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.

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.

We investigated the influence of hypoxia on the asymptote (critical power, CP) and the curvature constant (W') of the hyperbolic power-duration relationship, as measured by both conventional and all-out testing procedures. 13 females completed 5 constant-power prediction trials and a 3-min all-out test to estimate CP and W', in both normoxia (N) and moderate hypoxia (H; FiO2=0.13). CP was significantly reduced in hypoxia compared to normoxia when estimated by conventional (H:132±17 vs. N:175±25 W; P

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.

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 

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.

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′. Copyright © 2013 by the American College of Sports Medicine.

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'.

PURPOSE: We investigated the influence of pacing strategy on the work completed above critical power (CP) before exhaustion (W>CP) and the peak V̇O2 attained during high-intensity cycling. METHODS: After the determination of V̇O2max 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 V̇O 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 V̇O2 during SPT was not significantly different from peak V̇O2 during CWR (4.20 ± 0.77 and 4.14 ± 0.75 L·min -1, respectively), and these values were similar to the V̇O 2max determined from INC and the peak V̇O2 during AOT (4.10 ± 0.79 L·min-1). CONCLUSION: Exhaustion during high-intensity exercise coincides with the achievement of the same peak V̇O2 (V̇O2max) 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. Copyright © 2013 by the American College of Sports Medicine.

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.

We tested the hypothesis that incremental cycling to exhaustion that is paced using clamps of the rating of perceived exertion (RPE) elicits higher V̇O2max values compared to a conventional ramp incremental protocol when test duration is matched. Seven males completed three incremental tests to exhaustion to measure V̇O2max. 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 V̇O2max 'verification' test at a fixed high-intensity power output and a 3-min all-out test. No difference was found for V̇O 2max 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 V̇O2max measured during the 3-min all-out test (4.33 ± 0.68 L min-1) or the V̇O2max 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 V̇O2max compared to conventional incremental protocols. The striking similarity of V̇O2max measured across an array of exercise protocols indicates that there are physiological limits to the attainment of V̇O2max that cannot be exceeded by self-pacing. © 2012 Springer-Verlag.

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 V̇O 2 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 V̇O 2 and integrated EMG with time. © 2012 by the American College of Sports Medicine.

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.

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 laboratorybased 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 [NO2 -] (BR: 472 ± 96 vs. PL: 379 ± 94 nM; P0.05) but oxygen uptake ( VO2) tended to be lower in BR (P = 0.06), resulting in a significantly greater PO/ VO2 ratio (BR: 67.4 ± 5.5 vs. PL: 65.3 ± 4.8 W L min-1; P

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). 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 

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.

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′. © Springer-Verlag 2011.

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

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 lowerbody 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 31P-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. © Springer-Verlag 2012.

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.

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.

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.

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.

There are reports of abnormal pulmonary oxygen uptake (Vo(2)) and deoxygenated hemoglobin ([HHb]) kinetics in individuals with Type 2 diabetes (T2D) below 50 yr of age with disease durations of

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.

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.

The purpose of this study was to elucidate the mechanistic bases for the reported reduction in the O(2) cost of exercise following short-term dietary nitrate (NO(3)(-)) supplementation. In a randomized, double-blind, crossover study, seven men (aged 19-38 yr) consumed 500 ml/day of either nitrate-rich beet root juice (BR, 5.1 mmol of NO(3)(-)/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 (using (31)P-MRS) and pulmonary oxygen uptake (Vo(2)) 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 Vo(2) (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 Vo(2) (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 microM/s; P < 0.05) and high-intensity (PL 607 +/- 65 vs. BR 436 +/- 43 microM/s; P < 0.05) exercise. Thus the reduced O(2) cost of exercise following dietary NO(3)(-) supplementation appears to be due to a reduced ATP cost of muscle force production. The reduced muscle metabolic perturbation with NO(3)(-) supplementation allowed high-intensity exercise to be tolerated for a greater period of time.

Metabolic transitions from rest to high-intensity exercise were divided into two discrete steps (i.e. rest-to-moderate-intensity (R-->M) and moderate-to-high-intensity (M-->H)) to explore the effect of prior high-intensity 'priming' exercise on intramuscular [PCr] and pulmonary VO₂ kinetics for different sections of the motor unit pool. It was hypothesized that [PCr] and VO₂ kinetics would be unaffected by priming during R-->M exercise, but that the time constants (tau) describing the fundamental [PCr] response and the phase II VO₂ response would be significantly reduced by priming for M-->H exercise. On three separate occasions, six male subjects completed two identical R-->M/M-->H 'work-to-work' prone knee-extension exercise bouts separated by 5min rest. Two trials were performed with measurement of pulmonary VO₂ and the integrated electromyogram (iEMG) of the right m. vastus lateralis. The third trial was performed within the bore of a 1.5-T superconducting magnet for (31)P-MRS assessment of muscle metabolic responses. Priming did not significantly affect the [PCr] or VO₂ tau during R-->M ([PCr] tau Unprimed: 24+/-16 vs. Primed: 22+/-14s; VO₂ tau Unprimed: 26+/-8 vs. Primed: 25+/-9s) or M-->H transitions ([PCr] tau Unprimed: 30+/-5 vs. Primed: 32+/-7s; VO₂ tau Unprimed: 37+/-5 vs. Primed: 38+/-9s). However, it did reduce the amplitudes of the [PCr] and VO₂ slow components by 50% and 46%, respectively, during M-->H (PH exercise after priming. It is concluded that the tau for the initial exponential change of muscle [PCr] and pulmonary VO₂ following the transition from moderate-to-high-intensity prone knee-extension exercise is not altered by priming exercise.

Fatigue of the respiratory muscles during intense exercise might compromise leg blood flow, thereby constraining oxygen uptake (Vo(2)) and limiting exercise tolerance. We tested the hypothesis that inspiratory muscle training (IMT) would reduce inspiratory muscle fatigue, speed Vo(2) kinetics and enhance exercise tolerance. Sixteen recreationally active subjects (mean + or - SD, age 22 + or - 4 yr) were randomly assigned to receive 4 wk of either pressure threshold IMT [30 breaths twice daily at approximately 50% of maximum inspiratory pressure (MIP)] or sham treatment (60 breaths once daily at approximately 15% of MIP). The subjects completed moderate-, severe- and maximal-intensity "step" exercise transitions on a cycle ergometer before (Pre) and after (Post) the 4-wk intervention period for determination of Vo(2) kinetics and exercise tolerance. There were no significant changes in the physiological variables of interest after Sham. After IMT, baseline MIP was significantly increased (Pre vs. Post: 155 + or - 22 vs. 181 + or - 21 cmH(2)O; P < 0.001), and the degree of inspiratory muscle fatigue was reduced after severe- and maximal-intensity exercise. During severe exercise, the Vo(2) slow component was reduced (Pre vs. Post: 0.60 + or - 0.20 vs. 0.53 + or - 0.24 l/min; P < 0.05) and exercise tolerance was enhanced (Pre vs. Post: 765 + or - 249 vs. 1,061 + or - 304 s; P < 0.01). Similarly, during maximal exercise, the Vo(2) slow component was reduced (Pre vs. Post: 0.28 + or - 0.14 vs. 0.18 + or - 0.07 l/min; P < 0.05) and exercise tolerance was enhanced (Pre vs. Post: 177 + or - 24 vs. 208 + or - 37 s; P < 0.01). Four weeks of IMT, which reduced inspiratory muscle fatigue, resulted in a reduced Vo(2) slow-component amplitude and an improved exercise tolerance during severe- and maximal-intensity exercise. The results indicate that the enhanced exercise tolerance observed after IMT might be related, at least in part, to improved Vo(2) dynamics, presumably as a consequence of increased blood flow to the exercising limbs.

We manipulated the baseline metabolic rate and body position to explore the effect of the interaction between recruitment of discrete sections of the muscle fiber pool and muscle O(2) delivery on pulmonary O(2) uptake (VO(2)) kinetics during cycle exercise. We hypothesized that phase II VO(2) kinetics (tau(p)) in the transition from moderate- to severe-intensity exercise would be significantly slower in the supine than upright position because of a compromise to muscle perfusion and that a priming bout of severe-intensity exercise would return tau(p) during supine exercise to tau(p) during upright exercise. Eight male subjects [35 +/- 13 (SD) yr] completed a series of "step" transitions to severe-intensity cycle exercise from an "unloaded" (20-W) baseline and a baseline of moderate-intensity exercise in the supine and upright body positions. tau(p) was not significantly different between supine and upright exercise during transitions from a 20-W baseline to moderate- or severe-intensity exercise but was significantly greater during moderate- to severe-intensity exercise in the supine position (54 +/- 19 vs. 38 +/- 10 s, P < 0.05). Priming significantly reduced tau(p) during moderate- to severe-intensity supine exercise (34 +/- 9 s), returning it to a value that was not significantly different from tau(p) in the upright position. This effect occurred in the absence of changes in estimated muscle fractional O(2) extraction (from the near-infrared spectroscopy-derived deoxygenated Hb concentration signal), such that the priming-induced facilitation of muscle blood flow matched increased O(2) utilization in the recruited fibers, resulting in a speeding of VO(2) kinetics. These findings suggest that, during supine cycling, priming speeds VO(2) kinetics by providing an increased driving pressure for O(2) diffusion in the higher-order (i.e. type II) fibers, which would be recruited in the transition from moderate- to severe-intensity exercise and are known to be especially sensitive to limitations in O(2) supply.

Pharmacological sodium nitrate supplementation has been reported to reduce the O2 cost of submaximal exercise in humans. In this study, we hypothesized that dietary supplementation with inorganic nitrate in the form of beetroot juice (BR) would reduce the O2 cost of submaximal exercise and enhance the tolerance to high-intensity exercise. In a double-blind, placebo (PL)-controlled, crossover study, eight men (aged 19-38 yr) consumed 500 ml/day of either BR (containing 11.2 +/- 0.6 mM of nitrate) or blackcurrant cordial (as a PL, with negligible nitrate content) for 6 consecutive days and completed a series of "step" moderate-intensity and severe-intensity exercise tests on the last 3 days. On days 4-6, plasma nitrite concentration was significantly greater following dietary nitrate supplementation compared with PL (BR: 273 +/- 44 vs. PL: 140 +/- 50 nM; P < 0.05), and systolic blood pressure was significantly reduced (BR: 124 +/- 2 vs. PL: 132 +/- 5 mmHg; P < 0.01). During moderate exercise, nitrate supplementation reduced muscle fractional O2 extraction (as estimated using near-infrared spectroscopy). The gain of the increase in pulmonary O2 uptake following the onset of moderate exercise was reduced by 19% in the BR condition (BR: 8.6 +/- 0.7 vs. PL: 10.8 +/- 1.6 ml.min(-1).W(-1); P < 0.05). During severe exercise, the O2 uptake slow component was reduced (BR: 0.57 +/- 0.20 vs. PL: 0.74 +/- 0.24 l/min; P < 0.05), and the time-to-exhaustion was extended (BR: 675 +/- 203 vs. PL: 583 +/- 145 s; P < 0.05). The reduced O2 cost of exercise following increased dietary nitrate intake has important implications for our understanding of the factors that regulate mitochondrial respiration and muscle contractile energetics in humans.

We hypothesised that dichloroacetate (DCA) would reduce blood lactate accumulation, pulmonary carbon dioxide output (.V(CO2)) and ventilation (.V(E)) at sub-maximal work rates, and improve exercise tolerance during incremental exercise in healthy humans. Nine males (mean+/-SD, age 27+/-4 years) completed, in random order, two ramp incremental cycle ergometer tests to the limit of tolerance following the intravenous infusion of DCA (75 mg/kg body mass in 80 ml saline) or an equivalent volume of saline (as placebo). Relative to control, blood [lactate] was significantly reduced by DCA immediately before exercise (CON: 0.7+/-0.2 vs. DCA: 0.5+/-0.2mM; P

We hypothesized that increasing skeletal muscle total creatine (Cr) content through dietary Cr supplementation would result in slower muscle phosphocreatine concentration ([PCr]) kinetics, as assessed using (31)P magnetic resonance spectroscopy, following the onset and offset of both moderate-intensity (Mod) and heavy-intensity (Hvy) exercise. Seven healthy males (age 29 +/- 6 yr, mean +/- SD) completed a series of square-wave transitions to Mod and Hvy knee extensor exercise inside the bore of a 1.5-T superconducting magnet both before and after a 5-day period of Cr loading (4x 5 g/day of creatine monohydrate). Cr supplementation resulted in an approximately 8% increase in the resting muscle [PCr]-to-[ATP] ratio (4.66 +/- 0.27 vs. 5.04 +/- 0.22; P < 0.05), consistent with a significant increase in muscle total Cr content consequent to the intervention. The time constant for muscle [PCr] kinetics was increased following Cr loading for Mod exercise (control: 15 +/- 8 vs. Cr: 25 +/- 9 s; P < 0.05) and subsequent recovery (control: 14 +/- 8 vs. Cr: 27 +/- 8 s; P < 0.05) and for Hvy exercise (control: 54 +/- 18 vs. Cr: 72 +/- 30 s; P < 0.05), but not for subsequent recovery (control: 41 +/- 11 vs. Cr: 44 +/- 6 s). The magnitude of the increase in [PCr] following Cr loading was correlated (P < 0.05) with the extent of the slowing of the [PCr] kinetics for the moderate off-transient (r = 0.92) and the heavy on-transient (r = 0.71). These data demonstrate, for the first time in humans, that an increase in muscle [PCr] results in a slowing of [PCr] dynamics in exercise and subsequent recovery.

We used extreme pedal rates to investigate the influence of muscle fibre recruitment on pulmonary V(O)(2) kinetics during unloaded-to-moderate-intensity (U-->M), unloaded-to-high-intensity (U-->H), and moderate-intensity to high-intensity (M-->H) cycling transitions. Seven healthy men completed transitions to 60% of the difference between gas-exchange threshold and peak V(O)(2) from both an unloaded and a moderate-intensity (95% GET) baseline at cadences of 35 and 115rpm. Pulmonary gas exchange was measured breath-by-breath and iEMG of the m. vastus lateralis and m. gluteus maximus was measured during all tests. At 35rpm, the phase II time constant (tau(p)) values for U-->M, U-->H, and M-->H were 26+/-7, 31+/-7 and 36+/-8s with the value for M-->H being longer than for U-->M (PM, U-->H, and M-->H were 29+/-8, 48+/-16 and 53+/-20s with the value for U-->M being shorter than for the other two conditions (P

We used extreme pedal rates to investigate the influence of muscle fibre recruitment on pulmonary over(V, ̇)O2 kinetics during unloaded-to-moderate-intensity (U → M), unloaded-to-high-intensity (U → H), and moderate-intensity to high-intensity (M → H) cycling transitions. Seven healthy men completed transitions to 60% of the difference between gas-exchange threshold and peak over(V, ̇)O2 from both an unloaded and a moderate-intensity (95% GET) baseline at cadences of 35 and 115 rpm. Pulmonary gas exchange was measured breath-by-breath and iEMG of the m. vastus lateralis and m. gluteus maximus was measured during all tests. At 35 rpm, the phase II time constant (τp) values for U → M, U → H, and M → H were 26 ± 7, 31 ± 7 and 36 ± 8 s with the value for M → H being longer than for U → M (P < 0.05). At 115 rpm, the τp values for U → M, U → H, and M → H were 29 ± 8, 48 ± 16 and 53 ± 20 s with the value for U → M being shorter than for the other two conditions (P < 0.05). The over(V, ̇)O2 slow component was similar at both cadences, but iEMG only increased beyond minute 2 during high-intensity cycling at 115 rpm. These results demonstrate that over(V, ̇)O2 kinetics are influenced by an interaction of exercise intensity and pedal rate and are consistent with the notion that changes in muscle fibre recruitment are responsible for slower phase II over(V, ̇)O2 kinetics during high-intensity and work-to-work exercise transitions. © 2009 Elsevier B.V. All rights reserved.

We investigated the pedal rate dependency of the effect of priming exercise on pulmonary oxygen uptake (Vo(2)) kinetics. Seven healthy men completed two, 6-min bouts of high-intensity cycle exercise (separated by 6 min of rest) using different combinations of extreme pedal rates for the priming and criterion exercise bouts (i.e. 35-->35, 35-->115, 115-->35, and 115-->115 rev/min). Pulmonary gas exchange and heart rate were measured breath-by-breath, and muscle oxygenation was assessed using near-infrared spectroscopy. When the priming bout was performed at 35 rev/min (35-->35 and 35-->115 conditions), the phase II Vo(2) time constant (tau) was not significantly altered (bout 1: 31 +/- 7 vs. bout 2: 30 +/- 5 s and bout 1: 48 +/- 16 vs. bout 2: 46 +/- 21 s, respectively). However, when the priming bout was performed at 115 rev/min (115-->35 and 115-->115 conditions), the phase II tau was significantly reduced (bout 1: 31 +/- 7 vs. bout 2: 26 +/- 5 s and bout 1: 48 +/- 16 vs. bout 2: 39 +/- 9 s, respectively, P < 0.05). Muscle oxygenation was significantly higher after priming exercise in all four conditions, but significant effects on Vo(2) kinetics were only evident when muscle O(2) extraction (measured as Delta[deoxyhemoglobin]/DeltaVo(2)) was elevated in the fundamental response phase. These data indicate that prior high-intensity exercise at a high pedal rate can speed Vo(2) kinetics during subsequent high-intensity exercise, presumably through specific priming effects on type II muscle fibers.

We hypothesized that a short-term training program involving repeated all-out sprint training (RST) would be more effective than work-matched, low-intensity endurance training (ET) in enhancing the kinetics of oxygen uptake (Vo(2)) and muscle deoxygenation {deoxyhemoglobin concentration ([HHb])} following the onset of exercise. Twenty-four recreationally active subjects (15 men, mean +/- SD: age 21 +/- 4 yr, height 173 +/- 9 cm, body mass 71 +/- 11 kg) were allocated to one of three groups: RST, which completed six sessions of four to seven 30-s RSTs; ET, which completed six sessions of work-matched, moderate-intensity cycling; and a control group (CON). All subjects completed moderate-intensity and severe-intensity "step" exercise transitions before (Pre) and after the 2-wk intervention period (Post). Following RST, [HHb] kinetics were speeded, and the amplitude of the [HHb] response was increased during both moderate and severe exercise (P < 0.05); the phase II Vo(2) kinetics were accelerated for both moderate (Pre: 28 +/- 8, Post: 21 +/- 8 s; P < 0.01) and severe (Pre: 29 +/- 5, Post: 23 +/- 5 s; P < 0.05) exercise; the amplitude of the Vo(2) slow component was reduced (Pre: 0.52 +/- 0.19, Post: 0.40 +/- 0.17 l/min; P < 0.01); and exercise tolerance during severe exercise was improved by 53% (Pre: 700 +/- 234, Post: 1,074 +/- 431 s; P < 0.01). None of these parameters was significantly altered in the ET and CON groups. Six sessions of RST, but not ET, resulted in changes in [HHb] kinetics consistent with enhanced fractional muscle O(2) extraction, faster Vo(2) kinetics, and an increased tolerance to high-intensity exercise.

It has been suggested that a prior bout of high-intensity exercise has the potential to enhance performance during subsequent high-intensity exercise by accelerating the O(2) uptake (Vo(2)) on-response. However, the optimal combination of prior exercise intensity and subsequent recovery duration required to elicit this effect is presently unclear. Eight male participants, aged 18-24 yr, completed step cycle ergometer exercise tests to 80% of the difference between the preestablished gas exchange threshold and maximal Vo(2) (i.e. 80%Delta) after no prior exercise (control) and after six different combinations of prior exercise intensity and recovery duration: 40%Delta with 3 min (40-3-80), 9 min (40-9-80), and 20 min (40-20-80) of recovery and 70%Delta with 3 min (70-3-80), 9 min (70-9-80), and 20 min (70-20-80) of recovery. Overall Vo(2) kinetics were accelerated relative to control in all conditions except for 40-9-80 and 40-20-80 conditions as a consequence of a reduction in the Vo(2) slow component amplitude; the phase II time constant was not significantly altered with any prior exercise/recovery combination. Exercise tolerance at 80%Delta was improved by 15% and 30% above control in the 70-9-80 and 70-20-80 conditions, respectively, but was impaired by 16% in the 70-3-80 condition. Prior exercise at 40%Delta did not significantly influence exercise tolerance regardless of the recovery duration. These data demonstrate that prior high-intensity exercise ( approximately 70%Delta) can enhance the tolerance to subsequent high-intensity exercise provided that it is coupled with adequate recovery duration (>or=9 min). This combination presumably optimizes the balance between preserving the effects of prior exercise on Vo(2) kinetics and providing sufficient time for muscle homeostasis (e.g. muscle phosphocreatine and H(+) concentrations) to be restored.

Unaccustomed eccentric exercise has a profound impact on muscle structure and function. However, it is not known whether associated microvascular dysfunction disrupts the matching of O2 delivery (Qo2) to O2 utilization (Vo2). Near-infrared spectroscopy (NIRS) was used to test the hypothesis that eccentric exercise-induced muscle damage would elevate the muscle Qo2:Vo2 ratio during severe-intensity exercise while preserving the speed of the Vo2 kinetics at exercise onset. Nine physically active men completed "step" tests to severe-intensity exercise from an unloaded baseline on a cycle ergometer before (Pre) and 48 h after (Post) eccentric exercise (100 squats with a load corresponding to 70% of body mass). NIRS and breath-by-breath pulmonary Vo2 were measured continuously during the exercise tests and subsequently modeled using standard nonlinear regression techniques. There were no changes in phase II pulmonary Vo2 kinetics following the onset of exercise (time constant: Pre, 25 +/- 4 s; Post, 24 +/- 2 s; amplitude: Pre, 2.36 +/- 0.23 l/min; Post, 2.37 +/- 0.23 l/min; all P > 0.05). However, the primary (Pre, 14 +/- 3 s; Post, 19 +/- 3 s) and overall (Pre, 16 +/- 4 s; Post, 21 +/- 4 s) mean response time of the [HHb] response was significantly slower following eccentric exercise (P < 0.05). The slower [HHb] kinetics observed following eccentric exercise is consistent with an increased Qo2:Vo2 ratio during transitions to severe-intensity exercise. We propose that unchanged primary phase Vo2 kinetics are associated with an elevated Qo2:Vo2 ratio that preserves blood-myocyte O2 flux.

Seven male subjects completed cycle exercise bouts to the limit of tolerance on three occasions: (1) at a constant work rate (340+/-57 W; even-pace strategy; ES); (2) at a work rate that was initially 10% lower than that in the ES trial but which then increased with time such that it was 10% above that in the ES trial after 120 s of exercise (slow-start strategy; SS); and, (3) at a work rate that was initially 10% higher than that in the ES trial but which then decreased with time such that it was 10% below that in the ES trial after 120 s of exercise (fast-start strategy; FS). The expected time to exhaustion predicted from the pre-established power-time relationship was 120 s in all three conditions. However, the time to exhaustion was significantly greater (P

It has been suggested that the slower O2 uptake (VO2) kinetics observed when exercise is initiated from an elevated baseline metabolic rate are linked to an impairment of muscle O2 delivery. We hypothesized that "priming" exercise would significantly reduce the phase II time constant (tau) during subsequent severe-intensity cycle exercise initiated from an elevated baseline metabolic rate. Seven healthy men completed exercise transitions to 70% of the difference between gas exchange threshold (GET) and peak VO2 from a moderate-intensity baseline (90% GET) on three occasions in each of the "unprimed" and "primed" conditions. Pulmonary gas exchange, heart rate, and the electromyogram of m. vastus lateralis were measured during all tests. The phase II VO2 kinetics were slower when severe exercise was initiated from a baseline of moderate exercise compared with unloaded pedaling (mean+/-SD tau, 42+/-15 vs. 33+/-8 s; P0.05). The amplitude of the VO2 slow component and the change in electromyogram from minutes 2 to 6 were both significantly reduced following priming exercise (VO2 slow component: from 0.47+/-0.09 to 0.27+/-0.13 l/min; change in integrated electromyogram between 2 and 6 min: from 51+/-35 to 26+/-43% of baseline; P

(31)Phosphate-magnetic resonance spectroscopy and near infrared spectroscopy (NIRS) were used for the simultaneous assessment of changes in quadriceps muscle metabolism and oxygenation during consecutive bouts of high-intensity exercise. Six male subjects completed two 6 min bouts of single-legged knee-extension exercise at 80% of the peak work rate separated by 6 min of rest while positioned inside the bore of a 1.5 T superconducting magnet. The total haemoglobin and oxyhaemoglobin concentrations in the area of the quadriceps muscle interrogated with NIRS were significantly higher in the baseline period prior to the second compared with the first exercise bout, consistent with an enhanced muscle oxygenation. Intramuscular phosphorylcreatine concentration ([PCr]) dynamics were not different over the fundamental region of the response (time constant for bout 1, 51 +/- 15 s versus bout 2, 52 +/- 17 s). However, the [PCr] dynamics over the entire response were faster in the second bout (mean response time for bout 1, 72 +/- 16 s versus bout 2, 57 +/- 8 s; P < 0.05), as a consequence of a greater fall in [PCr] in the fundamental phase and a reduction in the magnitude of the 'slow component' in [PCr] beyond 3 min of exercise (bout 1, 10 +/- 6% versus bout 2, 5 +/- 3%; P < 0.05). These data suggest that the increased muscle O(2) availability afforded by the performance of a prior bout of high-intensity exercise does not significantly alter the kinetics of [PCr] hydrolysis at the onset of a subsequent bout of high-intensity exercise. The greater fall in [PCr] over the fundamental phase of the response following prior high-intensity exercise indicates that residual fatigue acutely reduces muscle efficiency.

The kinetics of pulmonary O(2) uptake is known to be substantially slower when exercise is initiated from a baseline of lower-intensity exercise rather than from rest. However, it is not known whether putative intracellular regulators of mitochondrial respiration (and in particular the phosphocreatine concentration, [PCr]) show similar non-linearities in their response dynamics. The purpose of this study was therefore to investigate the influence of baseline metabolic rate on muscle [PCr] kinetics (as assessed using (31)P-magnetic resonance spectroscopy) following the onset of exercise. Seven male subjects completed 'step' tests to heavy-intensity exercise (80% of peak work-rate) from a resting baseline and also from a baseline of moderate-intensity exercise (40% of peak work-rate) using a single-leg knee-extensor ergometer situated inside the bore of a 1.5 T super-conducting magnet. The time constant describing the kinetics of the initial exponential-like fall in [PCr] was significantly different between rest-to-moderate (25 +/- 14 s), rest-to-heavy (48 +/- 11 s) and moderate-to-heavy exercise (95 +/- 40 s) (P < 0.05 for all comparisons). A delayed-onset 'slow component' in the [PCr] response was observed in all subjects during rest-to-heavy exercise, but was attenuated in the moderate-to-heavy exercise condition. These data indicate that muscle [PCr] kinetics does not conform to 'linear, first-order' behaviour during dynamic exercise, and thus have implications for understanding the regulation of muscle oxidative metabolism.

We tested the hypothesis that the asymptote of the hyperbolic relationship between work rate and time to exhaustion during muscular exercise, the "critical power" (CP), represents the highest constant work rate that can be sustained without a progressive loss of homeostasis [as assessed using (31)P magnetic resonance spectroscopy (MRS) measurements of muscle metabolites]. Six healthy male subjects initially completed single-leg knee-extension exercise at three to four different constant work rates to the limit of tolerance (range 3-18 min) for estimation of the CP (mean +/- SD, 20 +/- 2 W). Subsequently, the subjects exercised at work rates 10% below CP (CP) for as long as possible, while the metabolic responses in the contracting quadriceps muscle, i.e. phosphorylcreatine concentration ([PCr]), P(i) concentration ([P(i)]), and pH, were estimated using (31)P-MRS. All subjects completed 20 min of CP exercise was 14.7 +/- 7.1 min. During CP exercise, however, [PCr] continued to fall to the point of exhaustion and [P(i)] and pH changed precipitously to values that are typically observed at the termination of high-intensity exhaustive exercise (end-exercise values = 26 +/- 16% of baseline [PCr], 564 +/- 167% of baseline [P(i)], and pH 6.87 +/- 0.10, all P < 0.05 vs.

The incremental or ramp exercise test to the limit of tolerance has become a popular test for determination of maximal O(2) uptake (VO(2max)). However, many subjects do not evidence a definitive plateau of the VO(2) -work rate relationship on this test and secondary criteria based upon respiratory exchange ratio (RER), maximal heart rate (HR(max)) or blood [lactate] have been adopted to provide confidence in the measured VO(2max). We hypothesized that verification of VO(2max) using these variables is fundamentally flawed in that their use could either allow underestimation of VO(2max) (if, for any reason, a test were ended at a sub-maximal [Formula: see text]), or alternatively preclude subjects from recording a valid VO(2max). Eight healthy male subjects completed a ramp exercise test (at 20 W/min) to the limit of tolerance on an electrically braked cycle ergometer during which pulmonary gas exchange was measured breath-by-breath and blood [lactate] was determined every 90 s. Using the most widely used criterion values of RER (1.10 and 1.15), VO(2max) as determined during the ramp test (4.03 +/- 0.10 l/min) could be undermeasured by 27% (2.97 +/- 0.24 l/min) and 16% (3.41 +/- 0.15 l/min), respectively (both P < 0.05). The criteria of HR(max) (age predicted HR(max) +/- 10 b/min) and blood [lactate] (> or = 8 mM) were untenable because they resulted in rejection of 3/8 and 6/8 of the subjects, most of whom (5/8) had demonstrated a plateau of VO(2max) at VO(2max). These findings provide a clear mandate for rejecting these secondary criteria as a means of validating VO(2max) on ramp exercise tests.

We hypothesised that initiating heavy-intensity exercise from an elevated baseline metabolic rate would result in slower Phase II O2 uptake V(O2) kinetics and a greater overall 'gain' in V(O2) per unit increase in work rate. Seven healthy males performed a series of like-transitions on a cycle ergometer: (1) from light exercise to 'moderate' exercise (80% of the gas exchange threshold, GET; L-->M); (2) from light exercise to 'heavy' exercise (40% of the difference between GET and V(O2) peak; L-->H); (3) from moderate exercise to heavy exercise (M-->H). The Phase II time constant (tau) was significantly (PH condition (48+/-11 s) compared to the L-->M and L-->H conditions (26+/-6 s versus 27+/-4 s, respectively). Moreover, the end-exercise 'gain' values were significantly different between the three conditions (L-->M, 8.1+/-0.7 mL min-1 W-1; L-->H, 9.7+/-0.4 mL min-1 W-1; M-->H, 10.7+/-0.7 mL min-1 W-1; P

We hypothesized that a period of endurance training would result in a speeding of muscle phosphocreatine concentration ([PCr]) kinetics over the fundamental phase of the response and a reduction in the amplitude of the [PCr] slow component during high-intensity exercise. Six male subjects (age 26 +/- 5 yr) completed 5 wk of single-legged knee-extension exercise training with the alternate leg serving as a control. Before and after the intervention period, the subjects completed incremental and high-intensity step exercise tests of 6-min duration with both legs separately inside the bore of a whole-body magnetic resonance spectrometer. The time-to-exhaustion during incremental exercise was not changed in the control leg [preintervention group (PRE): 19.4 +/- 2.3 min vs. postintervention group (POST): 19.4 +/- 1.9 min] but was significantly increased in the trained leg (PRE: 19.6 +/- 1.6 min vs. POST: 22.0 +/- 2.2 min; P < 0.05). During step exercise, there were no significant changes in the control leg, but end-exercise pH and [PCr] were higher after vs. before training. The time constant for the [PCr] kinetics over the fundamental exponential region of the response was not significantly altered in either the control leg (PRE: 40 +/- 13 s vs. POST: 43 +/- 10 s) or the trained leg (PRE: 38 +/- 8 s vs. POST: 40 +/- 12 s). However, the amplitude of the [PCr] slow component was significantly reduced in the trained leg (PRE: 15 +/- 7 vs. POST: 7 +/- 7% change in [PCr]; P < 0.05) with there being no change in the control leg (PRE: 13 +/- 8 vs. POST: 12 +/- 10% change in [PCr]). The attenuation of the [PCr] slow component might be mechanistically linked with enhanced exercise tolerance following endurance training.

We hypothesized that the performance of prior heavy exercise would speed the phase 2 oxygen consumption (VO2) kinetics during subsequent heavy exercise in the supine position (where perfusion pressure might limit muscle O2 supply) but not in the upright position. Eight healthy men (mean +/- SD age 24 +/- 7 yr; body mass 75.0 +/- 5.8 kg) completed a double-step test protocol involving two bouts of 6 min of heavy cycle exercise, separated by a 10-min recovery period, on two occasions in each of the upright and supine positions. Pulmonary O2 uptake was measured breath by breath and muscle oxygenation was assessed using near-infrared spectroscopy (NIRS). The NIRS data indicated that the performance of prior exercise resulted in hyperemia in both body positions. In the upright position, prior exercise had no significant effect on the time constant tau of the VO2 response in phase 2 (bout 1: 29 +/- 10 vs. bout 2: 28 +/- 4 s; P = 0.91) but reduced the amplitude of the VO2 slow component (bout 1: 0.45 +/- 0.16 vs. bout 2: 0.22 +/- 0.14 l/min; P = 0.006) during subsequent heavy exercise. In contrast, in the supine position, prior exercise resulted in a significant reduction in the phase 2 tau (bout 1: 38 +/- 18 vs. bout 2: 24 +/- 9 s; P = 0.03) but did not alter the amplitude of the VO2 slow component (bout 1: 0.40 +/- 0.29 vs. bout 2: 0.41 +/- 0.20 l/min; P = 0.86). These results suggest that the performance of prior heavy exercise enables a speeding of phase 2 VO2 kinetics during heavy exercise in the supine position, presumably by negating an O2 delivery limitation that was extant in the control condition, but not during upright exercise, where muscle O2 supply was probably not limiting.

The purpose of this study was to examine the influence of acute plasma volume expansion (APVE) on oxygen uptake (Vo(2)) kinetics, Vo(2) (peak), and time to exhaustion during severe-intensity exercise. Eight recreationally active men performed "step" cycle ergometer exercise tests at a work rate requiring 70% of the difference between the gas-exchange threshold and Vo(2) (max) on three occasions: twice as a "control" (Con) and once after intravenous infusion of a plasma volume expander (Gelofusine; 7 ml/kg body mass). Pulmonary gas exchange was measured breath by breath. APVE resulted in a significant reduction in hemoglobin concentration (preinfusion: 16.0 +/- 1.0 vs. postinfusion: 14.7 +/- 0.8 g/dl; P < 0.001) and hematocrit (preinfusion: 44 +/- 2 vs. postinfusion: 41 +/- 3%; P < 0.01). Despite this reduction in arterial O-2 content, APVE had no effect on Vo(2) kinetics ( phase II time constant, Con: 33 +/- 15 vs. APVE: 34 +/- 12 s; P = 0.74), and actually resulted in an increased Vo(2 peak) ( Con: 3.90 +/- 0.56 vs. APVE: 4.12 +/- 0.55 l/min; P = 0.006) and time to exhaustion ( Con: 365 +/- 58 vs. APVE: 424 +/- 64 s; P = 0.04). The maximum O-2 pulse was also enhanced by the treatment ( Con: 21.3 +/- 3.4 vs. APVE: 22.7 +/- 3.4 ml/beat; P = 0.04). In conclusion, APVE does not alter Vo(2) kinetics but enhances Vo(2 peak) and exercise tolerance during high-intensity cycle exercise in young recreationally active subjects.

We hypothesised that the fundamental (Phase II) component of pulmonary oxygen uptake (VO(2)) kinetics would be significantly slower when step transitions to severe intensity cycle exercise were initiated from elevated baseline metabolic rates, and that this would be associated with evidence for a greater activation of higher-order (i.e. type II) muscle fibres. Seven male subjects (age 22-34 years) completed repeat step transitions to a severe (S) work rate, estimated to require 100% VO(2) peak, from a baseline of: (1) 3 min of unloaded cycling (L-->S); (2) 6 min of moderate exercise (M-->S); (3) 6 min of heavy exercise (H-->S). Pulmonary gas exchange and the electromyogram (EMG) of the m. vastus lateralis were measured throughout all exercise tests. The Phase II VO(2) kinetics became progressively slower at higher baseline metabolic rates (tau was 37 +/- 6, 59 +/- 23, and 93 +/- 50 s for L-->S, M-->S, and H-->S, respectively; P < 0.05 between L-->S and H-->S). Both the integrated EMG and the mean power frequency were significantly higher immediately before the step transition to severe exercise when it was initiated from higher metabolic rates. Although indirect, these data suggest that the slower Phase II VO(2) kinetics observed at higher baseline metabolic rates was related to alterations in muscle activation and fibre recruitment patterns.

Purpose: the influence of metabolic alkalosis (ALK) on pulmonary O-2 uptake (pVO(2)) kinetics during high-intensity cycle exercise is controversial. The purpose of this study was to examine the influence of ALK induced by sodium bicarbonate (NaHCO3) ingestion on pVO(2) kinetics, using a sufficient number of repeat-step transitions to provide high confidence in the results obtained. Methods: Seven healthy males completed step tests to a work rate requiring 80% pVO(2max) on six separate occasions: three times after ingestion of 0.3 g(.)kg(-1) body mass NaHCO3 in 1 L of fluid, and three times after ingestion of a placebo (CON). Blood samples were taken to assess changes in acid-base balance, and pVO(2) was measured breath-by-breath. Results: NaHCO3 ingestion significantly increased blood pH and [bicarbonate] both before and during exercise relative to the control condition (P < 0.001). The time constant of the phase II pVO(2) response was not different between conditions (CON: 29 +/- 6 vs ALK: 32 +/- 7 s; P = 0.21). However, the onset of the pVO(2) Slow component was delayed by NaHCO3 ingestion (CON: 120 +/- 19 vs ALK: 147 34 s; P < 0.01), resulting in a significantly reduced end-exercise pVO(2) (CON: 2.88 +/- 0.19 vs ALK: 2.79 +/- 0.23 L(.)min(-1); P < 0.05). Conclusions: Metabolic alkalosis has no effect on phase II pVO(2) kinetics but alters the pVO(2) slow-component response, possibly as a result of the effects of NaHCO3 ingestion on muscle pH.

The purpose of this study was to characterise, for the first time, the pulmonary O2 uptake (V(O2)) on-kinetic responses to step transitions to moderate and heavy intensity rowing ergometer exercise, and to compare the responses to those observed during upright cycle ergometer exercise. We hypothesised that the recruitment of a greater muscle mass in rowing ergometer exercise (Row) might limit muscle perfusion and result in slower Phase II V(O2) kinetics compared to cycle exercise (Cyc). Eight healthy males (aged 28+/-5 years) performed a series of step transitions to moderate (90% of the mode-specific gas exchange threshold, GET) and heavy (50% of the difference between the mode-specific GET and V(O2) max) work rates, for both Row and Cyc exercise. Pulmonary V(O2) was measured breath-by-breath and the V(O2) on-kinetics were described using standard non-linear regression techniques. With the exception of delta V(O2)delta WR which was approximately 12% greater for Row, the V(O2) kinetic responses were similar between the exercise modes. There was no significant difference in the time constant describing the Phase II V(O2) kinetics between the exercise modes for either moderate (rowing: 25.9+/-6.8 s versus cycling: 25.7+/-8.6 s) or heavy (rowing: 26.5+/-3.0 s versus cycling: 27.8+/-5.1s) exercise. Furthermore, there was no significant difference in the amplitude of the V(O2) slow component between the exercise modes (rowing: 0.34+/-0.13 L min(-1) versus cycling: 0.35+/-0.12 L min(-1)). These data suggest that muscle V(O2) increases towards the anticipated steady-state requirement at essentially the same rate following a step increase in ATP turnover in the myocytes, irrespective of the mode of exercise, at least in subjects with no particular sport specialism. The recruitment of a greater muscle mass in rowing compared to cycling apparently did not compromise muscle perfusion sufficiently to result either in slower Phase II V(O2) kinetics or a greater V(O2) slow component amplitude during heavy exercise.

We hypothesised that pharmacological activation of the pyruvate dehydrogenase enzyme complex (PDC) by dichloroacetate (DCA) would speed phase-II pulmonary O2 uptake (VO2) kinetics following the onset of high-intensity, sub-maximal exercise. Eight healthy males (aged 19-33 years) completed two "square-wave" transitions of 6 min duration from unloaded cycling to a work-rate equivalent to approximately 80% of peak VO2 either with or without prior i.v. infusion of DCA (50 mg kg(-1) body mass in 50 ml saline). Pulmonary VO2 was measured breath-by-breath throughout all tests, and VO2 kinetics were determined using non-linear regression techniques from the averaged individual response to each of the conditions. Infusion of DCA resulted in significantly lower blood [lactate] during the baseline cycling period (means+/-SEM: control 0.9+/-0.1, DCA 0.5+/-0.1 mM; P

We hypothesized that the metabolic acidosis resulting from the performance of multiple-sprint exercise would enhance muscle perfusion and result in a speeding of pulmonary oxygen uptake (VO2)kinetics during subsequent perimaximal-intensity constant work rate exercise, if O2 availability represented a limitation to VO2 kinetics in the control (i.e. no prior exercise) condition. On two occasions, seven healthy subjects completed two bouts of exhaustive cycle exercise at a work rate corresponding to approximately 105% of the predetermined Vo2 peak, separated by 3 x 30-s maximal sprint cycling and 15-min recovery (MAX1 and MAX2). Blood lactate concentration (means +/- SD: MAX1: 1.3 +/- 0.4 mM vs. MAX2: 7.7 +/- 0.9 mM; P < 0.01) was significantly greater immediately before, and heart rate was significantly greater both before and during, perimaximal exercise when it was preceded by multiple-sprint exercise. Near-infrared spectroscopy also indicated that muscle blood volume and oxygenation were enhanced when perimaximal exercise was preceded by multiple-sprint exercise. However, the time constant describing the primary component (i.e. phase II) increase in VO2 was not significantly different between the two conditions (MAX1: 33.8 +/- 5.5 s vs. MAX2: 33.2 +/- 7.7 s). Rather, the asymptotic "gain" of the primary Vo2 response was significantly increased by the performance of prior sprint exercise (MAX1: 8.1 +/- 0.9 ml.min(-1).W(-1) vs. MAX2: 9.0 +/- 0.7 ml.min(-1).W(-1); P < 0.05), such that VO2 was projecting to a higher "steady-state" amplitude with the same time constant. These data suggest that priming exercise, which apparently increases muscle O2 availability, does not influence the time constant of the primary-component VO2 response but does increase the amplitude to which VO2 may rise following the onset of perimaximal-intensity cycle exercise.

It has recently been reported that the 'gain' of Phase II increase in pulmonary oxygen uptake (i.e. the 'fundamental' increase in V(O(2)) per unit increase in work rate; G(p)) does not attain the anticipated value of approximately 10 ml min(-1)W(-1) following the onset of high-intensity exercise. In the present study, we hypothesised that G(p) would fall significantly below 10 ml min(-1)W(-1) only when the work rate exceeded the so-called 'critical power' (CP). Seven healthy males completed several 'square-wave' transitions from 'unloaded' cycling to work rates requiring 60 and 90% of the gas exchange threshold (GET), 40 and 80% of the difference between the GET and V(O(2)) peak (i.e. below and above the CP, respectively), and 100, 110 and 120% of V(O(2)) peak. Pulmonary V(O(2)) was measured breath-by-breath and V(O(2)) kinetics were determined using non-linear regression techniques. The asymptotic G(p) was significantly lower at work rates above (7.2-8.6 ml min(-1)W(-1)) compared to work rates below (9.3-9.7 ml min(-1)W(-1)) the CP (P < 0.05). We conclude that the gain of Phase II increase in V(O(2)) becomes significantly reduced when the work rate exceeds the CP.

PURPOSE: to test the hypothesis that pharmacological activation of the pyruvate dehydrogenase enzyme complex (PDC) with dichloroacetate (DCA) would speed phase II pulmonary oxygen uptake ((.-)V(O2)) kinetics after the onset of subsequent moderate-intensity (40-45% ((.-)V(O2)) peak) cycle exercise. METHODS: Seven healthy males (mean +/- SD age 25 +/- 4 yr, body mass 75.3 +/- 9.4 kg) performed four "square-wave" transitions from unloaded cycling to a work rate requiring 90% of the predetermined gas exchange threshold either with or without prior infusion of DCA (50 mg x kg body mass in 50 mL saline). Pulmonary ((.-)V(O2)) was measured breath-by-breath in all tests and ((.-)V(O2)) kinetics were determined from the averaged individual response to each condition using nonlinear regression techniques. RESULTS: the blood [lactate] measured immediately before the onset of exercise was significantly reduced in the DCA condition (C: 1.1 +/- 0.3 vs DCA: 0.6 +/- 0.3 mM; P < 0.01) consistent with successful activation of the PDC. However, DCA had no discernible effect on the rate at which ((.-)V(O2)) increased toward the steady state after the onset of exercise as reflected in the phase II time constant (C: 28.5 +/- 11.8 vs DCA: 29.4 +/- 14.9 s). CONCLUSIONS: the results suggest that PDC activation does not represent a principal intramuscular limitation to ((.-)V(O2)) kinetics after the onset of moderate-intensity exercise.

We hypothesized that inhibition of nitric oxide synthase (NOS) by N(G)-nitro-L-arginine methyl ester (L-NAME) would alleviate the inhibition of mitochondrial oxygen uptake (Vo(2)) by nitric oxide and result in a speeding of phase II pulmonary Vo(2) kinetics at the onset of heavy-intensity exercise. Seven men performed square-wave transitions from unloaded cycling to a work rate requiring 40% of the difference between the gas exchange threshold and peak Vo(2) with and without prior intravenous infusion of L-NAME (4 mg/kg in 50 ml saline over 60 min). Pulmonary gas exchange was measured breath by breath, and Vo(2) kinetics were determined from the averaged response to two exercise bouts performed in each condition. There were no significant differences between the control (C) and L-NAME conditions (L) for baseline Vo(2), the duration of phase I, or the amplitude of the primary Vo(2) response. However, the time constant of the Vo(2) response in phase II was significantly smaller (mean +/- SE: C: 25.1 +/- 3.0 s; L: 21.8 +/- 3.3 s; P < 0.05), and the amplitude of the Vo(2) slow component was significantly greater (C: 240 +/- 47 ml/min; L: 363 +/- 24 ml/min; P < 0.05) after L-NAME infusion. These data indicate that inhibition of NOS by L-NAME results in a significant (13%) speeding of Vo(2) kinetics and a significant increase in the amplitude of the Vo(2) slow component in the transition to heavy-intensity cycle exercise in men. The speeding of the primary component Vo(2) kinetics after L-NAME infusion indicates that at least part of the intrinsic inertia to oxidative metabolism at the onset of heavy-intensity exercise may result from inhibition of mitochondrial Vo(2) by nitric oxide. The cause of the larger Vo(2) slow-component amplitude with L-NAME requires further investigation but may be related to differences in muscle blood flow early in the rest-to-exercise transition.

We have recently reported that inhibition of nitric oxide synthase (NOS) with N(G)-nitro-L-arginine methyl ester (L-NAME) accelerates the 'phase II' pulmonary O2 uptake (VO2) kinetics following the onset of moderate and heavy intensity submaximal exercise in humans. These data suggest that the influence of nitric oxide (NO) on mitochondrial function is an important factor in the inertia to aerobic respiration that is evident in the transition from a lower to a higher metabolic rate. The purpose of the present study was to investigate the influence of L-NAME on pulmonary VO2 kinetics following the onset of supra-maximal exercise, where it has been suggested that O2 availability represents an additional limitation to VO2 kinetics. Seven healthy young men volunteered to participate in this study. Following an incremental cycle ergometer test for the determination of VO2max, the subjects returned on two occasions to perform a 'step' exercise test from a baseline of unloaded cycling to a work rate calculated to require 105% VO2max, preceded either by systemic infusion of L-NAME (4 mg kg(-1) in 50 ml saline) or 50 ml saline as a control (Con). Pulmonary gas exchange was measured on a breath-by-breath basis throughout the exercise tests. The duration of 'phase I' was greater with L-NAME (Con: 14.0 +/- 2.1 versus L-NAME: 16.0 +/- 1.6 s; P = 0.03), suggestive of a slower cardiovascular adaptation following the onset of exercise. However, the phase II VO2 time constant was reduced by 44% with L-NAME (Con: 36.3 +/- 17.3 versus L-NAME: 20.4 +/- 8.3 s; P = 0.01). The accumulation of blood lactate during exercise was also reduced with L-NAME (Con: 4.0 +/- 1.1 versus L-NAME: 2.7 +/- 2.1 mM; P = 0.04). These data indicate that skeletal muscle NO production represents an important limitation to the acceleration of oxidative metabolism following the onset of supra-maximal exercise in humans.

We hypothesized that the effective inhibition of nitric oxide synthase (NOS), achieved via systemic infusion of N(G)-nitro-l-arginine methyl ester (l-NAME), would reduce the gas exchange threshold (GET) and the maximal oxygen uptake (V(.)(O(2)max)) during incremental cycle exercise in man if NO is important in the regulation of muscle vasodilatation. Seven healthy males, aged 18-34 years, volunteered to participate in this ethically approved study. On two occasions, the subjects completed an incremental exercise test to exhaustion on an electrically braked cycle ergometer following the infusion of either l-NAME (4 mg kg(-1) in 50 ml saline) or placebo (50 ml saline, CON). At rest, the infusion of l-NAME resulted in a significant increase in mean arterial pressure (MAP; CON vs. l-NAME, 89 +/- 8 vs. 103 +/- 11 mmHg (mean +/- s.d.; P < 0.05)) and a significant reduction in heart rate (HR; CON vs. l-NAME, 60 +/- 12 vs. 51 +/- 8 beats min(-1); P < 0.01). At submaximal work rates, there was no significant difference in V(.)(O(2)) between the conditions and no difference in the GET (CON vs. l-NAME, 1.94 +/- 0.47 vs. 2.01 +/- 0.41 l min(-1)). However, at higher work rates, differences in V(.)(O(2)) between the conditions became more pronounced such that V(.)(O(2)max) was significantly lower with l-NAME (CON vs. l-NAME, 4.02 +/- 0.41 vs. 3.80 +/- 0.34 l min(-1); P < 0.05). The reduction in V(.)(O(2)max) was associated with a reduction in HR(max) (CON vs. l-NAME, 186 +/- 10 vs. 178 +/- 7 beats min(-1); P < 0.01). These results demonstrate that NOS inhibition with l-NAME has no effect on GET but reduces V(.)(O(2)max) during large muscle group exercise in man, presumably by direct or indirect effects on cardiac output and muscle blood flow.

There is evidence that the rate at which oxygen uptake (.VO2) rises at the transition to higher metabolic rates within the moderate exercise intensity domain is modulated by oxidative enzyme inertia, and also that nitric oxide regulates mitochondrial function through competitive inhibition of cytochrome c oxidase in the electron transport chain. We therefore hypothesised that inhibition of nitric oxide synthase (NOS) by nitro-L-arginine methyl ester (L-NAME) would alleviate the inhibition of mitochondrial. VO2 by nitric oxide and result in a speeding of. VO2 kinetics at the onset of moderate-intensity exercise. Seven males performed square-wave transitions from unloaded cycling to a work rate requiring 90 % of predetermined gas exchange threshold with and without prior intravenous infusion of L-NAME (4 mg kg-1 in 50 ml saline over 60 min). Pulmonary gas exchange was measured breath-by-breath and. VO2 kinetics were determined from the averaged response to four exercise bouts performed in each condition using a mono-exponential function following elimination of the phase I response. There were no significant differences between the control and L-NAME conditions for baseline. VO2 (means +/- S.E.M. 797 +/- 32 vs. 794 +/- 29), the duration of phase I (15.4 +/- 0.8 vs. 17.2 +/- 0.6), or the steady-state increment in. VO2 above baseline (1000 +/- 83 vs. 990 +/- 85 ml min-1), respectively. However, the phase II time constant of the. VO2 response was significantly smaller following L-NAME infusion (22.1 +/- 2.4 vs. 17.9 +/- 2.3; P < 0.05). These data indicate that inhibition of NOS by L-NAME results in a significant (19 %) speeding of pulmonary. VO2 kinetics in the transition to moderate-intensity cycle exercise in man. At least part of the intrinsic inertia to oxidative metabolism at the onset of moderate-intensity exercise may result from competitive inhibition of mitochondrial. VO2 by nitric oxide at cytochrome c oxidase, although other mechanisms for the effect of L-NAME on. VO2 kinetics remain to be explored.

PURPOSE: to test the hypothesis that prior heavy exercise increases the time to exhaustion during subsequent perimaximal exercise. METHODS: Seven healthy males (mean +/- SD 27 +/- 3 yr; 78.4 +/- 0.7 kg) completed square-wave transitions from unloaded cycling to work rates equivalent to 100, 110, and 120% of the work rate at VO2peak (W-[VO2peak) after no prior exercise (control, C) and 10 min after a 6-min bout of heavy exercise at 50% Delta (HE; half-way between the gas exchange threshold (GET) and VO2peak), in a counterbalanced design. RESULTS: Blood [lactate] was significantly elevated before the onset of the perimaximal exercise bouts after prior HE (approximately 2.5 vs approximately 1.1 mM; P < 0.05). Prior HE increased time to exhaustion at 100% (mean +/- SEM. C: 386 +/- 92 vs HE: 613 +/- 161 s), 110% (C: 218 +/- 26 vs HE: 284 +/- 47 s), and 120% (C: 139 +/- 18 vs HE: 180 +/- 29 s) of W-VO2peak, (all P < 0.01). VO2 was significantly higher at 1 min into exercise after prior HE at 110% W-VO2peak (C: 3.11 +/- 0.14 vs HE: 3.42 +/- 0.16 L x min(-1); P < 0.05), and at 1 min into exercise (C: 3.25 +/- 0.12 vs HE: 3.67 +/- 0.15; P < 0.01) and at exhaustion (C: 3.60 +/- 0.08 vs HE: 3.95 +/- 0.12 L x min(-1); P < 0.01) at 120% of W-VO2peak. CONCLUSIONS: This study demonstrate that prior HE, which caused a significant elevation of blood [lactate], resulted in an increased time to exhaustion during subsequent perimaximal exercise presumably by enabling a greater aerobic contribution to the energy requirement of exercise.