Introduction: Cardiovascular disease (CVD) is the leading cause of mortality globally, accounting for approximately 17.5 million deaths annually. Hypertension is both the strongest predictor and most preventable risk factor of CVD; thus, the prevention of hypertension is central to reducing CVD-associated mortality. Dietary nitrate (NO3-) supplementation has emerged as a potential therapeutic strategy to manage hypertension and prevent CVD. Therefore, it is also possible that dietary NO3- deprivation may cause hypertension. However, research is required to investigate whether dietary NO3- deprivation causes a measurable increase in blood pressure in humans. Furthermore, rodent studies have demonstrated a ‘super compensation’ effect when NO3- supplementation is administered after a period of dietary NO3- deprivation. This phenomenon may have important applications as an anti-hypersensitive intervention. This thesis investigates the effect of dietary NO3- deprivation and subsequent supplementation on blood pressure in humans.
Methods: in a repeated measures, crossover design study, thirteen healthy subjects ingested 180 mg.d-1 NO3- for 3 days, followed by a low NO3- diet (< 30 mg.d-1 NO3-) or a standard NO3- diet (180 mg.d-1 NO3- ) for 7 days. Finally subjects ingested > 800 mg.d-1 NO3- for 3 days. Subjects reported to the lab after each diet allocation for blood pressure measurements.
Results: No interaction effects were observed following 7 days dietary NO3- deprivation for systolic blood pressure (SBP), diastolic blood pressure (DBP) or mean arterial pressure (MAP) (P > 0.05). However, a significant main effect of time was observed (P < 0.05; η2p= 0.30) in SBP with post-hoc t-test analysis demonstrating a significant decrease after 3 days NO3- supplementation compared to baseline (- 4 ± 3 mmHg; P = 0.001) in the standard condition. There were no significant differences in blood pressure variables following NO3- deprivation (P > 0.05). Additionally, NO3- supplementation following NO3- deprivation did not reduce blood pressure to a greater extent than NO3- supplementation following a standard NO3- diet.
Conclusion: 7 days dietary NO3- deprivation does not cause a significant increase in blood pressure within healthy humans. Moreover, 3 days NO3- supplementation reduced SBP following a standard diet. However, supplementation, when administered after a period of deprivation does not accentuate the blood pressure-lowering effects of dietary NO3-. These findings contribute to our understanding of the regulation of blood pressure by dietary NO3-. Specifically, the results suggest that the NOS-dependent pathway performs compensatory NO generation which offsets the decrease in NO generation from the NO3--NO2--NO pathway during a period of dietary NO3- deprivation.

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].

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.

Both psychological and physiological factors contribute to exercise performance at different exercise intensities. Measuring the characteristic physiological responses of an athlete at different exercise intensities makes it possible to predict the tolerance for exercise at a given work rate using the so-called power-duration relationship. While estimating athletic performance in this way is widely practiced, it is possible that the physiological responses typically measured at a given work rate are altered by factors relating to fatigue during long duration events. The purpose of this thesis was to investigate the plasticity of the power-duration relationship in the face of psychological stress and prolonged fatiguing exercise. Firstly, the thesis showed that severe-intensity time trial performance was not different after a prolonged cognitive function task compared to control, in either untrained men or in competitive athletes. Secondly, the thesis investigated the effects of prolonged, fatiguing endurance exercise on the power-duration relationship. Initially, the power asymptote of the hyperbolic power-time relationship critical power (CP) or end test power and the curvature constant of this relationship Wʹ or work done above end test power were not different and highly correlated when estimated from two different 3-min all-out exercise tests (3MT) preceded by 2 h of heavy-intensity exercise. After 2 h of heavy-intensity exercise both EP and WEP were lower compared to no prior exercise (control). Importantly, critical power and W′ established from three separate severe-intensity predication trials conducted immediately following 2 h of heavy-intensity exercise did not differ from F-EP and F-WEP established from a 3MT. F-EP and F-CP as well as F-W′ and F-WEP was ~11% and ~20% lower than C-EP and C-WEP, respectively. Furthermore, C-EP estimated from a 3MT was not different when established after 40 min, 80 min and 2 h of prior heavy-intensity exercise consuming carbohydrates. However, EP estimated after 2 h of heavy-intensity exercise without carbohydrate consumption was lower than all. C-WEP was higher compared to WEP estimated after 80 min of prior heavy-intensity exercise, 2 h of heavy-intensity exercise with and without carbohydrate consumption but was not different compared to estimates established after 40 min of prior heavy-intensity exercise. Firstly, this thesis has demonstrated that time trial performance is not affected by the psychological stress induced by prolonged cognitive tasks in trained athletes. Secondly, it has been demonstrated that prolonged heavy-intensity exercise alters both CP and W′. Thirdly, the results showed that the 3MT is a reliable and valid test to estimate CP and W′ in a fatigued state and that the decrease in CP, but not W′, after prolonged fatiguing exercise can be mitigated by the consumption of carbohydrates.

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.

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.

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.

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.

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 ± 625 μM) compared to the high-nitrate high-thiocyanate smoothie (941 ± 532 μM; P 

We hypothesized that 4 wk of dietary nitrate supplementation would enhance exercise performance and muscle metabolic adaptations to sprint interval training (SIT). Thirty-six recreationally active subjects, matched on key variables at baseline, completed a series of exercise tests before and following a 4-wk period in which they were allocated to one of the following groups: 1) SIT and [Formula: see text]-depleted beetroot juice as a placebo (SIT+PL); 2) SIT and [Formula: see text]-rich beetroot juice (~13 mmol [Formula: see text]/day; SIT+BR); or 3) no training and [Formula: see text]-rich beetroot juice (NT+BR). During moderate-intensity exercise, pulmonary oxygen uptake was reduced by 4% following 4 wk of SIT+BR and NT+BR (P < 0.05) but not SIT+PL. The peak work rate attained during incremental exercise increased more in SIT+BR than in SIT+PL (P < 0.05) or NT+BR (P < 0.001). The reduction in muscle and blood [lactate] and the increase in muscle pH from preintervention to postintervention were greater at 3 min of severe-intensity exercise in SIT+BR compared with SIT+PL and NT+BR (P < 0.05). However, the change in severe-intensity exercise performance was not different between SIT+BR and SIT+PL (P > 0.05). The relative proportion of type IIx muscle fibers in the vastus lateralis muscle was reduced in SIT+BR only (P < 0.05). These findings suggest that BR supplementation may enhance some aspects of the physiological adaptations to SIT.NEW & NOTEWORTHY We investigated the influence of nitrate-rich and nitrate-depleted beetroot juice on the muscle metabolic and physiological adaptations to 4 wk of sprint interval training. Compared with placebo, dietary nitrate supplementation reduced the O2 cost of submaximal exercise, resulted in greater improvement in incremental (but not severe-intensity) exercise performance, and augmented some muscle metabolic adaptations to training. Nitrate supplementation may facilitate some of the physiological responses to sprint interval training.

Lactate or gas exchange threshold (GET) and critical power (CP) are closely associated with human exercise performance. We tested the hypothesis that the limit of tolerance (Tlim) during cycle exercise performed within the exercise intensity domains demarcated by GET and CP is linked to discrete muscle metabolic and neuromuscular responses. Eleven men performed a ramp incremental exercise test, 4-5 severe-intensity (SEV; >CP) constant-work-rate (CWR) tests until Tlim, a heavy-intensity (HVY; GET) CWR test until Tlim, and a moderate-intensity (MOD;. 0.05) muscle metabolic milieu (i.e. low pH and [PCr] and high [lactate]) was attained at Tlim (approximately 2-14 min) for all SEV exercise bouts. The muscle metabolic perturbation was greater at Tlim following SEV compared with HVY, and also following SEV and HVY compared with MOD (all P < 0.05). The normalized M-wave amplitude for the vastus lateralis (VL) muscle decreased to a similar extent following SEV (-38 ± 15%), HVY (-68 ± 24%), and MOD (-53 ± 29%), (P > 0.05). Neural drive to the VL increased during SEV (4 ± 4%; P < 0.05) but did not change during HVY or MOD (P > 0.05). During SEV and HVY, but not MOD, the rates of change in M-wave amplitude and neural drive were correlated with changes in muscle metabolic ([PCr], [lactate]) and blood ionic/acid-base status ([lactate], [K+]) (P < 0.05). The results of this study indicate that the metabolic and neuromuscular determinants of fatigue development differ according to the intensity domain in which the exercise is performed.NEW & NOTEWORTHY the gas exchange threshold and the critical power demarcate discrete exercise intensity domains. For the first time, we show that the limit of tolerance during whole-body exercise within these domains is characterized by distinct metabolic and neuromuscular responses. Fatigue development during exercise greater than critical power is associated with the attainment of consistent "limiting" values of muscle metabolites, whereas substrate availability and limitations to muscle activation may constrain performance at lower intensities.

We hypothesised that: 1) the critical power (CP) will represent a boundary separating steady state from non-steady state muscle metabolic responses during whole-body exercise and 2) that the CP and the W′ (curvature constant of the power-time relationship for high-intensity exercise) will be correlated with type I and type IIx muscle fibre distributions, respectively. Four men and four women performed a 3-min all-out cycling test for the estimation of CP and constant work rate (CWR) tests slightly >CP until exhaustion (Tlim), slightly CP Tlim isotime to test hypothesis 1. Eleven men performed 3-min all-out tests and donated muscle biopsies to test hypothesis 2. Below CP, muscle [PCr] (42.6±7.1 vs 49.4±6.9 mmol/kgDW), [La-] (34.8±12.6 vs 35.5±13.2 mmol/kgDW) and pH (7.11±0.08 vs 7.10±0.11) remained stable between ~12 and 24 min (P>0.05 for all), whereas these variables changed with time >CP such that they were greater ([La-] 95.6±14.1 mmol/kgDW) and lower ([PCr] 24.2±3.9 mmol/kgDW; pH 6.84±0.06) (P

UNLABELLED: it is possible that dietary nitrate (NO3 (-)) supplementation may improve both physical and cognitive performance via its influence on blood flow and cellular energetics. PURPOSE: to investigate the effects of dietary NO3 (-) supplementation on exercise performance and cognitive function during a prolonged intermittent sprint test (IST) protocol, which was designed to reflect typical work patterns during team sports. METHODS: in a double-blind randomised crossover study, 16 male team-sport players received NO3 (-)-rich (BR; 140 mL day(-1); 12.8 mmol of NO3 (-)), and NO3 (-)-depleted (PL; 140 mL day(-1); 0.08 mmol NO3 (-)) beetroot juice for 7 days. On day 7 of supplementation, subjects completed the IST (two 40-min "halves" of repeated 2-min blocks consisting of a 6-s "all-out" sprint, 100-s active recovery and 20 s of rest), on a cycle ergometer during which cognitive tasks were simultaneously performed. RESULTS: Total work done during the sprints of the IST was greater in BR (123 ± 19 kJ) compared to PL (119 ± 17 kJ; P < 0.05). Reaction time of response to the cognitive tasks in the second half of the IST was improved in BR compared to PL (BR first half: 820 ± 96 vs. second half: 817 ± 86 ms; PL first half: 824 ± 114 vs. second half: 847 ± 118 ms; P < 0.05). There was no difference in response accuracy. CONCLUSIONS: These findings suggest that dietary NO3 (-) enhances repeated sprint performance and may attenuate the decline in cognitive function (and specifically reaction time) that may occur during prolonged intermittent exercise.