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.

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.

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.

.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 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'.

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.

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.

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.

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.

Influence of priming exercise on pulmonary O2 uptake kinetics during transitions to high-intensity exercise at extreme pedal rates.

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.

Influence of repeated sprint training on pulmonary O2 uptake and muscle deoxygenation kinetics in humans.

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.

Muscle [phosphocreatine] dynamics following the onset of exercise in humans: the influence of baseline work-rate.

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.

Influence of priming exercise on pulmonary O2 uptake kinetics during transitions to high-intensity exercise from an elevated baseline.

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; P<0.05), but were not accelerated by priming exercise (42+/-17 s; P>0.05). 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<0.05 for both comparisons). These results indicate that the slower phase II VO2 kinetics observed during transitions to severe exercise from an elevated baseline are not altered by priming exercise, but that the reduced VO2 slow component may be linked to changes in muscle fiber activation.

Effect of eccentric exercise-induced muscle damage on the dynamics of muscle oxygenation and pulmonary oxygen uptake.

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.

Effects of baseline metabolic rate on pulmonary O2 uptake on-kinetics during heavy-intensity exercise in humans.

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 (P<0.01) greater in the M-->H 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<0.05). This 'non-linearity' in the pulmonary V(O2) response to exercise might be attributed, at least in part, to differences in the metabolic properties of the muscle fibres recruited in the abrupt transition from a lower to a higher work rate.

Effects of "priming" exercise on pulmonary O2 uptake and muscle deoxygenation kinetics during heavy-intensity cycle exercise in the supine and upright positions.

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.

Influence of acute plasma volume expansion on VO2 kinetics, VO2 peak, and performance during high-intensity cycle exercise.

The purpose of this study was to examine the influence of acute plasma volume expansion (APVE) on oxygen uptake (V(O2)) kinetics, V(O2peak), 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 V(O2max) 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 V(O2) kinetics (phase II time constant, Con: 33 +/- 15 vs. APVE: 34 +/- 12 s; P = 0.74), and actually resulted in an increased V(O2peak) (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 V(O2) kinetics but enhances V(O2peak) and exercise tolerance during high-intensity cycle exercise in young recreationally active subjects.

Influence of initial metabolic rate on pulmonary O2 uptake on-kinetics during severe intensity exercise.

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.