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.

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.

Effect of nitrate supplementation on hepatic blood flow and glucose homeostasis: a double-blind, placebo-controlled, randomized control trial.

Nitric oxide alters gastric blood flow, improves vascular function, and mediates glucose uptake within the intestines and skeletal muscle. Dietary nitrate, acting as a source of nitric oxide, appears to be a potential low-cost therapy that may help maintain glucose homeostasis. In a randomized, double-blind, placebo-controlled crossover study, 31 young and older adult participants had a standardized breakfast, supplemented with either nitrate-rich beetroot juice (11.91 mmol nitrate) or nitrate-depleted beetroot juice as placebo (0.01 mmol nitrate). MRI was used to assess apparent diffusion coefficient (ADC), portal vein flux, and velocity. Plasma glucose, incretin, and C-peptide concentrations and blood pressure were assessed. Outcome variables were measured at baseline and hourly for 3 h. Compared with a placebo, beetroot juice resulted in a significant elevation in plasma nitrate and plasma nitrite concentration. No differences were seen for the young or older adult cohorts between placebo and beetroot juice for ADC, or portal vein flux. There was an interaction effect in the young adults between visits for portal vein velocity. Nitrate supplementation did not reduce plasma glucose, active GLP-1, total GLP-1, or plasma C-peptide concentrations for the young or older adult cohorts. Despite a significant elevation in plasma nitrite concentration following an acute dose of (11.91 mmol) nitrate, there was no effect on hepatic blood flow, plasma glucose, C-peptide, or incretin concentration in healthy adults.

Unchanged content of oxidative enzymes in fast-twitch muscle fibers and V˙O2 kinetics after intensified training in trained cyclists.

The present study examined if high intensity training (HIT) could increase the expression of oxidative enzymes in fast-twitch muscle fibers causing a faster oxygen uptake (V˙O2) response during intense (INT), but not moderate (MOD), exercise and reduce the V˙O2 slow component and muscle metabolic perturbation during INT. Pulmonary V˙O2 kinetics was determined in eight trained male cyclists (V˙O2-max: 59 ± 4 (means ± SD) mL min(-1) kg(-1)) during MOD (205 ± 12 W ~65% V˙O2-max) and INT (286 ± 17 W ~85% V˙O2-max) exercise before and after a 7-week HIT period (30-sec sprints and 4-min intervals) with a 50% reduction in volume. Both before and after HIT the content in fast-twitch fibers of CS (P < 0.05) and COX-4 (P < 0.01) was lower, whereas PFK was higher (P < 0.001) than in slow-twitch fibers. Content of CS, COX-4, and PFK in homogenate and fast-twitch fibers was unchanged with HIT. Maximal activity (µmol g DW(-1) min(-1)) of CS (56 ± 8 post-HIT vs. 59 ± 10 pre-HIT), HAD (27 ± 6 vs. 29 ± 3) and PFK (340 ± 69 vs. 318 ± 105) and the capillary to fiber ratio (2.30 ± 0.16 vs. 2.38 ± 0.20) was unaltered following HIT. V˙O2 kinetics was unchanged with HIT and the speed of the primary response did not differ between MOD and INT. Muscle creatine phosphate was lower (42 ± 15 vs. 66 ± 17 mmol kg DW(-1)) and muscle lactate was higher (40 ± 18 vs. 14 ± 5 mmol kg DW(-1)) at 6 min of INT (P < 0.05) after compared to before HIT. A period of intensified training with a volume reduction did not increase the content of oxidative enzymes in fast-twitch fibers, and did not change V˙O2 kinetics.

Effects of dietary nitrate supplementation on the oxygen cost of exercise and walking performance in individuals with type 2 diabetes: a randomized, double-blind, placebo-controlled crossover trial.

Dietary nitrate supplementation has been shown to reduce the oxygen (O2) cost of exercise and enhance exercise tolerance in healthy individuals. This study assessed whether similar effects could be observed in individuals with type 2 diabetes (T2DM). In a randomized, double-blind, placebo-controlled crossover study, 48 participants with T2DM supplemented their diet for 4 days with either nitrate-rich beetroot juice (70ml/day, 6.43mmol nitrate/day) or nitrate-depleted beetroot juice as placebo (70ml/day, 0.07mmol nitrate/day). After each intervention period, resting plasma nitrate and nitrite concentrations were measured subsequent to participants completing moderate-paced walking. Pulmonary gas exchange was measured to assess the O2 cost of walking. After a rest period, participants performed the 6-min walk test (6MWT). Relative to placebo, beetroot juice resulted in a significant increase in plasma nitrate (placebo, 57±66 vs beetroot, 319±110µM; P < 0.001) and plasma nitrite concentration (placebo, 680±256 vs beetroot, 1065±607nM; P < 0.001). There were no differences between placebo juice and beetroot juice for the O2 cost of walking (946±221 vs 939±223ml/min, respectively; P = 0.59) and distance covered in the 6MWT (550±83 vs 554±90m, respectively; P = 0.17). Nitrate supplementation did not affect the O2 cost of moderate-paced walking or improve performance in the 6MWT. These findings indicate that dietary nitrate supplementation does not modulate the response to exercise in individuals with T2DM.

The effect of dietary nitrate supplementation on the oxygen cost of cycling, walking performance and resting blood pressure in individuals with chronic obstructive pulmonary disease: A double blind placebo controlled, randomised control trial.

BACKGROUND: Chronic obstructive pulmonary disease (COPD) results in exercise intolerance. Dietary nitrate supplementation has been shown to lower blood pressure (BP), reduce the oxygen cost of exercise, and enhance exercise tolerance in healthy volunteers. This study assessed the effects of dietary nitrate on the oxygen cost of cycling, walking performance and BP in individuals with mild-moderate COPD. METHODS: Thirteen patients with mild-moderate COPD were recruited. Participants consumed 70 ml of either nitrate-rich (6.77 mmol nitrate; beetroot juice) or nitrate-depleted beetroot juice (0.002 mmol nitrate; placebo) twice a day for 2.5 days, with the final supplement ~3 hours before testing. BP was measured before completing two bouts of moderate-intensity cycling, where pulmonary gas exchange was measured throughout. The six-minute walk test (6 MWT) was completed 30 minutes subsequent to the second cycling bout. RESULTS: Plasma nitrate concentration was significantly elevated following beetroot juice vs. placebo (placebo; 48 ± 86 vs. beetroot juice; 215 ± 84 µM, P = 0.002). No significant differences were observed between placebo vs. beetroot juice for oxygen cost of exercise (933 ± 323 vs. 939 ± 302 ml: min(-1); P = 0.88), distance covered in the 6 MWT (456 ± 86 vs. 449 ± 79 m; P = 0.37), systolic BP (123 ± 14 vs. 123 ± 14 mmHg; P = 0.91), or diastolic BP (77 ± 9 vs. 79 ± 9 mmHg; P = 0.27). CONCLUSION: Despite a large rise in plasma nitrate concentration, two days of nitrate supplementation did not reduce the oxygen cost of moderate intensity cycling, increase distance covered in the 6 MWT, or lower BP.

Effects of nitrate on the power-duration relationship for severe-intensity exercise.

PURPOSE: The power asymptote (critical power [CP]) and curvature constant (W') of the power-duration relationship dictate the tolerance to severe-intensity exercise. We tested the hypothesis that dietary nitrate supplementation would increase the CP and/or the W' during cycling exercise. METHODS: In a double-blind, randomized, crossover study, nine recreationally active male subjects supplemented their diet with either nitrate-rich concentrated beetroot juice (BR; 2 × 250 mL·d, ∼8.2 mmol·d nitrate) or a nitrate-depleted BR placebo (PL; 2 × 250 mL·d, ∼0.006 mmol·d nitrate). In each condition, the subjects completed four separate severe-intensity exercise bouts to exhaustion at 60% of the difference between the gas exchange threshold and the peak power attained during incremental exercise (60% Δ), 70% Δ, 80% Δ, and 100% peak power, and the results were used to establish CP and W'. RESULTS: Nitrate supplementation improved exercise tolerance during exercise at 60% Δ (BR, 696 ± 120 vs PL, 593 ± 68 s; P < 0.05), 70% Δ (BR, 452 ± 106 vs PL, 390 ± 86 s; P < 0.05), and 80% Δ (BR, 294 ± 50 vs PL, 263 ± 50 s; P < 0.05) but not 100% peak power (BR, 182 ± 37 vs PL, 166 ± 26 s; P = 0.10). Neither CP (BR, 221 ± 27 vs PL, 218 ± 26 W) nor W' (BR, 19.3 ± 4.6 vs PL, 17.8 ± 3 kJ) were significantly altered by BR. CONCLUSION: Dietary nitrate supplementation improved endurance during severe-intensity exercise in recreationally active subjects without significantly increasing either the CP or the W'.

Effects of pacing strategy on work done above critical power during high-intensity exercise.

PURPOSE: We investigated the influence of pacing strategy on the work completed above critical power (CP) before exhaustion (W>CP) and the peak V˙O2 attained during high-intensity cycling. METHODS: After the determination of VO(2max) from a ramp incremental cycling (INC) test and the estimation of the parameters of the power-duration relationship for high-intensity exercise (i.e., CP and W') from a 3-min all-out cycling test (AOT), eight male subjects completed a cycle test to exhaustion at a severe-intensity constant work rate (CWR) estimated to result in exhaustion in 3 min and a self-paced 3-min cycling time trial (SPT). RESULTS: The VO(2max) determined from INC was 4.24 ± 0.69 L · min(-1), and the CP and the W' estimated from AOT were 260 ± 60 W and 16.5 ± 4.0 kJ, respectively. W>CP during SPT was not significantly different from W>CP during CWR (15.3 ± 5.6 and 16.6 ± 7.4 kJ, respectively), and these values were also similar to W(>CP) during INC (16.4 ± 4.0 kJ) and W' estimated from AOT. The peak VO(2) during SPT was not significantly different from peak VO(2) during CWR (4.20 ± 0.77 and 4.14 ± 0.75 L · min(-1), respectively), and these values were similar to the VO(2max) determined from INC and the peak VO(2) during AOT (4.10 ± 0.79 L · min(-1)). CONCLUSION: Exhaustion during high-intensity exercise coincides with the achievement of the same peak VO2 (VO(2max)) and the completion of the same W>CP, irrespective of the work rate forcing function (INC or CWR) or pacing strategy (enforced pace or self-paced). These findings indicate that exhaustion during high-intensity exercise is based on highly predictable physiological processes, which are unaffected when pacing strategy is self-selected.

.VO2max is not altered by self-pacing during incremental exercise.

We tested the hypothesis that incremental cycling to exhaustion that is paced using clamps of the rating of perceived exertion (RPE) elicits higher .VO2max values compared to a conventional ramp incremental protocol when test duration is matched. Seven males completed three incremental tests to exhaustion to measure .VO2max. The incremental protocols were of similar duration and included: a ramp test at 30 W min(-1) with constant cadence (RAMP1); a ramp test at 30 W min(-1) with cadence free to fluctuate according to subject preference (RAMP2); and a self-paced incremental test in which the power output was selected by the subject according to prescribed increments in RPE (SPT). The subjects also completed a .VO2max 'verification' test at a fixed high-intensity power output and a 3-min all-out test. No difference was found for .VO2max between the incremental protocols (RAMP1 = 4.33 ± 0.60 L min(-1); RAMP2 = 4.31 ± 0.62 L min(-1); SPT = 4.36 ± 0.59 L min(-1); P > 0.05) nor between the incremental protocols and the peak.VO2max measured during the 3-min all-out test (4.33 ± 0.68 L min(-1)) or the .VO2max measured in the verification test (4.32 ± 0.69 L min(-1)). The integrated electromyogram, blood lactate concentration, heart rate and minute ventilation at exhaustion were not different (P > 0.05) between the incremental protocols. In conclusion, when test duration is matched, SPT does not elicit a higher .VO2max compared to conventional incremental protocols. The striking similarity of .VO2max measured across an array of exercise protocols indicates that there are physiological limits to the attainment of .VO2max that cannot be exceeded by self-pacing.

Influence of exercise intensity on skeletal muscle blood flow, O2 extraction and O2 uptake on-kinetics.

Following the start of low-intensity exercise in healthy humans, it has been established that the kinetics of skeletal muscle O(2) delivery is faster than, and does not limit, the kinetics of muscle O(2) uptake (V(O(2)(m))). Direct data are lacking, however, on the question of whether O(2) delivery might limit (V(O(2)(m))) kinetics during high-intensity exercise. Using multiple exercise transitions to enhance confidence in parameter estimation, we therefore investigated the kinetics of, and inter-relationships between, muscle blood flow (Q(m)), a-(V(O(2))) difference and (V(O(2)(m))) following the onset of low-intensity (LI) and high-intensity (HI) exercise. Seven healthy males completed four 6 min bouts of LI and four 6 min bouts of HI single-legged knee-extension exercise. Blood was frequently drawn from the femoral artery and vein during exercise and Q(m), a-(V(O(2))) difference and (V(O(2)(m))) were calculated and subsequently modelled using non-linear regression techniques. For LI, the fundamental component mean response time (MRT(p)) for Q(m) kinetics was significantly shorter than (V(O(2)(m))) kinetics (mean ± SEM, 18 ± 4 vs. 30 ± 4 s; P < 0.05), whereas for HI, the MRT(p) for Q(m) and (V(O(2)(m))) was not significantly different (27 ± 5 vs. 29 ± 4 s, respectively). There was no difference in the MRT(p) for either Q(m) or (V(O(2)(m))) between the two exercise intensities; however, the MRT(p)for a-(V(O(2)) difference was significantly shorter for HI compared with LI (17 ± 3 vs. 28 ± 4 s; P < 0.05). Excess O(2), i.e. oxygen not taken up (Q(m) x (V(O(2))), was significantly elevated within the first 5 s of exercise and remained unaltered thereafter, with no differences between LI and HI. These results indicate that bulk O(2) delivery does not limit (V(O(2)(m))) kinetics following the onset of LI or HI knee-extension exercise.

Influence of acute dietary nitrate supplementation on 50 mile time trial performance in well-trained cyclists.

Dietary nitrate supplementation has been reported to improve short distance time trial (TT) performance by 1-3 % in club-level cyclists. It is not known if these ergogenic effects persist in longer endurance events or if dietary nitrate supplementation can enhance performance to the same extent in better trained individuals. Eight well-trained male cyclists performed two laboratory-based 50 mile TTs: (1) 2.5 h after consuming 0.5 L of nitrate-rich beetroot juice (BR) and (2) 2.5 h after consuming 0.5 L of nitrate-depleted BR as a placebo (PL). BR significantly elevated plasma [NO(2) (-)] (BR: 472 ± 96 vs. PL: 379 ± 94 nM; P < 0.05) and reduced completion time for the 50 mile TT by 0.8 % (BR: 136.7 ± 5.6 vs. PL: 137.9 ± 6.4 min), which was not statistically significant (P > 0.05). There was a significant correlation between the increased post-beverage plasma [NO(2) (-)] with BR and the reduction in TT completion time (r = -0.83, P = 0.01). Power output (PO) was not different between the conditions at any point (P > 0.05) but oxygen uptake ([Formula: see text]O(2)) tended to be lower in BR (P = 0.06), resulting in a significantly greater PO/[Formula: see text]O(2) ratio (BR: 67.4 ± 5.5 vs. PL: 65.3 ± 4.8 W L min(-1); P < 0.05). In conclusion, acute dietary supplementation with beetroot juice did not significantly improve 50 mile TT performance in well-trained cyclists. It is possible that the better training status of the cyclists in this study might reduce the physiological and performance response to NO(3) (-) supplementation compared with the moderately trained cyclists tested in earlier studies.

Influence of passive lower-body heating on muscle metabolic perturbation and high-intensity exercise tolerance in humans.

The purpose of this investigation was to determine the influence of heat stress on the dynamics of muscle metabolic perturbation during high-intensity exercise. Seven healthy males completed single-legged knee-extensor exercise until the limit of tolerance on two separate occasions. In a randomized order the subjects underwent 40 min of lower-body immersion in warm water at 42°C prior to exercise (HOT) or received no prior thermal manipulation (CON). Following the intervention, muscle metabolism was measured at rest and throughout exercise using (31)P-MRS. The tolerable duration of high-intensity exercise was reduced by 36% after passive heating (CON: 474 ± 146 vs. HOT: 303 ± 76 s; P = 0.005). Intramuscular pH was lower over the first 60 s of exercise (CON: 7.05 ± 0.02 vs. HOT: 7.00 ± 0.03; P = 0.019) in HOT compared to CON. The rate of muscle [PCr] degradation during exercise was greater in the HOT condition (CON: -0.17 ± 0.08 vs. HOT: -0.25 ± 0.10% s(-1); P = 0.006) and pH also tended to change more rapidly in HOT (P = 0.09). Muscle [PCr] (CON: 26 ± 14 vs. HOT: 29 ± 10%), [Pi] (CON: 504 ± 236 vs. HOT: 486 ± 186%) and pH (CON: 6.84 ± 0.13 vs. HOT: 6.80 ± 0.14; P > 0.05) were not statistically different at the limit of tolerance (P > 0.05 for all comparisons). These results suggest that the reduced time-to-exhaustion during high-intensity knee-extensor exercise following lower-body heating might be related, in part, to accelerated rates of change of intramuscular [PCr] and pH towards 'critical' values that limit muscle function.

Exercise tolerance in intermittent cycling: application of the critical power concept.

PURPOSE: This study tested the relevance of the critical power (CP) model for explaining exercise tolerance during intermittent high-intensity exercise with different recovery intensities. METHODS: After estimation of CP and W' from a 3-min all-out test, seven male subjects completed, in randomized order, a cycle test to exhaustion at a severe-intensity constant-work-rate (S-CWR) and four cycle tests to exhaustion using different intermittent ("work-recovery") protocols (i.e., severe-severe (S-S), severe-heavy (S-H), severe-moderate (S-M), and severe-light (S-L)). RESULTS: The tolerable duration of exercise in S-CWR was 384 ± 48 s, and this was increased by 47%, 100%, and 219% for S-H, S-M, and S-L, respectively (all P < 0.05). Consistent with this, compared with S-CWR (22.9 ± 7.4 kJ), the work done above the CP was significantly greater by 46%, 98%, and 220% for S-H, S-M, and S-L, respectively (all P < 0.05). The slope of the relationship between V˙O2 and time was significantly reduced for S-H, S-M, and S-L (0.09 ± 0.02, 0.09 ± 0.01, and 0.07 ± 0.02 L·min⁻², respectively) compared with S-CWR (0.16 ± 0.03 L·min⁻², P < 0.05). In addition, the slope of the relationship between integrated EMG and time showed a systematic decline for S-H, S-M, and S-L compared with S-CWR (P < 0.05). CONCLUSIONS: These results indicate that, when recovery intervals during intermittent exercise are performed below the CP, exercise tolerance is improved in proportion to the reconstitution of the finite W'. The enhanced exercise tolerance with the lower-intensity recovery intervals was associated with a blunted increase in both V˙O2 and integrated EMG with time.

Influence of initial metabolic rate on the power-duration relationship for all-out exercise.

A single 3-min all-out cycling test can be used to estimate the power asymptote (critical power, CP) and the curvature constant (W') of the power-duration relationship for severe-intensity exercise. It was hypothesized that when exercise immediately preceding the 3-min all-out test was performed CP would systematically reduce the W' without affecting the CP. Seven physically active males completed 3-min all-out cycling tests in randomized order immediately preceded by: unloaded cycling (control); 6-min moderate; 6-min heavy; 2-min severe (S2); or 4-min severe (S4) intensity exercise. The CP was estimated from the mean power output over the final 30 s of the test and the W' was estimated as the power-time integral above end-test power. There were no significant differences in the CP between control (279 ± 62), moderate (275 ± 52), heavy (286 ± 66 W), S2 (274 ± 55), or S4 (273 ± 65 W). The W' was significantly lower (P < 0.05) in S2 (11.5 ± 2.5) and S4 (8.9 ± 2.2) than in control (16.3 ± 2.3), moderate (17.2 ± 2.4) and heavy (15.6 ± 2.3 kJ). These results support the notion that the W' is predictably depleted only at a power output >CP whereas the CP is independent of the mechanisms which reduce W'.

Acute dietary nitrate supplementation improves cycling time trial performance.

PURPOSE: Dietary nitrate supplementation has been shown to reduce the O2 cost of submaximal exercise and to improve high-intensity exercise tolerance. However, it is presently unknown whether it may enhance performance during simulated competition. The present study investigated the effects of acute dietary nitrate supplementation on power output (PO), VO2, and performance during 4- and 16.1-km cycling time trials (TT). METHODS: After familiarization, nine club-level competitive male cyclists were assigned in a randomized, crossover design to consume 0.5 L of beetroot juice (BR; containing ∼ 6.2 mmol of nitrate) or 0.5 L of nitrate-depleted BR (placebo, PL; containing ∼ 0.0047 mmol of nitrate), ∼ 2.5 h before the completion of a 4- and a 16.1-km TT. RESULTS: BR supplementation elevated plasma [nitrite] (PL = 241 ± 125 vs BR = 575 ± 199 nM, P < 0.05). The VO2 values during the TT were not significantly different between the BR and PL conditions at any elapsed distance (P > 0.05), but BR significantly increased mean PO during the 4-km (PL = 279 ± 51 vs BR = 292 ± 44 W, P < 0.05) and 16.1-km TT (PL = 233 ± 43 vs BR = 247 ± 44 W, P < 0.01). Consequently, BR improved 4-km performance by 2.8% (PL = 6.45 ± 0.42 vs BR = 6.27 ± 0.35 min, P < 0.05) and 16.1-km performance by 2.7% (PL = 27.7 ± 2.1 vs BR = 26.9 ± 1.8 min, P < 0.01). CONCLUSIONS: These results suggest that acute dietary nitrate supplementation with 0.5 L of BR improves cycling economy, as demonstrated by a higher PO for the same VO2 and enhances both 4- and 16.1-km cycling TT performance.

Influence of N-acetylcysteine administration on pulmonary O2 uptake kinetics and exercise tolerance in humans.

We investigated the influence of the antioxidant N-acetylcysteine (NAC) on plasma nitrite concentration ([NO2⁻]), pulmonary oxygen uptake (V(O2)) kinetics and exercise tolerance. Eight males completed 'step' moderate- and severe-intensity cycle exercise tests following infusion of either NAC (125 mg kg⁻¹ h⁻¹ for 15 min followed by 25 mg kg⁻¹ h⁻¹ until the termination of exercise) or Placebo (PLA; saline). Following the initial loading phase, NAC infusion elevated plasma free sulfhydryl groups compared to placebo (PLA: 4 ± 2 vs. NAC: 13 ± 3 µ M g⁻¹; P < 0.05) and this elevation was preserved throughout the protocol. The administration of NAC did not significantly influence plasma [NO2⁻] or V(O2) kinetics during either moderate- or severe-intensity exercise. Although NAC did not significantly alter severe-intensity exercise tolerance at the group mean level (PLA: 776 ± 181 vs. NAC: 878 ± 284 s; P > 0.05), there was appreciable inter-subject variability in the response: four subjects had small reductions in exercise tolerance with NAC compared to PLA (-4%, -8%, -11%, and -14%) while the other four showed substantial improvements (+24%, +24%, +40%, and +69%). The results suggest that exercise-induced redox perturbations may contribute to fatigue development in recreationally-active adults.

Fast-start strategy improves VO2 kinetics and high-intensity exercise performance.

PURPOSE: The purpose of this study was to investigate the influence of pacing strategy on pulmonary VO2 kinetics and performance during high-intensity exercise. METHODS: Seven males completed 3- and 6-min bouts of cycle exercise on three occasions with the bouts initiated using an even-start (ES; constant work rate), fast-start (FS), or slow-start (SS) pacing strategy. In all conditions, subjects completed an all-out sprint over the final 60 s of the test as a measure of performance. RESULTS: For the 3-min exercise bouts, the mean response time (MRT) for the VO2 kinetics over the pacing phase was shortest in FS (35 ± 6 s), longest in SS (55 ± 14 s), and intermediate in ES (41 ± 10 s) (P < 0.05 for all comparisons). For the 6-min bouts, the VO2 MRT was longer in SS (56 ± 15 s) than that in FS and ES (38 ± 7 and 42 ± 6 s, respectively, P < 0.05). The VO2 at the end of exercise was not different from the VO2max during the 6-min exercise bouts or 3-FS but was lower than VO2max for 3-ES and 3-SS (P < 0.05). The end-sprint performance was significantly enhanced in 3-FS compared with 3-ES and 3-SS (mean power = 374 ± 68 vs 348 ± 61 and 345 ± 71 W, respectively; P < 0.05). However, end-sprint performance was unaffected by pacing strategy in the 6-min bouts. CONCLUSIONS: These data indicate that an FS pacing strategy significantly improves performance during 3-min bouts of high-intensity exercise by speeding VO2 kinetics and enabling the attainment of VO2max.

Acute L-arginine supplementation reduces the O2 cost of moderate-intensity exercise and enhances high-intensity exercise tolerance.

It has recently been reported that dietary nitrate (NO(3)(-)) supplementation, which increases plasma nitrite (NO(2)(-)) concentration, a biomarker of nitric oxide (NO) availability, improves exercise efficiency and exercise tolerance in healthy humans. We hypothesized that dietary supplementation with L-arginine, the substrate for NO synthase (NOS), would elicit similar responses. In a double-blind, crossover study, nine healthy men (aged 19-38 yr) consumed 500 ml of a beverage containing 6 g of l-arginine (Arg) or a placebo beverage (PL) and completed a series of "step" moderate- and severe-intensity exercise bouts 1 h after ingestion of the beverage. Plasma NO(2)(-) concentration was significantly greater in the Arg than the PL group (331 ± 198 vs. 159 ± 102 nM, P < 0.05) and systolic blood pressure was significantly reduced (123 ± 3 vs. 131 ± 5 mmHg, P < 0.01). The steady-state O(2) uptake (VO(2)) during moderate-intensity exercise was reduced by 7% in the Arg group (1.48 ± 0.12 vs. 1.59 ± 0.14 l/min, P < 0.05). During severe-intensity exercise, the Vo(2) slow component amplitude was reduced (0.58 ± 0.23 and 0.76 ± 0.29 l/min in Arg and PL, respectively, P < 0.05) and the time to exhaustion was extended (707 ± 232 and 562 ± 145 s in Arg and PL, respectively, P < 0.05) following consumption of Arg. In conclusion, similar to the effects of increased dietary NO(3)(-) intake, elevating NO bioavailability through dietary L-Arg supplementation reduced the O(2) cost of moderate-intensity exercise and blunted the VO(2) slow component and extended the time to exhaustion during severe-intensity exercise.

Acute and chronic effects of dietary nitrate supplementation on blood pressure and the physiological responses to moderate-intensity and incremental exercise.

Dietary nitrate (NO(3)(-)) supplementation with beetroot juice (BR) over 4-6 days has been shown to reduce the O(2) cost of submaximal exercise and to improve exercise tolerance. However, it is not known whether shorter (or longer) periods of supplementation have similar (or greater) effects. We therefore investigated the effects of acute and chronic NO(3)(-) supplementation on resting blood pressure (BP) and the physiological responses to moderate-intensity exercise and ramp incremental cycle exercise in eight healthy subjects. Following baseline tests, the subjects were assigned in a balanced crossover design to receive BR (0.5 l/day; 5.2 mmol of NO(3)(-)/day) and placebo (PL; 0.5 l/day low-calorie juice cordial) treatments. The exercise protocol (two moderate-intensity step tests followed by a ramp test) was repeated 2.5 h following first ingestion (0.5 liter) and after 5 and 15 days of BR and PL. Plasma nitrite concentration (baseline: 454 ± 81 nM) was significantly elevated (+39% at 2.5 h postingestion; +25% at 5 days; +46% at 15 days; P < 0.05) and systolic and diastolic BP (baseline: 127 ± 6 and 72 ± 5 mmHg, respectively) were reduced by ∼4% throughout the BR supplementation period (P < 0.05). Compared with PL, the steady-state Vo(2) during moderate exercise was reduced by ∼4% after 2.5 h and remained similarly reduced after 5 and 15 days of BR (P < 0.05). The ramp test peak power and the work rate at the gas exchange threshold (baseline: 322 ± 67 W and 89 ± 15 W, respectively) were elevated after 15 days of BR (331 ± 68 W and 105 ± 28 W; P < 0.05) but not PL (323 ± 68 W and 84 ± 18 W). These results indicate that dietary NO(3)(-) supplementation acutely reduces BP and the O(2) cost of submaximal exercise and that these effects are maintained for at least 15 days if supplementation is continued.