scholarly journals Maternal Dietary Nitrate Supplementation Lowers Incidence of Stillbirth in Hyper Prolific Sows under Commercial Circumstances

Animals ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 3364
Author(s):  
Moniek van den Bosch ◽  
Bram Bronsvoort ◽  
Bas Kemp ◽  
Henry van den Brand

The objective of the current experiment was to investigate whether or not maternal dietary nitrate supplementation, a nitric oxide (NO) precursor, could reduce piglet losses under commercial circumstances. In the current experiment, 120 hyper prolific gilts and sows (Landrace x Yorkshire: Danbred) on a commercial farm in Denmark received either a control lactation diet or a lactation diet containing 0.1% of calcium nitrate (containing 63.1% of nitrate) from approximately 5 days pre-farrowing until day 4 of lactation. The number of piglets born total, alive, and stillborn, as well as birth weights, weights after cross-fostering (approximately 1 day of age), 24 h after cross-fostering, day 3 of age, and at weaning was recorded. Placentas of sows were collected after expulsion and scored on redness. No effect of nitrate supplementation was found on piglet weight, piglet growth, placental redness score, and pre-weaning mortality during lactation. Maternal dietary nitrate supplementation decreased stillbirth percentage with 2.5% (9.9 vs. 7.4%; p = 0.05). It can be concluded that maternal dietary nitrate supplementation shows the potential to decrease the incidence of stillbirth in hyper prolific sows.

2017 ◽  
Vol 313 (1) ◽  
pp. H59-H65 ◽  
Author(s):  
Karambir Notay ◽  
Anthony V. Incognito ◽  
Philip J. Millar

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.


Nutrients ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3611
Author(s):  
Rocío González-Soltero ◽  
María Bailén ◽  
Beatriz de Lucas ◽  
Maria Isabel Ramírez-Goercke ◽  
Helios Pareja-Galeano ◽  
...  

Nitrate supplementation is an effective, evidence-based dietary strategy for enhancing sports performance. The effects of dietary nitrate seem to be mediated by the ability of oral bacteria to reduce nitrate to nitrite, thus increasing the levels of nitrite in circulation that may be further reduced to nitric oxide in the body. The gut microbiota has been recently implicated in sports performance by improving muscle function through the supply of certain metabolites. In this line, skeletal muscle can also serve as a reservoir of nitrate. Here we review the bacteria of the oral cavity involved in the reduction of nitrate to nitrite and the possible changes induced by nitrite and their effect on gastrointestinal balance and gut microbiota homeostasis. The potential role of gut bacteria in the reduction of nitrate to nitrite and as a supplier of the signaling molecule nitric oxide to the blood circulation and muscles has not been explored in any great detail.


Author(s):  
Candace L Doepker ◽  
Melissa M Heintz ◽  
Jennifer van de Ligt ◽  
Daniele S Wikoff

Abstract Calcium nitrate has been reported to benefit reproductive outcomes in sows and their offspring when administered via the feed (15–19 mg/kg-bw/day) during the periparturient period. Traditionally, dietary nitrate had been considered a methemoglobinemia (MetHb) risk in swine. Similar hazard concerns have existed in humans, but a recent benefit/risk analysis established that nitrate levels associated with well-recognized health benefits outweigh potential risks. A similar benefit/risk perspective in swine was lacking and challenged by sparse published hazard data, often referenced within larger reviews related to all livestock. The objective of this review was to better characterize the potential for adverse health and performance effects reported in the literature for swine consuming nitrate, and to provide metrics for evaluating the reliability of the studies reviewed. Supplemental exposure via feed or drinking water was considered for any life stage, dose, and exposure duration. More than 30 relevant studies, including case reports and reviews, examined calcium, potassium, sodium, or unspecified nitrate salts at doses up to 1,800 mg nitrate/kg-bw/day for exposures ranging from 1 to 105 days. The studies primarily evaluated weight gain, blood methemoglobin levels, or vitamin A homeostasis in sows or growing swine. An extensive review of the literature showed reports of adverse effects at low nitrate doses to be of low reliability. Conversely, reliable studies corroborate nitrate intake from feed or drinking water at levels equal to or greater than EFSA’s no-observed-adverse-effect level (NOAEL) for swine of 410 mg nitrate/kg-bw/day, with no MetHb or other adverse effects on reproduction, growth, or vitamin A levels. Using a weight-of-evidence evaluation, we have moderate to high confidence that the NOAEL for nitrate supplementation in swine is likely between 600 and 800 mg/kg-bw/day. These levels are several-fold higher than dietary nitrate concentrations (19 mg/kg-bw/day) that are known to benefit birth outcomes in sows. This review elucidates the quality and reliability of the information sources historically used to characterize nitrate in swine feed as a contaminant of concern. Results from this evaluation can assist risk managers (e.g., regulatory officials and veterinarians) in consideration of proposed benefits, as well as reassuring swine producers that low-level nitrate supplementation is not anticipated to be a concern.


2019 ◽  
Vol 3 (1) ◽  
pp. 464-472
Author(s):  
Moniek van den Bosch ◽  
Jan Wijnen ◽  
Irene B van de Linde ◽  
Ad A M van Wesel ◽  
Delphine Melchior ◽  
...  

Abstract The objective of this study was to evaluate effects of different dosages of dietary nitrate supplementation to sows from d 108 of gestation until d 5 of lactation on reproductive performance of sows and piglet performance from birth until weaning. Dietary nitrate supplementation leads to nitric oxide (NO) formation that can potentially increase blood flow to the fetuses (by the vasodilative effect of NO), leading to a decrease in the loss of potential viable piglets in the form of stillbirth and preweaning mortality. Three hundred and five gilts and sows were allocated to one of six diets from d 108 of gestation until d 5 of lactation, containing 0.00% (Control), 0.03%, 0.06%, 0.09%, 0.12%, or 0.15% of dietary nitrate. The source of nitrate used was calcium nitrate double salt. Calcium levels were kept the same among diets by using limestone. Gilts and sows were weighed and backfat was measured at arrival to the farrowing room (d 108 of gestation) and at weaning (d 27 of age). Data included number of piglets born alive, born dead, and weaned, as well as individual piglet weights at d 0, 72 h of age and weaning. Preweaning mortality was determined throughout lactation. Body weight d 0 (P = 0.04) as well as BW at 72 h of age (P < 0.01) increased linearly with increasing dosages of nitrate in the maternal diet. Litter uniformity (SD) at birth was not affected by maternal nitrate supplementation level (P > 0.10), but tended to be higher at 72 h of age in the control treatment than in all nitrate-supplemented treatments (P = 0.07), and SD decreased linearly (increased uniformity) at weaning with increasing dosages of nitrate (P = 0.05). BW at weaning (P > 0.05) and average daily gain of piglets during lactation (P > 0.05) were not affected by maternal nitrate supplementation. A tendency for a quadratic effect (P = 0.10) of the dosage of maternal dietary nitrate was found on preweaning mortality of piglets with the lowest level of mortality found at 0.09% to 0.12% of maternal nitrate supplementation. We conclude that the use of nitrate in the maternal diet of sows during the perinatal period might stimulate preweaning piglet vitality. Exact mode of action and optimal dose of nitrate still need to be elucidated.


2019 ◽  
Vol 127 (1) ◽  
pp. 81-88 ◽  
Author(s):  
Christopher J. de Vries ◽  
Darren S. DeLorey

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.


2017 ◽  
Vol 123 (3) ◽  
pp. 594-605 ◽  
Author(s):  
Robert F. Bentley ◽  
Jeremy J. Walsh ◽  
Patrick J. Drouin ◽  
Aleksandra Velickovic ◽  
Sarah J. Kitner ◽  
...  

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.


Circulation ◽  
2018 ◽  
Vol 137 (suppl_1) ◽  
Author(s):  
Haley M Fair ◽  
Caleb D Harrison ◽  
Evan J Bockover ◽  
Brycen J Ratcliffe ◽  
Sierra Crowe ◽  
...  

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.


2001 ◽  
Vol 120 (5) ◽  
pp. A245-A245
Author(s):  
E HENY ◽  
K IIJIMA ◽  
A MORIYA ◽  
K MCELROY ◽  
J GRANT ◽  
...  
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