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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.

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.

We tested the hypothesis that the time constants (τ) of postexercise T2* MRI signal intensity (an index of O2delivery) and muscle [PCr] (an index of metabolic perturbation, measured by31P-MRS) in hypoxia would be accelerated after dietary nitrate (NO3−) supplementation. In a double-blind crossover design, eight moderately trained subjects underwent 5 days of NO3−(beetroot juice, BR; 8.2 mmol/day NO3−) and placebo (PL; 0.003 mmol/day NO3−) supplementation in four conditions: normoxic PL (N-PL), hypoxic PL (H-PL; 13% O2), normoxic NO3−(N-BR), and hypoxic NO3−(H-BR). The single-leg knee-extension protocol consisted of 10 min of steady-state exercise and 24 s of high-intensity exercise. The [PCr] recovery τ was greater in H-PL (30 ± 4 s) than H-BR (22 ± 4 s), N-PL (24 ± 4 s) and N-BR (22 ± 4 s) ( P < 0.05) and the maximal rate of mitochondrial ATP resynthesis (Qmax) was lower in the H-PL (1.12 ± 0.16 mM/s) compared with H-BR (1.35 ± 0.26 mM/s), N-PL (1.47 ± 0.28 mM/s), and N-BR (1.40 ± 0.21 mM/s) ( P < 0.05). The τ of postexercise T2* signal intensity was greater in H-PL (47 ± 14 s) than H-BR (32 ± 10 s), N-PL (38 ± 9 s), and N-BR (27 ± 6 s) ( P < 0.05). The postexercise [PCr] and T2* recovery τ were correlated in hypoxia ( r = 0.60; P < 0.05), but not in normoxia ( r = 0.28; P > 0.05). These findings suggest that the NO3−-NO2−-NO pathway is a significant modulator of muscle energetics and O2delivery during hypoxic exercise and subsequent recovery.

Dietary supplementation with beetroot juice (BR), containing approximately 5–8 mmol inorganic nitrate (NO3−), increases plasma nitrite concentration ([NO2−]), reduces blood pressure, and may positively influence the physiological responses to exercise. However, the dose-response relationship between the volume of BR ingested and the physiological effects invoked has not been investigated. In a balanced crossover design, 10 healthy men ingested 70, 140, or 280 ml concentrated BR (containing 4.2, 8.4, and 16.8 mmol NO3−, respectively) or no supplement to establish the effects of BR on resting plasma [NO3−] and [NO2−] over 24 h. Subsequently, on six separate occasions, 10 subjects completed moderate-intensity and severe-intensity cycle exercise tests, 2.5 h postingestion of 70, 140, and 280 ml BR or NO3−-depleted BR as placebo (PL). Following acute BR ingestion, plasma [NO2−] increased in a dose-dependent manner, with the peak changes occurring at approximately 2–3 h. Compared with PL, 70 ml BR did not alter the physiological responses to exercise. However, 140 and 280 ml BR reduced the steady-state oxygen (O2) uptake during moderate-intensity exercise by 1.7% ( P = 0.06) and 3.0% ( P < 0.05), whereas time-to-task failure was extended by 14% and 12% (both P < 0.05), respectively, compared with PL. The results indicate that whereas plasma [NO2−] and the O2 cost of moderate-intensity exercise are altered dose dependently with NO3−-rich BR, there is no additional improvement in exercise tolerance after ingesting BR containing 16.8 compared with 8.4 mmol NO3−. These findings have important implications for the use of BR to enhance cardiovascular health and exercise performance in young adults.

Dietary supplementation with beetroot juice (BR) has been shown to reduce resting blood pressure and the O2cost of submaximal exercise and to increase tolerance to high-intensity cycling. We tested the hypothesis that the physiological effects of BR were consequent to its high NO3−content per se, and not the presence of other potentially bioactive compounds. We investigated changes in blood pressure, mitochondrial oxidative capacity (Qmax), and physiological responses to walking and moderate- and severe-intensity running following dietary supplementation with BR and NO3−-depleted BR [placebo (PL)]. After control (nonsupplemented) tests, nine healthy, physically active male subjects were assigned in a randomized, double-blind, crossover design to receive BR (0.5 l/day, containing ∼6.2 mmol of NO3−) and PL (0.5 l/day, containing ∼0.003 mmol of NO3−) for 6 days. Subjects completed treadmill exercise tests on days 4 and 5 and knee-extension exercise tests for estimation of Qmax(using31P-magnetic resonance spectroscopy) on day 6 of the supplementation periods. Relative to PL, BR elevated plasma NO2−concentration (183 ± 119 vs. 373 ± 211 nM, P < 0.05) and reduced systolic blood pressure (129 ± 9 vs. 124 ± 10 mmHg, P < 0.01). Qmaxwas not different between PL and BR (0.93 ± 0.05 and 1.05 ± 0.22 mM/s, respectively). The O2cost of walking (0.87 ± 0.12 and 0.70 ± 0.10 l/min in PL and BR, respectively, P < 0.01), moderate-intensity running (2.26 ± 0.27 and 2.10 ± 0.28 l/min in PL and BR, respectively, P < 0.01), and severe-intensity running (end-exercise O2uptake = 3.77 ± 0.57 and 3.50 ± 0.62 l/min in PL and BL, respectively, P < 0.01) was reduced by BR, and time to exhaustion during severe-intensity running was increased by 15% (7.6 ± 1.5 and 8.7 ± 1.8 min in PL and BR, respectively, P < 0.01). In contrast, relative to control, PL supplementation did not alter plasma NO2−concentration, blood pressure, or the physiological responses to exercise. These results indicate that the positive effects of 6 days of BR supplementation on the physiological responses to exercise can be ascribed to the high NO3−content per se.

The purpose of this study was to elucidate the mechanistic bases for the reported reduction in the O2cost of exercise following short-term dietary nitrate (NO3−) supplementation. In a randomized, double-blind, crossover study, seven men (aged 19–38 yr) consumed 500 ml/day of either nitrate-rich beetroot juice (BR, 5.1 mmol of NO3−/day) or placebo (PL, with negligible nitrate content) for 6 consecutive days, and completed a series of low-intensity and high-intensity “step” exercise tests on the last 3 days for the determination of the muscle metabolic (using31P-MRS) and pulmonary oxygen uptake (V̇o2) responses to exercise. On days 4–6, BR resulted in a significant increase in plasma [nitrite] (mean ± SE, PL 231 ± 76 vs. BR 547 ± 55 nM; P < 0.05). During low-intensity exercise, BR attenuated the reduction in muscle phosphocreatine concentration ([PCr]; PL 8.1 ± 1.2 vs. BR 5.2 ± 0.8 mM; P < 0.05) and the increase in V̇o2(PL 484 ± 41 vs. BR 362 ± 30 ml/min; P < 0.05). During high-intensity exercise, BR reduced the amplitudes of the [PCr] (PL 3.9 ± 1.1 vs. BR 1.6 ± 0.7 mM; P < 0.05) and V̇o2(PL 209 ± 30 vs. BR 100 ± 26 ml/min; P < 0.05) slow components and improved time to exhaustion (PL 586 ± 80 vs. BR 734 ± 109 s; P < 0.01). The total ATP turnover rate was estimated to be less for both low-intensity (PL 296 ± 58 vs. BR 192 ± 38 μM/s; P < 0.05) and high-intensity (PL 607 ± 65 vs. BR 436 ± 43 μM/s; P < 0.05) exercise. Thus the reduced O2cost of exercise following dietary NO3−supplementation appears to be due to a reduced ATP cost of muscle force production. The reduced muscle metabolic perturbation with NO3−supplementation allowed high-intensity exercise to be tolerated for a greater period of time.

to the editor: The letter of Lundberg et al. ([12][1]) does not relate directly to any of the articles we published in this journal ([1][2], [2][3], [6][4]). Rather, the correspondents make a general point on the potential risks to athletes who might choose to supplement their diet with nitrate or (

to the editor: The points made by Derave and Taes ([2][1]) in relation to our recent article ([1][2]) are important. We are very much aware of the literature concerning nitrate toxicity, which is extensive and complex. Concern about dietary nitrate began in the 1970's ([5][3], [6][4]) with the