res

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Ingestion of fruit and vegetables rich in inorganic nitrate (NO(3)(-)) has emerged as an effective method for acutely elevating vascular nitric oxide (NO) levels through formation of an NO(2)(-) intermediate. As such a number of beneficial effects of NO(3)(-) and NO(2)(-) ingestion have been demonstrated including reductions in blood pressure, measures of arterial stiffness and platelet activity. The pathway for NO generation from such dietary interventions involves the activity of facultative oral microflora that facilitate the reduction of inorganic NO(3)(-), ingested in the diet, to inorganic NO(2)(-). This NO(2)(-) then eventually enters the circulation where, through the activity of one or more of a range of distinct NO(2)(-) reductases, it is chemically reduced to NO. This pathway provides an alternative route for in vivo NO generation that could be utilized for therapeutic benefit in those cardiovascular disease states where reduced bioavailable NO is thought to contribute to pathogenesis. Indeed, the cardiovascular benefits of NO(2)(-) and NO(3)(-) are now starting to be translated in patients in several clinical trials. In this review, we discuss recent evidence supporting the potential utility of delivery of NO(3)(-) or NO(2)(-) for the treatment of cardiovascular diseases.

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Acute dietary nitrate supplementation does not augment submaximal forearm exercise hyperemia in healthy young men

Cited by 41 publications

References 40 publications

Effects of acute nitric oxide precursor intake on peripheral and central fatigue during knee extensions in healthy men

Effects of acute nitric oxide precursor intake on peripheral and central fatigue during knee extensions in healthy men

Acute ingestion of dietary nitrate increases muscle blood flow via local vasodilation during handgrip exercise in young adults

A ‘green’ diet‐based approach to cardiovascular health? Is inorganic nitrate the answer?

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