Accounting for Dynamic Changes in the Power-Duration Relationship Improves the Accuracy of W' Balance Modeling.

PURPOSE: This study aimed 1) to examine the accuracy with which W' reconstitution (W' REC ) is estimated by the W' balance (W' BAL ) models after a 3-min all-out cycling test (3MT), 2) to determine the effects of a 3MT on the power-duration relationship, and 3) to assess whether accounting for changes in the power-duration relationship during exercise improved estimates of W' REC . METHODS: The power-duration relationship and the actual and estimated W' REC were determined for 12 data sets extracted from our laboratory database where participants had completed two 3MT separated by 1-min recovery (i.e., control [C-3MT] and fatigued [F-3MT]). RESULTS: Actual W' REC (6.3 ± 1.4 kJ) was significantly overestimated by the W' BAL·ODE (9.8 ± 1.3 kJ; P < 0.001) and the W' BAL·MORTON (16.9 ± 2.6 kJ; P < 0.001) models but was not significantly different to the estimate provided by the W' BAL·INT (7.5 ± 1.5 kJ; P > 0.05) model. End power (EP) was 7% lower in the F-3MT (263 ± 40 W) compared with the C-3MT (282 ± 44 W; P < 0.001), and work done above EP (WEP) was 61% lower in the F-3MT (6.3 ± 1.4 kJ) compared with the C-3MT (16.9 ± 3.2 kJ). The size of the error in the estimated W' REC was correlated with the reduction in WEP for the W' BAL·INT and W' BAL·ODE models (both r > -0.74, P < 0.01) but not the W' BAL·MORTON model ( r = -0.18, P > 0.05). Accounting for the changes in the power-duration relationship improved the accuracy of the W' BAL·ODE and W' BAL·MORTON , but they remained significantly different to actual W' REC . CONCLUSIONS: These findings demonstrate that the power-duration relationship is altered after a 3MT, and accounting for these changes improves the accuracy of the W' BAL·ODE and the W' BAL·MORTON , but not W' BAL·INT models. These results have important implications for the design and use of mathematical models describing the energetics of exercise performance.

Effects of dietary nitrate on the O2 cost of submaximal exercise: Accounting for "noise" in pulmonary gas exchange measurements.

Dietary nitrate (NO3-) supplementation can reduce the oxygen cost of submaximal exercise, but this has not been reported consistently. We hypothesised that the number of step transitions to moderate-intensity exercise, and corresponding effects on the signal-to-noise ratio for pulmonary V˙ O2, may be important in this regard. Twelve recreationally active participants were assigned in a randomised, double-blind, crossover design to supplement for 4 days in three conditions: 1) control (CON; water); 2); PL (NO3--depleted beetroot juice); and 3) BR (NO3--rich beetroot juice). On days 3 and 4, participants completed two 6-min step transitions to moderate-intensity cycle exercise. Breath-by-breath V˙ O2 data were collected and V˙ O2 kinetic responses were determined for a single transition and when the responses to 2, 3 and 4 transitions were ensemble-averaged. Steady-state V˙ O2 was not different between PL and BR when the V˙ O2 response to one-, two- or three-step transition was compared but was significantly lower in BR compared to PL when four-step transitions was considered (PL: 1.33 ± 0.34 vs. BR: 1.31 ± 0.34 L·min-1, P < 0.05). There were no differences in pulmonary V˙ O2 responses between CON and PL (P > 0.05). Multiple step transitions may be required to detect the influence of NO3- supplementation on steady-state V˙ O2.

Time course of human skeletal muscle nitrate and nitrite concentration changes following dietary nitrate ingestion.

Dietary nitrate (NO3-) ingestion can be beneficial for health and exercise performance. Recently, based on animal and limited human studies, a skeletal muscle NO3- reservoir has been suggested to be important in whole body nitric oxide (NO) homeostasis. The purpose of this study was to determine the time course of changes in human skeletal muscle NO3- concentration ([NO3-]) following the ingestion of dietary NO3-. Sixteen participants were allocated to either an experimental group (NIT: n = 11) which consumed a bolus of ∼1300 mg (12.8 mmol) potassium nitrate (KNO3), or a placebo group (PLA: n = 5) which consumed a bolus of potassium chloride (KCl). Biological samples (muscle (vastus lateralis), blood, saliva and urine) were collected shortly before NIT or PLA ingestion and at intervals over the course of the subsequent 24 h. At baseline, no differences were observed for muscle [NO3-] and [NO2-] between NIT and PLA (P > 0.05). In PLA, there were no changes in muscle [NO3-] or [NO2-] over time. In NIT, muscle [NO3-] was significantly elevated above baseline (54 ± 29 nmol/g) at 0.5 h, reached a peak at 3 h (181 ± 128 nmol/g), and was not different to baseline from 9 h onwards (P > 0.05). Muscle [NO2-] did not change significantly over time. Following ingestion of a bolus of dietary NO3-, skeletal muscle [NO3-] increases rapidly, reaches a peak at ∼3 h and subsequently declines towards baseline values. Following dietary NO3- ingestion, human m. vastus lateralis [NO3-] expressed a slightly delayed pharmacokinetic profile compared to plasma [NO3-].

Preparation of Rat Skeletal Muscle Homogenates for Nitrate and Nitrite Measurements.

Nitrate ions (NO3-) were once thought to be inert end products of nitric oxide (NO) metabolism. However, previous studies demonstrated that nitrate ions can be converted back to NO in mammals through a two-step reduction mechanism: nitrate being reduced to nitrite (NO2-) mostly by oral commensal bacteria, then nitrite being reduced to NO by several mechanisms including via heme- or molybdenum-containing proteins. This reductive nitrate pathway contributes to enhancing NO-mediated signaling pathways, particularly in the cardiovascular system and during muscular exercise. The levels of nitrate in the body before such utilization are determined by two different sources: endogenous NO oxidation and dietary nitrate intake, principally from plants. To elucidate the complex NO cycle in physiological circumstances, we have examined further the dynamics of its metabolites, nitrate and nitrite ions, which are relatively stable compared to NO. In previous studies skeletal muscle was identified as a major storage organ for nitrate ions in mammals, as well as a direct source of NO during exercise. Therefore, establishing a reliable methodology to measure nitrate and nitrite levels in skeletal muscle is important and should be helpful in extending its application to other tissue samples. This paper explains in detail the preparation of skeletal muscle samples, using three different homogenization methods, for nitrate and nitrite measurements and discusses important issues related to homogenization processes, including the size of the samples. Nitrate and nitrite concentrations have also been compared across four different muscle groups.

S-nitrosothiols, and other products of nitrate metabolism, are increased in multiple human blood compartments following ingestion of beetroot juice.

Ingested inorganic nitrate (NO3⁻) has multiple effects in the human body including vasodilation, inhibition of platelet aggregation, and improved skeletal muscle function. The functional effects of oral NO3⁻ involve the in vivo reduction of NO3⁻ to nitrite (NO2⁻) and thence to nitric oxide (NO). However, the potential involvement of S-nitrosothiol (RSNO) formation is unclear. We hypothesised that the RSNO concentration ([RSNO]) in red blood cells (RBCs) and plasma is increased by NO3⁻-rich beetroot juice ingestion. In healthy human volunteers, we tested the effect of dietary supplementation with NO3⁻-rich beetroot juice (BR) or NO3⁻-depleted beetroot juice (placebo; PL) on [RSNO], [NO3⁻] and [NO2⁻] in RBCs, whole blood and plasma, as measured by ozone-based chemiluminescence. The median basal [RSNO] in plasma samples (n = 22) was 10 (5-13) nM (interquartile range in brackets). In comparison, the median values for basal [RSNO] in the corresponding RBC preparations (n = 19) and whole blood samples (n = 19) were higher (p < 0.001) than in plasma, being 40 (30-60) nM and 35 (25-80) nM, respectively. The median RBC [RSNO] in a separate cohort of healthy subjects (n = 5) was increased to 110 (93-125) nM after ingesting BR (12.8 mmol NO3⁻) compared to a corresponding baseline value of 25 (21-31) nM (Mann-Whitney test, p < 0.01). The median plasma [RSNO] in another cohort of healthy subjects (n = 14) was increased almost ten-fold to 104 (58-151) nM after BR supplementation (7 × 6.4 mmol of NO3⁻ over two days, p < 0.01) compared to PL. In conclusion, RBC and plasma [RSNO] are increased by BR ingestion. In addition to NO2⁻, RSNO may be involved in dietary NO3⁻ metabolism/actions.

Network analysis of nitrate-sensitive oral microbiome reveals interactions with cognitive function and cardiovascular health across dietary interventions.

Many oral bacteria reduce inorganic nitrate, a natural part of a vegetable-rich diet, into nitrite that acts as a precursor to nitric oxide, a regulator of vascular tone and neurotransmission. Aging is hallmarked by reduced nitric oxide production with associated detriments to cardiovascular and cognitive function. This study applied a systems-level bacterial co-occurrence network analysis across 10-day dietary nitrate and placebo interventions to test the stability of relationships between physiological and cognitive traits and clusters of co-occurring oral bacteria in older people. Relative abundances of Proteobacteria increased, while Bacteroidetes, Firmicutes and Fusobacteria decreased after nitrate supplementation. Two distinct microbiome modules of co-occurring bacteria, that were sensitive to nitrate supplementation, showed stable relationships with cardiovascular (Rothia-Streptococcus) and cognitive (Neisseria-Haemophilus) indices of health across both dietary conditions. A microbiome module (Prevotella-Veillonella) that has been associated with pro-inflammatory metabolism was diminished after nitrate supplementation, including a decrease in relative abundance of pathogenic Clostridium difficile. These nitrate-sensitive oral microbiome modules are proposed as potential pre- and probiotic targets to ameliorate age-induced impairments in cardiovascular and cognitive health.

Physiological demands of running at 2-hour marathon race pace.

The requirements of running a 2-h marathon have been extensively debated but the actual physiological demands of running at ∼21.1 km/h have never been reported. We therefore conducted laboratory-based physiological evaluations and measured running economy (O2 cost) while running outdoors at ∼21.1 km/h, in world-class distance runners as part of Nike's "Breaking 2" marathon project. On separate days, 16 world-class male distance runners (age, 29 ± 4 yr; height, 1.72 ± 0.04 m; mass, 58.9 ± 3.3 kg) completed an incremental treadmill test for the assessment of V̇O2peak, O2 cost of submaximal running, lactate threshold and lactate turn-point, and a track test during which they ran continuously at 21.1 km/h. The laboratory-determined V̇O2peak was 71.0 ± 5.7 mL/kg/min with lactate threshold and lactate turn-point occurring at 18.9 ± 0.4 and 20.2 ± 0.6 km/h, corresponding to 83 ± 5% and 92 ± 3% V̇O2peak, respectively. Seven athletes were able to attain a steady-state V̇O2 when running outdoors at 21.1 km/h. The mean O2 cost for these athletes was 191 ± 19 mL/kg/km such that running at 21.1 km/h required an absolute V̇O2 of ∼4.0 L/min and represented 94 ± 3% V̇O2peak. We report novel data on the O2 cost of running outdoors at 21.1 km/h, which enables better modeling of possible marathon performances by elite athletes. Using the value for O2 cost measured in this study, a sub 2-h marathon would require a 59 kg runner to sustain a V̇O2 of approximately 4.0 L/min or 67 mL/kg/min.NEW & NOTEWORTHY We report the physiological characteristics and O2 cost of running overground at ∼21.1 km/h in a cohort of the world's best male distance runners. We provide new information on the absolute and relative O2 uptake required to run at 2-h marathon pace.

Influence of muscle oxygenation and nitrate-rich beetroot juice supplementation on O2 uptake kinetics and exercise tolerance.

We tested the hypothesis that acute supplementation with nitrate (NO3-)-rich beetroot juice (BR) would improve quadriceps muscle oxygenation, pulmonary oxygen uptake (V˙O2) kinetics and exercise tolerance (Tlim) in normoxia and that these improvements would be augmented in hypoxia and attenuated in hyperoxia. In a randomised, double-blind, cross-over study, ten healthy males completed two-step cycle tests to Tlim following acute consumption of 210 mL BR (18.6 mmol NO3-) or NO3--depleted beetroot juice placebo (PL; 0.12 mmol NO3-). These tests were completed in normobaric normoxia [fraction of inspired oxygen (FIO2): 21%], hypoxia (FIO2: 15%) and hyperoxia (FIO2: 40%). Pulmonary V˙O2 and quadriceps tissue oxygenation index (TOI), derived from multi-channel near-infrared spectroscopy, were measured during all trials. Plasma [nitrite] was higher in all BR compared to all PL trials (P < 0.05). Quadriceps TOI was higher in normoxia compared to hypoxia (P < 0.05) and higher in hyperoxia compared to hypoxia and normoxia (P < 0.05). Tlim was improved after BR compared to PL ingestion in the hypoxic trials (250 ± 44 vs. 231 ± 41 s; P = 0.006; d = 1.13), with the magnitude of improvement being negatively correlated with quadriceps TOI at Tlim (r = -0.78; P < 0.05). Tlim was not improved following BR ingestion in normoxia (BR: 364 ± 98 vs. PL: 344 ± 78 s; P = 0.087, d = 0.61) or hyperoxia (BR: 492 ± 212 vs. PL: 472 ± 196 s; P = 0.273, d = 0.37). BR ingestion increased peak V˙O2 in hypoxia (P < 0.05), but not normoxia or hyperoxia (P > 0.05). These findings indicate that BR supplementation is more likely to improve Tlim and peak V˙O2 in situations when skeletal muscle is more hypoxic.

Dynamics of the power-duration relationship during prolonged endurance exercise and influence of carbohydrate ingestion.

We tested the hypotheses that the parameters of the power-duration relationship, estimated as the end-test power (EP) and work done above EP (WEP) during a 3-min all-out exercise test (3MT), would be reduced progressively after 40 min, 80 min, and 2 h of heavy-intensity cycling and that carbohydrate (CHO) ingestion would attenuate the reduction in EP and WEP. Sixteen participants completed a 3MT without prior exercise (control), immediately after 40 min, 80 min, and 2 h of heavy-intensity exercise while consuming a placebo beverage, and also after 2 h of heavy-intensity exercise while consuming a CHO supplement (60 g/h CHO). There was no difference in EP measured without prior exercise (260 ± 37 W) compared with EP after 40 min (268 ± 39 W) or 80 min (260 ± 40 W) of heavy-intensity exercise; however, after 2 h EP was 9% lower compared with control (236 ± 47 W; P < 0.05). There was no difference in WEP measured without prior exercise (17.9 ± 3.3 kJ) compared with after 40 min of heavy-intensity exercise (16.1 ± 3.3 kJ), but WEP was lower (P < 0.05) than control after 80 min (14.7 ± 2.9 kJ) and 2 h (13.8 ± 2.7 kJ). Compared with placebo, CHO ingestion negated the reduction of EP following 2 h of heavy-intensity exercise (254 ± 49 W) but had no effect on WEP (13.5 ± 3.4 kJ). These results reveal a different time course for the deterioration of EP and WEP during prolonged endurance exercise and indicate that EP is sensitive to CHO availability.NEW & NOTEWORTHY The parameters of the power-duration relationship [critical power (CP) and the curvature constant (W')] have typically been considered to be static. Here we report the time course for reductions in CP and W', as estimated with the 3-min all-out cycle test, during 2 h of heavy-intensity exercise. We also show that carbohydrate ingestion during exercise preserves CP, but not W', without altering muscle glycogen depletion. These results provide new mechanistic and practical insight into the power-duration curve and its relationship to exercise-related fatigue development.

Human skeletal muscle nitrate store: influence of dietary nitrate supplementation and exercise.

KEY POINTS: Nitric oxide (NO), a potent vasodilator and a regulator of many physiological processes, is produced in mammals both enzymatically and by reduction of nitrite and nitrate ions. We have previously reported that, in rodents, skeletal muscle serves as a nitrate reservoir, with nitrate levels greatly exceeding those in blood or other internal organs, and with nitrate being reduced to NO during exercise. In the current study, we show that nitrate concentration is substantially greater in skeletal muscle than in blood and is elevated further by dietary nitrate ingestion in human volunteers. We also show that high-intensity exercise results in a reduction in the skeletal muscle nitrate store following supplementation, likely as a consequence of its reduction to nitrite and NO. We also report the presence of sialin, a nitrate transporter, and xanthine oxidoreductase in human skeletal muscle, indicating that muscle has the necessary apparatus for nitrate transport, storage and metabolism. ABSTRACT: Rodent skeletal muscle contains a large store of nitrate that can be augmented by the consumption of dietary nitrate. This muscle nitrate reservoir has been found to be an important source of nitrite and nitric oxide (NO) via its reduction by tissue xanthine oxidoreductase. To explore if this pathway is also active in human skeletal muscle during exercise, and if it is sensitive to local nitrate availability, we assessed exercise-induced changes in muscle nitrate and nitrite concentrations in young healthy humans, under baseline conditions and following dietary nitrate consumption. We found that baseline nitrate and nitrite concentrations were far higher in muscle than in plasma (∼4-fold and ∼29-fold, respectively), and that the consumption of a single bolus of dietary nitrate (12.8 mmol) significantly elevated nitrate concentration in both plasma (∼19-fold) and muscle (∼5-fold). Consistent with these observations, and with previous suggestions of active muscle nitrate transport, we present western blot data to show significant expression of the active nitrate/nitrite transporter sialin in human skeletal muscle. Furthermore, we report an exercise-induced reduction in human muscle nitrate concentration (by ∼39%), but only in the presence of an increased muscle nitrate store. Our results indicate that human skeletal muscle nitrate stores are sensitive to dietary nitrate intake and may contribute to NO generation during exercise. Together, these findings suggest that skeletal muscle plays an important role in the transport, storage and metabolism of nitrate in humans.

Changes in the power-duration relationship following prolonged exercise: estimation using conventional and all-out protocols and relationship with muscle glycogen.

It is not clear how the parameters of the power-duration relationship [critical power (CP) and W'] are influenced by the performance of prolonged endurance exercise. We used severe-intensity prediction trials (conventional protocol) and the 3-min all-out test (3MT) to measure CP and W' following 2 h of heavy-intensity cycling exercise and took muscle biopsies to investigate possible relationships to changes in muscle glycogen concentration ([glycogen]). Fourteen participants completed a rested 3MT to establish end-test power (Control-EP) and work done above EP (Control-WEP). Subsequently, on separate days, immediately following 2 h of heavy-intensity exercise, participants completed a 3MT to establish Fatigued-EP and Fatigued-WEP and three severe-intensity prediction trials to the limit of tolerance (Tlim) to establish Fatigued-CP and Fatigued-W'. A muscle biopsy was collected immediately before and after one of the 2-h exercise bouts. Fatigued-CP (256 ± 41 W) and Fatigued-EP (256 ± 52 W), and Fatigued-W' (15.3 ± 5.0 kJ) and Fatigued-WEP (14.6 ± 5.3 kJ), were not different (P > 0.05) but were ~11% and ~20% lower than Control-EP (287 ± 46 W) and Control-WEP (18.7 ± 4.7 kJ), respectively (P < 0.05). The change in muscle [glycogen] was not significantly correlated with the changes in either EP (r = 0.19) or WEP (r = 0.07). The power-duration relationship is adversely impacted by prolonged endurance exercise. The 3MT provides valid estimates of CP and W' following 2 h of heavy-intensity exercise, but the changes in these parameters are not primarily determined by changes in muscle [glycogen].

Potential benefits of dietary nitrate ingestion in healthy and clinical populations: A brief review.

This article provides an overview of the current literature relating to the efficacy of dietary nitrate (NO3-) ingestion in altering aspects of cardiovascular and metabolic health and exercise capacity in healthy and diseased individuals. The consumption of NO3--rich vegetables, such as spinach and beetroot, have been variously shown to promote nitric oxide bioavailability, reduce systemic blood pressure, enhance tissue blood flow, modulate muscle O2 utilisation and improve exercise tolerance both in normoxia and in hypoxia, as is commonly observed in a number of disease states. NO3- ingestion may, therefore, act as a natural means for augmenting performance and attenuating complications associated with limited O2 availability or transport, hypertension and the metabolic syndrome. Recent studies indicate that dietary NO3- might also augment intrinsic skeletal muscle contractility and improve the speed and power of muscle contraction. Moreover, several investigations suggest that NO3- supplementation may improve aspects of cognitive performance both at rest and during exercise. Collectively, these observations position NO3- as more than a putative ergogenic aid and suggest that increasing natural dietary NO3- intake may act as a prophylactic in countering the predations of senescence and certain cardiovascular-metabolic diseases.

The quiet eye is sensitive to exercise-induced physiological stress.

The current study sought to explore attentional mechanisms underpinning visuomotor performance degradation following acute exercise. Ten experienced basketball players took free throws while wearing mobile eye tracking glasses, before and after performing a bout of cycling exercise. Shooting accuracy was measured using a 6-point scoring system, and quiet eye duration (the final fixation to a target) was adopted as an objective measure of top-down attentional control. Four intensities of exercise (based on an initial ramp test) were performed in a counterbalanced order: rest, moderate, heavy and severe. The four intensities resulted in participants reaching 52±4%, 58±4%, 76±6% and 86±5% of their heart rate max, respectively. Performance and quiet eye were only significantly impaired (19% and 45% drops, respectively) between pre- and post-intervention at the severe intensity workload level. Additionally, exercise-induced changes in quiet eye predicted 33% of the subsequent change in performance accuracy. The results suggest that attentional disruptions may at least partially explain why sporting skills break down under acute fatigue. Implications for training to mitigate against these impairments are discussed.

Dietary Nitrate and Physical Performance.

Nitric oxide (NO) plays a plethora of important roles in the human body. Insufficient production of NO (for example, during older age and in various disease conditions) can adversely impact health and physical performance. In addition to its endogenous production through the oxidation of l-arginine, NO can be formed nonenzymatically via the reduction of nitrate and nitrite, and the storage of these anions can be augmented by the consumption of nitrate-rich foodstuffs such as green leafy vegetables. Recent studies indicate that dietary nitrate supplementation, administered most commonly in the form of beetroot juice, can ( a) improve muscle efficiency by reducing the O2 cost of submaximal exercise and thereby improve endurance exercise performance and ( b) enhance skeletal muscle contractile function and thereby improve muscle power and sprint exercise performance. This review describes the physiological mechanisms potentially responsible for these effects, outlines the circumstances in which ergogenic effects are most likely to be evident, and discusses the effects of dietary nitrate supplementation on physical performance in a range of human populations.

A randomised controlled trial exploring the effects of different beverages consumed alongside a nitrate-rich meal on systemic blood pressure.

BACKGROUND:: Ingestion of nitrate (NO3-)-containing vegetables, alcohol and polyphenols, separately, can reduce blood pressure (BP). However, the pharmacokinetic response to the combined ingestion of NO3- and polyphenol-rich or low polyphenol alcoholic beverages is unknown. AIM:: The aim of this study was to investigate how the consumption of low and high polyphenolic alcoholic beverages combined with a NO3--rich meal can influence NO3- metabolism and systemic BP. METHODS:: In a randomised, crossover trial, 12 normotensive males (age 25 ± 5 years) ingested an acute dose of NO3- (∼6.05 mmol) in the form of a green leafy salad, in combination with either a polyphenol-rich red wine (NIT-RW), a low polyphenol alcoholic beverage (vodka; NIT-A) or water (NIT-CON). Participants also consumed a low NO3- salad and water as a control (CON; ∼0.69 mmol NO3-). BP and plasma, salivary and urinary [NO3-] and nitrite ([NO2-]) were determined before and up to 5 h post ingestion. RESULTS:: Each NO3--rich condition elevated nitric oxide (NO) biomarkers when compared with CON ( P < 0.05). The peak rise in plasma [NO2-] occurred 1 h after NIT-RW (292 ± 210 nM) and 2 h after NIT-A (318 ± 186 nM) and NIT-CON (367 ± 179 nM). Systolic BP was reduced 2 h post consumption of NIT-RW (-4 mmHg), NIT-A (-3 mmHg) and NIT-CON (-2 mmHg) compared with CON ( P < 0.05). Diastolic BP and mean arterial pressure were also lower in NIT-RW and NIT-A compared with NIT-CON ( P < 0.05). CONCLUSIONS:: A NO3--rich meal, consumed with or without an alcoholic beverage, increases plasma [NO2-] and lowers systemic BP for 2-3 h post ingestion.

Discrete physiological effects of beetroot juice and potassium nitrate supplementation following 4-wk sprint interval training.

The physiological and exercise performance adaptations to sprint interval training (SIT) may be modified by dietary nitrate ([Formula: see text]) supplementation. However, it is possible that different types of [Formula: see text] supplementation evoke divergent physiological and performance adaptations to SIT. The purpose of this study was to compare the effects of 4-wk SIT with and without concurrent dietary [Formula: see text] supplementation administered as either [Formula: see text]-rich beetroot juice (BR) or potassium [Formula: see text] (KNO3). Thirty recreationally active subjects completed a battery of exercise tests before and after a 4-wk intervention in which they were allocated to one of three groups: 1) SIT undertaken without dietary [Formula: see text] supplementation (SIT); 2) SIT accompanied by concurrent BR supplementation (SIT + BR); or 3) SIT accompanied by concurrent KNO3 supplementation (SIT + KNO3). During severe-intensity exercise, V̇o2peak and time to task failure were improved to a greater extent with SIT + BR than SIT and SIT + KNO3 ( P < 0.05). There was also a greater reduction in the accumulation of muscle lactate at 3 min of severe-intensity exercise in SIT + BR compared with SIT + KNO3 ( P < 0.05). Plasma [Formula: see text] concentration fell to a greater extent during severe-intensity exercise in SIT + BR compared with SIT and SIT + KNO3 ( P < 0.05). There were no differences between groups in the reduction in the muscle phosphocreatine recovery time constant from pre- to postintervention ( P > 0.05). These findings indicate that 4-wk SIT with concurrent BR supplementation results in greater exercise capacity adaptations compared with SIT alone and SIT with concurrent KNO3 supplementation. This may be the result of greater NO-mediated signaling in SIT + BR compared with SIT + KNO3. NEW & NOTEWORTHY We compared the influence of different forms of dietary nitrate supplementation on the physiological and performance adaptations to sprint interval training (SIT). Compared with SIT alone, supplementation with nitrate-rich beetroot juice, but not potassium [Formula: see text], enhanced some physiological adaptations to training.

Effects of Two Hours of Heavy-Intensity Exercise on the Power-Duration Relationship.

INTRODUCTION: Changes in the parameters of the power-time relationship (critical power (CP) and W') during endurance exercise would have important implications for performance. We tested the hypotheses that CP and W', estimated using the end-test power (EP) and the work done above EP (WEP), respectively, during a the 3-min all-out test (3MT), can be reliably determined, and would be lower, after completing 2 h of heavy-intensity exercise. METHODS: In study 1, six cyclists completed a 3MT immediately after 2 h of heavy-intensity exercise on two occasions to establish the reliability of EP and WEP. In study 2, nine cyclists completed a control 3MT, and a fatigued 3MT and constant power output tests to 30 min or the limit of tolerance (Tlim) below and above F-EP after 2 h of heavy-intensity exercise. RESULTS: In study 1, EP (273 ± 52 vs 276 ± 58 W) and WEP (12.4 ± 4.3 vs 12.8 ± 4.3 kJ) after 2 h of heavy-intensity exercise were not different (P > 0.05) and were highly correlated (r = 0.99; P < 0.001). In study 2, both EP (F-EP: 282 ± 52 vs C-EP: 306 ± 56 W; P < 0.01) and WEP (F-WEP: 14.7 ± 4.9 vs C-WEP: 18.3 ± 4.1 kJ; P < 0.05) were lower after 2-h heavy-intensity exercise. However, maximum O2 uptake was not achieved during exercise >F-EP and Tlim was shorter than 30 min during exercise

Lowering of blood pressure after nitrate-rich vegetable consumption is abolished with the co-ingestion of thiocyanate-rich vegetables in healthy normotensive males.

A diet rich in vegetables is known to provide cardioprotection. However, it is unclear how the consumption of different vegetables might interact to influence vascular health. This study tested the hypothesis that nitrate-rich vegetable consumption would lower systolic blood pressure but that this effect would be abolished when nitrate-rich and thiocyanate-rich vegetables are co-ingested. On four separate occasions, and in a randomized cross-over design, eleven healthy males reported to the laboratory and consumed a 750 mL vegetable smoothie that was either: low in nitrate (∼0.3 mmol) and thiocyanate (∼5 µmol), low in nitrate and high in thiocyanate (∼72 µmol), high in nitrate (∼4 mmol) and low in thiocyanate and high in nitrate and thiocyanate. Blood pressure as well as plasma and salivary [thiocyanate], [nitrate] and [nitrite] were assessed before and 3 h after smoothie consumption. Plasma [nitrate] and [nitrite] and salivary [nitrate] were not different after consuming the two high-nitrate smoothies, but salivary [nitrite] was higher after consuming the high-nitrate low-thiocyanate smoothie (1183 ±â€¯625 µM) compared to the high-nitrate high-thiocyanate smoothie (941 ±â€¯532 µM; P < .001). Systolic blood pressure was only lowered after consuming the high-nitrate low-thiocyanate smoothie (-3 ±â€¯5 mmHg; P < .05). The acute consumption of vegetables high in nitrate and low in thiocyanate lowered systolic blood pressure. However, when the same dose of nitrate-rich vegetables was co-ingested with thiocyanate-rich vegetables the increase in salivary [nitrite] was smaller and systolic blood pressure was not lowered. These findings might have implications for optimising dietary guidelines aimed at improving cardiovascular health.

Beetroot juice ingestion during prolonged moderate-intensity exercise attenuates progressive rise in O2 uptake.

Nitrate-rich beetroot juice (BR) supplementation has been shown to increase biomarkers of nitric oxide availability with implications for the physiological responses to exercise. We hypothesized that BR supplementation before and during prolonged moderate-intensity exercise would maintain an elevated plasma nitrite concentration ([[Formula: see text]]), attenuate the expected progressive increase in V̇o2 over time, and improve performance in a subsequent time trial (TT). In a double-blind, randomized, crossover design, 12 men completed 2 h of moderate-intensity cycle exercise followed by a 100-kJ TT in three conditions: 1) BR before and 1 h into exercise (BR + BR); 2) BR before and placebo (PL) 1 h into exercise (BR + PL); and 3) PL before and 1 h into exercise (PL + PL). During the 2-h moderate-intensity exercise bout, plasma [[Formula: see text]] declined by ~17% in BR + PL but increased by ~8% in BR + BR such that, at 2 h, plasma [[Formula: see text]] was greater in BR + BR than both BR + PL and PL + PL ( P < 0.05). V̇o2 was not different among conditions over the first 90 min of exercise but was lower at 120 min in BR + BR (1.73 ± 0.24 l/min) compared with BR + PL (1.80 ± 0.21 l/min; P = 0.08) and PL + PL (1.83 ± 0.27 l/min; P < 0.01). The decline in muscle glycogen concentration over the 2-h exercise bout was attenuated in BR + BR (~28% decline) compared with BR + PL (~44% decline) and PL + PL (~44% decline; n = 9, P < 0.05). TT performance was not different among conditions ( P > 0.05). BR supplementation before and during prolonged moderate-intensity exercise attenuated the progressive rise in V̇o2 over time and appeared to reduce muscle glycogen depletion but did not enhance subsequent TT performance. NEW & NOTEWORTHY We show for the first time that ingestion of nitrate during exercise preserves elevated plasma [nitrite] and negates the progressive rise in O2 uptake during prolonged moderate-intensity exercise.

Influence of dietary nitrate food forms on nitrate metabolism and blood pressure in healthy normotensive adults.

Inorganic nitrate (NO3-) supplementation has been shown to improve cardiovascular health indices in healthy adults. The purpose of this study was to investigate how the vehicle of NO3- administration can influence NO3- metabolism and the subsequent blood pressure response. Ten healthy males consumed an acute equimolar dose of NO3- (∼5.76 mmol) in the form of a concentrated beetroot juice drink (BR; 55 mL), a non-concentrated beetroot juice drink (BL; 456 mL) and a solid beetroot flapjack (BF; 60 g). A drink containing soluble beetroot crystals (BC; ∼1.40 mmol NO3-) and a control drink (CON; 70 mL deionised water) were also ingested. BP and plasma, salivary and urinary [NO3-] and [NO2-] were determined before and up to 24 h after ingestion. All NO3--rich vehicles elevated plasma, salivary and urinary nitric oxide metabolites compared with baseline and CON (P<0.05). The peak increases in plasma [NO2-] were greater in BF (371 ± 136 nM) and BR (369 ± 167 nM) compared to BL (283 ± 93 nM; all P<0.05) and BC (232 ± 51 nM). BR, but not BF, BL and BC, reduced systolic (∼5 mmHg) and mean arterial pressure (∼3-4 mmHg; P<0.05), whereas BF reduced diastolic BP (∼4 mmHg; P < 0.05). Although plasma [NO2-] was elevated in all conditions, the consumption of a small, concentrated NO3--rich fluid (BR) was the most effective means of reducing BP. These findings have implications for the use of dietary NO3-supplements when the main objective is to maintain or improve indices of cardiovascular health.