scholarly journals Effect of acute dietary nitrate supplementation on sympathetic vasoconstriction at rest and during exercise

2019 ◽  
Vol 127 (1) ◽  
pp. 81-88 ◽  
Author(s):  
Christopher J. de Vries ◽  
Darren S. DeLorey
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Skeletal Muscle ◽  
Beetroot Juice ◽  
Total Plasma ◽  
Dietary Nitrate ◽  
Arterial Blood ◽  
Sympathetic Vasoconstriction ◽  
Nitrate Supplementation ◽  
Healthy Males

Dietary nitrate ([Formula: see text]) supplementation has been shown to reduce resting blood pressure. However, the mechanism responsible for the reduction in blood pressure has not been identified. Dietary [Formula: see text] supplementation may increase nitric oxide (NO) bioavailability, and NO has been shown to inhibit sympathetic vasoconstriction in resting and contracting skeletal muscle. Therefore, the purpose of this study was to investigate the hypothesis that acute dietary [Formula: see text] supplementation would attenuate sympathetic vasoconstrictor responsiveness at rest and during exercise. In a double-blind randomized crossover design, 12 men (23 ± 5 yr) performed a cold-pressor test (CPT) at rest and during moderate- and heavy-intensity alternate-leg knee-extension exercise after consumption of [Formula: see text] rich beetroot juice (~12.9 mmol [Formula: see text]) or a [Formula: see text]-depleted placebo (~0.13 mmol [Formula: see text]). Venous blood was sampled before and 2.5 h after the consumption of beetroot juice for the measurement of total plasma nitrite/[Formula: see text] [NOx]. Beat-by-beat blood pressure was measured by Finometer. Leg blood flow was measured at the femoral artery via Doppler ultrasound, and leg vascular conductance (LVC) was calculated. Sympathetic vasoconstrictor responsiveness was calculated as the percentage decrease in LVC in response to the CPT. Total plasma [NOx] was greater ( P < 0.001) in the [Formula: see text] (285 ± 120 µM) compared with the placebo (65 ± 30 µM) condition. However, mean arterial blood pressure and plasma catecholamines were not different ( P > 0.05) between [Formula: see text] and placebo conditions at rest or during moderate- and heavy-intensity exercise. Sympathetic vasoconstrictor responsiveness (Δ% LVC) was not different ( P > 0.05) between [Formula: see text] and placebo conditions at rest ([Formula: see text]: −33 ± 10%; placebo: −35 ± 11%) or during moderate ([Formula: see text]: −18 ± 8%; placebo: −20 ± 10%)- and heavy ([Formula: see text]: −12 ± 8%; placebo: −11 ± 9%)-intensity exercise. These data demonstrate that acute dietary [Formula: see text] supplementation does not alter sympathetic vasoconstrictor responsiveness at rest or during exercise in young healthy males. NEW & NOTEWORTHY Dietary nitrate may increase nitric oxide bioavailability, and nitric oxide has been shown to attenuate sympathetic vasoconstriction in resting and contracting skeletal muscle and enhance functional sympatholysis. However, the effect of dietary nitrate on sympathetic vasoconstrictor responsiveness is unknown. Acute dietary nitrate supplementation did not alter blood pressure or sympathetic vasoconstrictor responsiveness at rest or during exercise in young healthy males.

scholarly journals Acute beetroot juice supplementation on sympathetic nerve activity: a randomized, double-blind, placebo-controlled proof-of-concept study

2017 ◽  
Vol 313 (1) ◽  
pp. H59-H65 ◽  
Author(s):  
Karambir Notay ◽  
Anthony V. Incognito ◽  
Philip J. Millar
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Sympathetic Outflow ◽  
Beetroot Juice ◽  
Proof Of Concept ◽  
Burst Frequency ◽  
Double Blind ◽  
Dietary Nitrate ◽  
Nitrate Supplementation ◽  
Central Sympathetic Outflow

Acute dietary nitrate ([Formula: see text]) supplementation reduces resting blood pressure in healthy normotensives. This response has been attributed to increased nitric oxide bioavailability and peripheral vasodilation, although nitric oxide also tonically inhibits central sympathetic outflow. We hypothesized that acute dietary [Formula: see text] supplementation using beetroot (BR) juice would reduce blood pressure and muscle sympathetic nerve activity (MSNA) at rest and during exercise. Fourteen participants (7 men and 7 women, age: 25 ± 10 yr) underwent blood pressure and MSNA measurements before and after (165–180 min) ingestion of 70ml high-[Formula: see text] (~6.4 mmol [Formula: see text]) BR or [Formula: see text]-depleted BR placebo (PL; ~0.0055 mmol [Formula: see text]) in a double-blind, randomized, crossover design. Blood pressure and MSNA were also collected during 2 min of static handgrip (30% maximal voluntary contraction). The changes in resting MSNA burst frequency (−3 ± 5 vs. 3 ± 4 bursts/min, P = 0.001) and burst incidence (−4 ± 7 vs. 4 ± 5 bursts/100 heart beats, P = 0.002) were lower after BR versus PL, whereas systolic blood pressure (−1 ± 5 vs. 2 ± 5 mmHg, P = 0.30) and diastolic blood pressure (4 ± 5 vs. 5 ± 7 mmHg, P = 0.68) as well as spontaneous arterial sympathetic baroreflex sensitivity ( P = 0.95) were not different. During static handgrip, the change in MSNA burst incidence (1 ± 8 vs. 8 ± 9 bursts/100 heart beats, P = 0.04) was lower after BR versus PL, whereas MSNA burst frequency (6 ± 6 vs. 11 ± 10 bursts/min, P = 0.11) as well as systolic blood pressure (11 ± 7 vs. 12 ± 8 mmHg, P = 0.94) and diastolic blood pressure (11 ± 4 vs. 11 ± 4 mmHg, P = 0.60) were not different. Collectively, these data provide proof of principle that acute BR supplementation can decrease central sympathetic outflow at rest and during exercise. Dietary [Formula: see text] supplementation may represent a novel intervention to target exaggerated sympathetic outflow in clinical populations. NEW & NOTEWORTHY The hemodynamic benefits of dietary nitrate supplementation have been attributed to nitric oxide-mediated peripheral vasodilation. Here, we provide proof of concept that acute dietary nitrate supplementation using beetroot juice can decrease muscle sympathetic outflow at rest and during exercise in a normotensive population. These results have applications for targeting central sympathetic overactivation in disease.

scholarly journals Dietary nitrate restores compensatory vasodilation and exercise capacity in response to a compromise in oxygen delivery in the noncompensator phenotype

2017 ◽  
Vol 123 (3) ◽  
pp. 594-605 ◽  
Author(s):  
Robert F. Bentley ◽  
Jeremy J. Walsh ◽  
Patrick J. Drouin ◽  
Aleksandra Velickovic ◽  
Sarah J. Kitner ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Exercise Capacity ◽  
Perfusion Pressure ◽  
Beetroot Juice ◽  
Local Pressure ◽  
Dietary Nitrate ◽  
Arterial Blood ◽  
Nitrate Supplementation ◽  
Plasma Nitrite

Recently, dietary nitrate supplementation has been shown to improve exercise capacity in healthy individuals through a potential nitrate-nitrite-nitric oxide pathway. Nitric oxide has been shown to play an important role in compensatory vasodilation during exercise under hypoperfusion. Previously, we established that certain individuals lack a vasodilation response when perfusion pressure reductions compromise exercising muscle blood flow. Whether this lack of compensatory vasodilation in healthy, young individuals can be restored with dietary nitrate supplementation is unknown. Six healthy (21 ± 2 yr), recreationally active men completed a rhythmic forearm exercise. During steady-state exercise, the exercising arm was rapidly transitioned from an uncompromised (below heart) to a compromised (above heart) position, resulting in a reduction in local pressure of −31 ± 1 mmHg. Exercise was completed following 5 days of nitrate-rich (70 ml, 0.4 g nitrate) and nitrate-depleted (70 ml, ~0 g nitrate) beetroot juice consumption. Forearm blood flow (in milliliters per minute; brachial artery Doppler and echo ultrasound), mean arterial blood pressure (in millimeters of mercury; finger photoplethysmography), exercising forearm venous effluent (ante-cubital vein catheter), and plasma nitrite concentrations (chemiluminescence) revealed two distinct vasodilatory responses: nitrate supplementation increased (plasma nitrite) compared with placebo (245 ± 60 vs. 39 ± 9 nmol/l; P < 0.001), and compensatory vasodilation was present following nitrate supplementation (568 ± 117 vs. 714 ± 139 ml ⋅ min−1 ⋅ 100 mmHg−1; P = 0.005) but not in placebo (687 ± 166 vs. 697 ± 171 min−1 ⋅ 100 mmHg−1; P = 0.42). As such, peak exercise capacity was reduced to a lesser degree (−4 ± 39 vs. −39 ± 27 N; P = 0.01). In conclusion, dietary nitrate supplementation during a perfusion pressure challenge is an effective means of restoring exercise capacity and enabling compensatory vasodilation. NEW & NOTEWORTHY Previously, we identified young, healthy persons who suffer compromised exercise tolerance when exercising muscle perfusion pressure is reduced as a result of a lack of compensatory vasodilation. The ability of nitrate supplementation to restore compensatory vasodilation in such noncompensators is unknown. We demonstrated that beetroot juice supplementation led to compensatory vasodilation and restored perfusion and exercise capacity. Elevated plasma nitrite is an effective intervention for correcting the absence of compensatory vasodilation in the noncompensator phenotype.

Effects of short-term dietary nitrate supplementation on blood pressure, O2 uptake kinetics, and muscle and cognitive function in older adults

2013 ◽  
Vol 304 (2) ◽  
pp. R73-R83 ◽  
Author(s):  
James Kelly ◽  
Jonathan Fulford ◽  
Anni Vanhatalo ◽  
Jamie R. Blackwell ◽  
Olivia French ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Older Adults ◽  
Cognitive Function ◽  
Metabolic Response ◽  
Treadmill Walking ◽  
Beetroot Juice ◽  
Dietary Nitrate ◽  
Resting Blood Pressure ◽  
Nitrate Supplementation ◽  
Plasma Nitrite

Dietary nitrate (NO3−) supplementation has been shown to reduce resting blood pressure and alter the physiological response to exercise in young adults. We investigated whether these effects might also be evident in older adults. In a double-blind, randomized, crossover study, 12 healthy, older (60–70 yr) adults supplemented their diet for 3 days with either nitrate-rich concentrated beetroot juice (BR; 2 × 70 ml/day, ∼9.6 mmol/day NO3−) or a nitrate-depleted beetroot juice placebo (PL; 2 × 70 ml/day, ∼0.01 mmol/day NO3−). Before and after the intervention periods, resting blood pressure and plasma [nitrite] were measured, and subjects completed a battery of physiological and cognitive tests. Nitrate supplementation significantly increased plasma [nitrite] and reduced resting systolic (BR: 115 ± 9 vs. PL: 120 ± 6 mmHg; P < 0.05) and diastolic (BR: 70 ± 5 vs. PL: 73 ± 5 mmHg; P < 0.05) blood pressure. Nitrate supplementation resulted in a speeding of the V̇o2 mean response time (BR: 25 ± 7 vs. PL: 28 ± 7 s; P < 0.05) in the transition from standing rest to treadmill walking, although in contrast to our hypothesis, the O2 cost of exercise remained unchanged. Functional capacity (6-min walk test), the muscle metabolic response to low-intensity exercise, brain metabolite concentrations, and cognitive function were also not altered. Dietary nitrate supplementation reduced resting blood pressure and improved V̇o2 kinetics during treadmill walking in healthy older adults but did not improve walking or cognitive performance. These results may have implications for the enhancement of cardiovascular health in older age.

scholarly journals No Effect of Beetroot Juice Supplementation on 100-m and 200-m Swimming Performance in Moderately Trained Swimmers

2019 ◽  
Vol 14 (6) ◽  
pp. 706-710 ◽  
Author(s):  
Ozcan Esen ◽  
Ceri Nicholas ◽  
Mike Morris ◽  
Stephen J. Bailey
Keyword(s):  
Blood Pressure ◽  
Swimming Performance ◽  
Time Trial ◽  
Upper Body ◽  
Beetroot Juice ◽  
Nitrite Concentration ◽  
Double Blind ◽  
Dietary Nitrate ◽  
Nitrate Supplementation ◽  
Plasma Nitrite

Purpose: Dietary nitrate supplementation has been reported to improve performance in kayaking and rowing exercise, which mandate significant recruitment of the upper-body musculature. Because the effect of dietary nitrate supplementation on swimming performance is unclear, the purpose of this study was to assess the effect of dietary nitrate supplementation on 100-m and 200-m swimming freestyle time-trial (TT) performance. Methods: In a double-blind, randomized crossover design, 10 moderately trained swimmers underwent 2 separate 3-d supplementation periods, with a daily dose of either 140 mL nitrate-rich (∼800 mg/d nitrate) or nitrate-depleted (PLA) beetroot juice (BRJ). After blood sampling on day 3, the swimmers performed both 200-m and 100-m freestyle swimming TTs, with 30 min recovery between trials. Results: Plasma nitrite concentration was greater after BRJ relative to PLA consumption (432 [203] nmol/L, 111 [56] nmol/L, respectively, P = .001). Systolic blood pressure was lowered after BRJ compared with PLA supplementation (114 [10], 120 [10] mm Hg, respectively P = .001), but time to complete the 200-m (BRJ 152.6 [14.1] s, PLA 152.5 [14.1] s) and 100-m (BRJ 69.5 [7.2] s, PLA 69.4 [7.4] s) freestyle swimming TTs was not different between BRJ and PLA (P > .05). Conclusions: Although 3 d of BRJ supplementation increased plasma nitrite concentration and lowered blood pressure, it did not improve 100-m and 200-m swimming TT performance. These results do not support an ergogenic effect of nitrate supplementation in moderately trained swimmers, at least for 100-m and 200-m freestyle swimming performance.

Abstract P242: Dietary Nitrate Does not Reduce Resting Metabolic Rate or Oxidative Stress in Healthy Males

Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Haley M Fair ◽  
Caleb D Harrison ◽  
Evan J Bockover ◽  
Brycen J Ratcliffe ◽  
Sierra Crowe ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Metabolic Rate ◽  
Resting Metabolic Rate ◽  
Dietary Nitrate ◽  
Young Males ◽  
Nitrate Supplementation ◽  
No Bioavailability ◽  
Plasma Nitrite ◽  
Healthy Males

Introduction: Nitric oxide (NO) is a vasodilator that increases blood flow by promoting relaxation of endothelium. Dietary nitrate supplementation increases plasma nitrite, a marker of overall NO bioavailability. Previously, acute dietary nitrate supplementation has been shown to reduce oxygen consumption and improve tolerance during submaximal exercise in healthy populations. Less is known about the effect of dietary nitrate on oxygen consumption at rest. Hypothesis: We hypothesized that dietary nitrate supplementation would reduce resting metabolic rate (RMR) and oxidative stress (8-isoprostane) at rest, via enhanced NO bioavailability via the oxygen independent Nitrate-Nitrite-Nitric Oxide pathway in healthy, young males. Methods: In a randomized, double-blind, cross-over study, ten healthy, young males (21 ± 2 years) visited the laboratory on 5 separate occasions. Participants completed informed consent paperwork and underwent protocol familiarization during visit 1. Prior to visits 2 and 4, participants fasted for 12 hours and adhered to an NIH-approved low-nitrate diet for 48 hours. During visits 2 and 4, an initial blood draw was performed to analyze baseline plasma nitrite and 8-isoprostane. Participants then completed a 30-minute resting metabolic rate (RMR) test. Two hours prior to visits 3 and 5, participants consumed either a placebo or dietary nitrate supplement (negligible and 6.2 mmol nitrate, respectively). During visits 3 and 5, participants also had blood drawn for analysis of the previously stated measurements, and completed an RMR test. Visits 2 and 3 were on consecutive days, followed by a week-long washout period between visit 3 and visit 4, while visit 4 and 5 also occurred on consecutive days. Results: Plasma nitrite significantly increased following dietary nitrate consumption compared to baseline values (27.56 ± 7.58 and 1.25 ± 1.51 arbitrary units, respectively). No difference was present between nitrate and baseline measurements for 8-isoprostane (155.75 ± 57.01 and 198.42 ± 66.44 pg/mL, respectively; p=0.55) and RMR (2086.60 ± 202.23 and 2050.00 ± 209.23 kcal/day, respectively; p=0.13). Conclusion: Dietary nitrate supplementation increases plasma nitrite, but does not change resting metabolic rate following an acute dose of dietary nitrate in healthy males. Individuals consuming dietary nitrate as an ergogenic aid during exercise may not, however, experience similar changes in their resting metabolism. The lack of change in oxidative stress may have been associated with the overall health of the cohort examined. Future research should investigate the clinical implications of dietary nitrate in populations with decreased NO bioavailability and associated endothelial disfunction (and elevated oxidative stress). In such populations, dietary nitrate may provide benefit. However, in a healthy cohort, dietary nitrate exerts minimal effects.

Effects of Neuroactive Amino Acids Derivatives on Cardiac and Cerebral Mitochondria and Endothelial functions in Animals Exposed to Stress

2017 ◽  
Vol 2 (2) ◽  
pp. 34
Author(s):  
TA Popova ◽  
II Prokofiev ◽  
IS Mokrousov ◽  
Valentina Perfilova ◽  
AV Borisov ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Platelet Aggregation ◽  
Atp Synthesis ◽  
Elevated Concentration ◽  
Blood Pressure Monitor ◽  
Pressure Monitor ◽  
Griess Reagent ◽  
Arterial Blood ◽  
Endothelial Functions

Introduction: To study the effects of glufimet, a new derivative of glutamic acid, and phenibut, a derivative of γ-aminobutyric acid (GABA), on cardiac and cerebral mitochondria and endothelial functions in animals following exposure to stress and inducible nitric oxide synthase (iNOS) inhibition. Methods: Rats suspended by their dorsal cervical skin fold for 24 hours served as the immobilization and pain stress model. Arterial blood pressure was determined using a non-invasive blood pressure monitor. Mitochondrial fraction of heart and brain homogenates were isolated by differential centrifugation and analysed for mitochondrial respiration intensity, lipid peroxidation (LPO) and antioxidant enzyme activity using polarographic method. The concentrations of nitric oxide (NO) terminal metabolites were measured using Griess reagent. Hemostasis indices were evaluated. Platelet aggregation was estimated using modified version of the Born method described by Gabbasov et al., 1989. Results: The present study demonstrated that stress leads to an elevated concentration of NO terminal metabolites and LPO products, decreased activity of antioxidant enzymes, reduced mitochondrial respiratory function, and endothelial dysfunction. Inhibition of iNOS by aminoguanidine had a protective effect. Phenibut and glufimet inhibited a rise in stress-induced nitric oxide production. This resulted in enhanced coupling of substrate peroxidation and ATP synthesis. The reduced LPO processes caused by glufimet and phenibut normalized the endothelial function which was proved by the absence of average daily blood pressure (BP) elevation episodes and a significant increase in platelet aggregation level. Conclusion: Glufimet and phenibut restrict the harmful effects of stress on the heart and brain possibly by modulating iNOS activity.

scholarly journals Dietary nitrate supplementation attenuates the reduction in exercise tolerance following blood donation

2016 ◽  
Vol 311 (6) ◽  
pp. H1520-H1529 ◽  
Author(s):  
Sinead T. J. McDonagh ◽  
Anni Vanhatalo ◽  
Jonathan Fulford ◽  
Lee J. Wylie ◽  
Stephen J. Bailey ◽  
...  
Keyword(s):  
Exercise Tolerance ◽  
Peak Power ◽  
Blood Donation ◽  
Hemoglobin Concentration ◽  
Moderate Intensity ◽  
Beetroot Juice ◽  
Moderate Intensity Exercise ◽  
Exercise Tests ◽  
Dietary Nitrate ◽  
Nitrate Supplementation

We tested the hypothesis that dietary nitrate (NO3−)-rich beetroot juice (BR) supplementation could partially offset deteriorations in O2transport and utilization and exercise tolerance after blood donation. Twenty-two healthy volunteers performed moderate-intensity and ramp incremental cycle exercise tests prior to and following withdrawal of ∼450 ml of whole blood. Before donation, all subjects consumed seven 70-ml shots of NO3−-depleted BR [placebo (PL)] in the 48 h preceding the exercise tests. During the 48 h after blood donation, subjects consumed seven shots of BR (each containing 6.2 mmol of NO3−, n = 11) or PL ( n = 11) before repeating the exercise tests. Hemoglobin concentration and hematocrit were reduced by ∼8–9% following blood donation ( P < 0.05), with no difference between the BR and PL groups. Steady-state O2uptake during moderate-intensity exercise was ∼4% lower after than before donation in the BR group ( P < 0.05) but was unchanged in the PL group. The ramp test peak power decreased from predonation (341 ± 70 and 331 ± 68 W in PL and BR, respectively) to postdonation (324 ± 69 and 322 ± 66 W in PL and BR, respectively) in both groups ( P < 0.05). However, the decrement in performance was significantly less in the BR than PL group (2.7% vs. 5.0%, P < 0.05). NO3−supplementation reduced the O2cost of moderate-intensity exercise and attenuated the decline in ramp incremental exercise performance following blood donation. These results have implications for improving functional capacity following blood loss.

scholarly journals Beneficial haemodynamic effect of indomethacin during endotoxin shock in anaesthetized pigsputative involvement of nitric oxide?

1995 ◽  
Vol 4 (2) ◽  
pp. 117-123 ◽  
Author(s):  
T. Mózes ◽  
E. M. van Gelderen ◽  
E. J. Mylecharane ◽  
P. R. Saxena
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Beneficial Effect ◽  
Endotoxic Shock ◽  
Haemodynamic Effect ◽  
Experimental Period ◽  
Endotoxin Shock ◽  
Arterial Blood ◽  
Imminent Death ◽  
Beneficial Haemodynamic Effect

Endotoxin shock was induced in 31 anaesthetized pigs by infusion of 5 μg/kg of Escbeicbia coli endotoxin (LPS) over 60 min into the superior mesenteric artery. Fifteen of these pigs died within 30 min of the start of LPS infusion whereas the remaining 16 survived the experimental period of 2 h. In a group of nine pigs indomethacin (2 mg/kg, i.v.)was inected 20–25 rain after the start of LPS infusion at which time mean arterial blood pressure (MABP) had decreased below 40 mmHg indicating imminent death. Indomethacin immediately reversed the hypotension. In another group of five pigs, NG-nitro L-arginine-methyl ester (L-NAME, 1 and 3 mg/kg)was iniected 10 and 5 min, respectively, before the expected death without any beneficial effect on the hypotension. Three rain after the last dose of L-NAME, indomethacin (2 mg/kg, i.v.) was iniected. In three animals the hypotension was reserved by indomethacin, although this beneficial effect was delayed in comparison with the LP-Streated group not receiving L-NAME. Four pigs were pretreated with L-NAME, 3 mg/kg, i.v., 10 min prior to LPS infusion. All pretreated animals tended to die within 30 min of the start of the LPS infusion. Five rain before the expected death (20–25 rain after the start of LPS infusion) indomethacin (2 mg/kg) was inected. In three of these animals indomethacin reversed hypotenston and prevented death. Interestingly, this rise in the MABP developed very slowly. These results suggest that the beneficial effect of indomethacin in endotoxin shock might be related partially to interference with nitric oxide, which is not the only factor determining blood pressure levels during endotoxic shock.

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