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The aim of this study was to compare the effects of two different kinds of prior exercise protocols [continuous exercise (CE) versus intermittent repeated sprint (IRS)] on oxygen uptake (VO2) kinetics parameters during high-intensity running.Thirteen male amateur futsal players (age 22.8 ± 6.1 years; mass 76.0 ± 10.2 kg; height 178.7 ± 6.6 cm; VO2max 58.1 ± 4.5 mL kg(-1) min(-1)) performed a maximal incremental running test for the determination of the gas exchange threshold (GET) and maximal VO2 (VO2max). On two different days, the subjects completed a 6-min bout of high-intensity running (50 % ∆) on a treadmill that was 6-min after (1) an identical bout of high-intensity exercise (from control to CE), and (2) a protocol of IRS (6 × 40 m).We found significant differences between CE and IRS for the blood lactate concentration ([La]; 6.1 versus 10.7 mmol L(-1), respectively), VO2 baseline (0.74 versus 0.93 L min(-1), respectively) and the heart rate (HR; 102 versus 124 bpm, respectively) before the onset of high-intensity exercise. However, both prior CE and prior IRS significantly increased the absolute primary VO2 amplitude (3.77 and 3.79 L min(-1), respectively, versus control 3.54 L min(-1)), reduced the amplitude of the VO2 slow component (0.26 and 0.21 L min(-1), respectively, versus control 0.50 L min(-1)), and decreased the mean response time (MRT; 28.9 and 28.0 s, respectively, versus control 36.9 s) during subsequent bouts.This study showed that different protocols and intensities of prior exercise trigger similar effects on VO2 kinetics during high-intensity running.

This study used priming exercise in young boys to investigate (i) how muscle oxygen delivery and oxygen utilization, and muscle activity modulate oxygen uptake kinetics during exercise; and (ii) whether the accelerated oxygen uptake kinetics following priming exercise can improve exercise tolerance. Seven boys that were aged 11.3 ± 1.6 years completed either a single bout (bout 1) or repeated bouts with 6 min of recovery (bout 2) of very heavy-intensity cycling exercise. During the tests oxygen uptake, muscle oxygenation, muscle electrical activity and exercise tolerance were measured. Priming exercise most likely shortened the oxygen uptake mean response time (change, ±90% confidence limits; –8.0 s, ±3.0), possibly increased the phase II oxygen uptake amplitude (0.11 L·min−1, ±0.09) and very likely reduced the oxygen uptake slow component amplitude (–0.08 L·min−1, ±0.07). Priming resulted in a likely reduction in integrated electromyography (–24% baseline, ±21% and –25% baseline, ±19) and a very likely reduction in Δ deoxyhaemoglobin/Δoxygen uptake (–0.16, ±0.11 and –0.09, ±0.05) over the phase II and slow component portions of the oxygen uptake response, respectively. A correlation was present between the change in tissue oxygenation index during bout 2 and the change in the phase II (r = –0.72, likely negative) and slow component (r = 0.72, likely positive) oxygen uptake amplitudes following priming exercise, but not for muscle activity. Exercise tolerance was likely reduced (change –177 s, ±180) following priming exercise. The altered phase II and slow component oxygen uptake amplitudes in boys following priming exercise are linked to an improved localised matching of muscle oxygen delivery to oxygen uptake and not muscle electrical activity. Despite more rapid oxygen uptake kinetics following priming exercise, exercise tolerance was not enhanced.

Context:An exercise bout completed several hours prior to an event may improve competitive performance later that same day.Purpose:To examine the influence of morning exercise on afternoon sprint-swimming performance.Methods:Thirteen competitive swimmers (7 male, mean age 19 ± 3 y; 6 female, mean age 17 ± 3 y) completed a morning session of 1200 m of variedintensity swimming (SwimOnly), a combination of varied-intensity swimming and a resistance-exercise routine (SwimDry), or no morning exercise (NoEx). After a 6-h break, swimmers completed a 100-m time trial.Results:Time-trial performance was faster in SwimOnly (1.6% ± 0.6, mean ± 90% confidence limit, P < .01) and SwimDry (1.7% ± 0.7%, P < .01) than in NoEx. Split times for the 25- to 50-m distance were faster in both SwimOnly (1.7% ± 1.2%, P = .02) and SwimDry (1.5% ± 0.8%, P = .01) than in NoEx. The first 50-m stroke rate was higher in SwimOnly (0.70 ± 0.21 Hz, mean ± SD, P = .03) and SwimDry (0.69 ± 0.18 Hz, P = .05) than in NoEx (0.64 ± 0.16 Hz). Before the afternoon session, core (0.2°C ± 0.1°C [mean ± 90% confidence limit], P = .04), body (0.2°C ± 0.1°C, P = .02), and skin temperatures (0.3°C ± 0.3°C, P = .02) were higher in SwimDry than in NoEx.Conclusions:Completion of a morning swimming session alone or together with resistance exercise can substantially enhance sprint-swimming performance completed later the same day.

Purpose:To assess the effects of different modes of morning (AM) exercise on afternoon (PM) performance and salivary hormone responses in professional rugby union players.Methods:On 4 occasions (randomized, crossover design), 15 professional rugby players provided AM (~8 AM) and PM (~2 PM) saliva samples before PM assessments of countermovement-jump height, reaction time, and repeated-sprint ability. Control (passive rest), weights (bench press: 5 × 10 repetitions, 75% 1-repetition maximum, 90-s intraset recovery), cycling (6 × 6-s maximal sprint cycling, 7.5% body mass load, 54-s intraset recovery), and running (6 × 40-m maximal sprints, 20-s intraset recovery) interventions preceded (~5 h) PM testing.Results:PM sprint performance improved (P < .05) after weights (>0.15 ± 0.19 s, >2.04% ± 2.46%) and running (>0.15 ± 0.17 s, >2.12% ± 2.22%) but not cycling (P > .05). PM jump height increased after cycling (0.012 ± 0.009 m, 2.31% ± 1.76%, P < .001) and running (0.020 ± 0.009 m, 3.90% ± 1.79%, P < .001) but not weights (P = .936). Reaction time remained unchanged between trials (P = .379). Relative to control (131 ± 21 pg/mL), PM testosterone was greater in weights (21 ± 23 pg/mL, 17% ± 18%, P = .002) and running (28 ± 26 pg/mL, 22% ± 20%, P = .001) but not cycling (P = .072). Salivary cortisol was unaffected by AM exercise (P = .540).Conclusions:All modes of AM exercise improved at least 1 marker of PM performance, but running appeared the most beneficial to professional rugby union players. A rationale therefore exists for preceding PM competition with AM exercise.

Research in paediatric exercise metabolism has been constrained by being unable to interrogate muscle in vivo . Conventionally, research has been limited to the estimation of muscle metabolism from observations of blood and respiratory gases during maximal or steady state exercise and the analysis of a few muscle biopsies taken at rest or post-exercise. The purpose of this paper is to review how the introduction of 31 P-magnetic resonance spectroscopy and breath-by-breath oxygen uptake kinetics studies has contributed to current understanding of exercise metabolism during growth and maturation. Methodologically robust studies using 31 P-magnetic resonance spectroscopy and oxygen uptake kinetics with children are sparse and some data are in conflict. However, it can be concluded that children respond to exercise with enhanced oxygen utilization within the myocyte compared with adults and that their responses are consistent with a greater recruitment of type I muscle fibres. Changes in muscle metabolism are age, maturation- and sex-related and dependent on the intensity of the exercise challenge. The introduction of experimental models such as “priming exercise” and “work-to-work” transitions provide intriguing avenues of research into the mechanisms underpinning exercise metabolism during growth and maturation.

This study examined the separate and combined effects of acute hypoxia (Hypo) and heavy-intensity “priming” exercise (Hvy) on pulmonary O2 uptake (V̇o2p) kinetics during moderate-intensity exercise (Mod). Breath-by-breath V̇o2p and near-infrared spectroscopy-derived muscle deoxygenation {deoxyhemoglobin concentration [HHb]} were monitored continuously in 10 men (23 ± 4 yr) during repetitions of a Mod 1-Hvy-Mod 2 protocol, where each of the 6-min (Mod or Hvy) leg-cycling bouts was separated by 6 min at 20 W. Subjects were exposed to Hypo [fraction of inspired O2 (FiO2) = 15%, Mod 2 + Hypo] or “sham” (FiO2 = 20.9%, Mod 2-N) 2 min following Hvy in half of these repetitions; Mod was also performed in Hypo without Hvy (Mod 1 + Hypo). On-transient V̇o2p and [HHb] responses were modeled as a monoexponential. Data were scaled to a relative percentage of the response (0–100%), the signals were time-aligned, and the individual [HHb]-to-V̇o2 ratio was calculated. Compared with control (Mod 1), τV̇o2p and the O2 deficit (26 ± 7 s and 638 ± 144 ml, respectively) were reduced ( P < 0.05) in Mod 2-N (20 ± 5 s and 529 ± 196 ml) and increased ( P < 0.05) in Mod 1 + Hypo (34 ± 14 s and 783 ± 184 ml); in Mod 2 + Hypo, τV̇o2p was increased (30 ± 8 s, P < 0.05), yet O2 deficit was unaffected (643 ± 193 ml, P > 0.05). The modest “overshoot” in the [HHb]-to-V̇o2 ratio (reflecting an O2 delivery-to-utilization mismatch) in Mod 1 (1.06 ± 0.04) was abolished in Mod 2-N (1.00 ± 0.05), persisted in Mod 2 + Hypo (1.09 ± 0.07), and tended to increase in Mod 1 + Hypo (1.10 ± 0.09, P = 0.13). The present data do not support an “O2 delivery-independent” speeding of τV̇o2p following Hvy (or Hvy + Hypo); rather, this study suggests that local muscle O2 delivery likely governs the rate of adjustment of V̇o2 at τV̇o2p greater than ∼20 s.

To investigate the effects of warm-up intensity on all-out sprint cycling performance, muscle oxygenation and metabolism, 8 trained male cyclists/triathletes undertook a 30-s sprint cycling test preceded by moderate, heavy or severe warm up and 10-min recovery. Muscle oxygenation was measured by near-infrared spectroscopy, with deoxyhaemoglobin ([HHb]) during the sprint analysed with monoexponential models with time delay. Aerobic, anaerobic-glycolytic and phosphocreatine energy provision to the sprint were estimated from oxygen uptake and lactate production. Immediately prior to the sprint, blood [lactate] was different for each warm up and higher than resting for the heavy and severe warm ups (mod. 0.94 ± 0.36, heavy 1.92 ± 0.64, severe 4.37 ± 0.93 mmol l(-1) P 0.05), although muscle oxygenation was equally raised above rest. Mean power during the sprint was lower following severe compared to moderate warm up (mod. 672 ± 54, heavy 666 ± 56, severe 655 ± 59 W, P 0.05). The [HHb] kinetics during the sprint were not different among conditions, although the time delay before [HHb] increased was shorter for severe versus moderate warm up (mod. 5.8 ± 0.6, heavy 5.6 ± 0.9, severe 5.2 ± 0.7 s, P 0.05). The severe warm up was without effect on estimated aerobic metabolism, but increased estimated phosphocreatine hydrolysis, the latter unable to compensate for the reduction in estimated anaerobic-glycolytic metabolism. It appears that despite all warm ups equally increasing muscle oxygenation, and indicators of marginally faster oxygen utilisation at the start of exercise following a severe-intensity warm up, other energy sources may not be able to fully compensate for a reduced glycolytic rate in sprint exercise with potential detrimental effects on performance.

International audience; During the early period of running after cycling, EMG patterns of the leg are modified in only some highly trained triathletes. The majority of studies have analysed muscle EMG patterns at arbitrary, predetermined time points. The purpose of this study was to examine changes to EMG patterns of the lower limb at physiologically determined times during the cycle-run transition period to better investigate neuromuscular adaptations. Six highly trained triathletes completed a 10 min isolated run (IR), 30 min of rest, then a 20 min cycling procedure, before a 10 min transition run (C-R). Surface EMG activity of eight lower limb muscles was recorded, normalised and quantified at four time points. Oxygen uptake and heart rate values were also collected. Across all muscles, mean (+/- SD) EMG patterns, demonstrated significant levels of reproducibility for each participant at all four time points (alpha < 0.05; r = 0.52-0.97). Mean EMG patterns during C-R correlated highly with the IR patterns (alpha < 0.05). These results show that EMG patterns during subsequent running are not significantly affected by prior cycling. However, variability of muscle recruitment activity does appear to increase during C-R transition when compared to IR.

The purpose of this study was to determine the effect of 6 min of prior-priming exercise on the incidence of plateau at VO(2max). Twelve trained cyclists (age, 21 ± 3 years; height, 175·0 ± 8·0 cm; weight, 69·0 ± 10·4 kg; maximal oxygen uptake (VO(2max)), 56·3 ± 6·9 ml kg(-1) min(-1)) completed three incremental tests to volitional exhaustion, which were classified as unprimed (UP), heavy-primed (HP) and severe-primed (SP), at a work rate of 1 W 2 s(-1), from an initial workload of 100 W, for the determination of VO(2max). VO(2max) trial in the HP and SP conditions was preceded by a period of 4-min unloaded cycling followed by a further 6 min of constant load cycling at Δ50% VO(2) gas exchange threshold (GET)-VO(2max) (HP) and Δ75% VO(2) GET-VO(2max) (SP). Expired air was recorded on a breath-by-breath basis during all trials. The criteria adopted for a plateau in VO(2max) was a ΔVO(2) over the final two consecutive 30-s sampling periods ≤ 2·1 ml kg(-1) min(-1). There was a significant increase in plateau responses between the UP (50%) and HP (100%) conditions (P = 0·001) coupled with a significant change in the slope of the regression line during the final 60 s of the VO(2max) test, UP and HP (P = 0·0299) and UP and SP (P = 0·0296). These data suggest that a bout of prior-priming exercise promotes an increased incidence of plateau responses at VO(2max) . It is suggested that future studies address how such an approach can be adopted without prior knowledge of GET.

Warm-up is generally considered beneficial for performance, although the reduction in anaerobic glycolytic metabolism may be detrimental to sprinting. This study examined the effect of warm-up intensity on metabolism and performance in sprint cycling. The mean power was determined during a 1-min sprint on 11 trained males preceded by easy (WE), moderate (WM) or hard (WH) warm-up and a 10-min recovery. Aerobic, anaerobic glycolytic and phosphocreatine energy provision to the sprint was determined from oxygen uptake and lactate production. Blood lactate concentration before the sprint increased with the warm-up intensity (WE: 1.2±0.3; WM: 2.0±0.3; WH: 4.2±0.9 mmol/L, P 0.05) due to increased oxygen uptake in WH during the sprint (WE: 3.2±0.4; WM: 3.3±0.3; WH: 3.4±0.4 liters, P

The present study examined the effect of priming exercise on O2 uptake (V̇o2) kinetics during subsequent very heavy exercise in eight 9- to 13-yr-old boys. We hypothesised that priming exercise would 1) elevate muscle O2 delivery prior to the subsequent bout of very heavy exercise, 2) have no effect on the phase II V̇o2 τ, 3) elevate the phase II V̇o2 total amplitude, and 4) reduce the magnitude of the V̇o2 slow component. Each participant completed repeat 6-min bouts of very heavy-intensity cycling exercise separated by 6 min of light pedaling. During the tests V̇o2, muscle oxygenation (near infrared spectroscopy), and cardiac output (Q̇) (thoracic impedance) were determined. Priming exercise increased baseline muscle oxygenation and elevated Q̇ at baseline and throughout the second exercise bout. The phase II V̇o2 τ was not altered by priming exercise ( bout 1: 22 ± 7 s vs. bout 2: 20 ± 4 s; P = 0.30). However, the time constant describing the entire V̇o2 response from start to end of exercise was accelerated ( bout 1: 43 ± 8 s vs. bout 2: 36 ± 5 s; P = 0.002) due to an increased total phase II V̇o2 amplitude ( bout 1: 1.73 ± 0.33 l/min vs. bout 2: 1.80 ± 0.59 l/min; P = 0.002) and a reduced V̇o2 slow component amplitude ( bout 1: 0.18 ± 0.08 l/min vs. bout 2: 0.12 ± 0.09 l/min; P = 0.048). These results suggest that phase II V̇o2 kinetics in young boys is principally limited by intrinsic muscle metabolic factors, whereas the V̇o2 total phase II and slow component amplitudes may be O2 delivery sensitive.

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 (P0.05 for both comparisons). These effects were accompanied by iEMG changes suggesting reduced muscle fiber activation during M--H 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.

The effects of a priming exercise bout on both muscle energy production and the pattern of muscle fibre recruitment during a subsequent exercise bout are poorly understood. The purpose of the present study was to determine whether a prior exercise bout which is known to increase O(2) supply and to induce a residual acidosis could alter energy cost and muscle fibre recruitment during a subsequent heavy-intensity knee-extension exercise. Fifteen healthy subjects performed two 6 min bouts of heavy exercise separated by a 6 min resting period. Rates of oxidative and anaerobic ATP production, determined with (31)P-magnetic resonance spectroscopy, and breath-by-breath measurements of pulmonary oxygen uptake were obtained simultaneously. Changes in muscle oxygenation and muscle fibre recruitment occurring within the quadriceps were measured using near-infrared spectroscopy and surface electromyography. The priming heavy-intensity exercise increased motor unit recruitment (P < 0.05) in the early part of the subsequent exercise bout but did not alter muscle energy cost. We also observed a reduced deoxygenation time delay, whereas the deoxygenation amplitude was increased (P < 0.01). These changes were associated with an increased oxidative ATP cost after approximately 50 s (P < 0.05) and a slight reduction in the overall anaerobic rate of ATP production (0.11 +/- 0.04 mM min(-1) W(-1) for bout 1 and 0.06 +/- 0.11 mM min(-1) W(-1) for bout 2; P < 0.05). We showed that a priming bout of heavy exercise led to an increased recruitment of motor units in the early part of the second bout of heavy exercise. Considering the increased oxidative cost and the unaltered energy cost, one could suggest that our results illustrate a reduced metabolic strain per fibre.

(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.

Other than during sleep and contrived laboratory testing protocols, humans rarely exist in prolonged metabolic steady states; rather, they transition among different metabolic rates (V O2). The dynamic transition of V O2 (V O2 kinetics), initiated, for example, at exercise onset, provides a unique window into understanding metabolic control. This brief review presents the state-of-the art regarding control of V O2 kinetics within the context of a simple model that helps explain the work rate dependence of V O2 kinetics as well as the effects of environmental perturbations and disease. Insights emerging from application of novel approaches and technologies are integrated into established concepts to assess in what circumstances O2 supply might exert a commanding role over V O2 kinetics, and where it probably does not. The common presumption that capillary blood flow dynamics can be extrapolated accurately from upstream arterial measurements is challenged. From this challenge, new complexities emerge with respect to the relationships between O2 supply and flux across the capillary-myocyte interface and the marked dependence of these processes on muscle fiber type. Indeed, because of interfiber type differences in O2 supply relative to V O2, the presence of much lower O2 levels in the microcirculation supplying fast-twitch muscle fibers, and the demonstrated metabolic sensitivity of muscle to O2, it is possible that fiber type recruitment profiles (and changes thereof) might help explain the slowing of V O2 kinetics at higher work rates and in chronic diseases such as heart failure and diabetes.

Purpose:To assess whether combining prior “priming” exercise with an all-out pacing strategy is more effective at improving oxygen-uptake (V̇O2) kinetics and cycling performance than either intervention administered independently.Methods:Nine men completed target-work cycling performance trials using a self-paced or all-out pacing strategy with or without prior severe-intensity (70%Δ) priming exercise. Breath-by-breath pulmonary V̇O2 and cycling power output were measured during all trials.Results:Compared with the self-paced unprimed control trial (22 ± 5 s), the V̇O2 mean response time (MRT) was shorter (V̇O2 kinetics were faster) with all-out pacing (17 ± 4 s) and priming (17 ± 3 s), with the lowest V̇O2 MRT observed when all-out pacing and priming were combined (15 ± 4 s) (P < .05). However, total O2 consumed and end-exercise V̇O2 were only higher than the control condition in the primed trials (P < .05). Similarly, cycling performance was improved compared with control (98 ± 11 s) in the self-paced primed (93 ± 8 s) and all-out primed (92 ± 8 s) trials (P < .05) but not the all-out unprimed trial (97 ± 5 s; P > .05).Conclusions:These findings suggest that combining an all-out start with severe-intensity priming exercise additively improves V̇O2 MRT but not total O2 consumption and cycling performance since these were improved by a similar magnitude in both primed trials relative to the self-paced unprimed control condition. Therefore, these results support the use of priming exercise as a precompetition intervention to improve oxidative metabolism and performance during short-duration high-intensity cycling exercise, independent of the pacing strategy adopted.

The adaptation of pulmonary oxygen uptake during the transition to moderate-intensity exercise (Mod) is faster following a prior bout of heavy-intensity exercise. In the present study we examined the activation of pyruvate dehydrogenase (PDHa) during Mod both with and without prior heavy-intensity exercise. Subjects (n= 9) performed a Mod1–heavy-intensity–Mod2 exercise protocol preceded by 20 W baseline. Breath-by-breath kinetics and near-infrared spectroscopy-derived muscle oxygenation were measured continuously, and muscle biopsy samples were taken at specific times during the transition to Mod. In Mod1, PDHa increased from baseline (1.08 ± 0.2 mmol min−1 (kg wet wt)−1) to 30 s (2.05 ± 0.2 mmol min−1 (kg wet wt)−1), with no additional change at 6 min exercise (2.07 ± 0.3 mmol min−1 (kg wet wt)−1). In Mod2, PDHa was already elevated at baseline (1.88 ± 0.3 mmol min−1 (kg wet wt)−1) and was greater than in Mod1, and did not change at 30 s (1.96 ± 0.2 mmol min−1 (kg wet wt)−1) but increased at 6 min exercise (2.70 ± 0.3 mmol min−1 (kg wet wt)−1). The time constant of was lower in Mod2 (19 ± 2 s) than Mod1 (24 ± 3 s). Phosphocreatine (PCr) breakdown from baseline to 30 s was greater (P < 0.05) in Mod1 (13.6 ± 6.7 mmol (kg dry wt)−1) than Mod2 (6.5 ± 6.2 mmol (kg dry wt)−1) but total PCr breakdown was similar between conditions (Mod1, 14.8 ± 7.4 mmol (kg dry wt)−1; Mod2, 20.1 ± 8.0 mmol (kg dry wt)−1). Both oxyhaemoglobin and total haemoglobin were elevated prior to and throughout Mod2 compared with Mod1. In conclusion, the greater PDHa at baseline prior to Mod2 compared with Mod1 may have contributed in part to the faster kinetics in Mod2. That oxyhaemoglobin and total haemoglobin were elevated prior to Mod2 suggests that greater muscle perfusion may also have contributed to the observed faster kinetics. These findings are consistent with metabolic inertia, via delayed activation of PDH, in part limiting the adaptation of pulmonary and muscle O2 consumption during the normal transition to exercise.

Prior heavy exercise markedly alters the O2 uptake (V̇o2) response to subsequent heavy exercise. However, the time required for V̇o2 to return to its normal profile following prior heavy exercise is not known. Therefore, we examined the V̇o2 responses to repeated bouts of heavy exercise separated by five different recovery durations. On separate occasions, nine male subjects completed two 6-min bouts of heavy cycle exercise separated by 10, 20, 30, 45, or 60 min of passive recovery. The second-by-second V̇o2 responses were modeled using nonlinear regression. Prior heavy exercise had no effect on the primary V̇o2 time constant (from 25.9 ± 4.7 s to 23.9 ± 8.8 s after 10 min of recovery; P = 0.338), but it increased the primary V̇o2 amplitude (from 2.42 ± 0.39 to 2.53 ± 0.41 l/min after 10 min of recovery; P = 0.001) and reduced the V̇o2 slow component (from 0.44 ± 0.13 to 0.21 ± 0.12 l/min after 10 min of recovery; P < 0.001). The increased primary amplitude was also evident after 20–45 min, but not after 60 min, of recovery. The increase in the primary V̇o2 amplitude was accompanied by an increased baseline blood lactate concentration (to 5.1 ± 1.0 mM after 10 min of recovery; P < 0.001). Baseline blood lactate concentration was still elevated after 20–60 min of recovery. The priming effect of prior heavy exercise on the V̇o2 response persists for at least 45 min, although the mechanism underpinning the effect remains obscure.

We investigated the hypothesis that the pulmonary oxygen uptake slow component is related to a progressive increase in muscle lactate concentration and that prior heavy exercise (PHE) with pronounced acidosis alters kinetics and reduces work efficiency. Subjects (n= 9) cycled at 75% of the peak for 10 min before (CON) and after (AC) PHE. was measured continuously (breath-by-breath) and muscle biopsies were obtained prior to and after 3 and 10 min of exercise. Muscle lactate concentration was stable between 3 and 10 min of exercise but was 2- to 3-fold higher during AC (P < 0.05 versus CON). Acetylcarnitine (ACn) concentration was 6-fold higher prior to AC and remained higher during exercise. Phosphocreatine (PCr) concentration was similar prior to exercise but the decrease was 2-fold greater during AC than during CON. The time constant for the initial kinetics (phase II) was similar but the asymptote was 14% higher during AC. The slow increase in between 3 and 10 min of exercise during CON (+7.9 ± 0.2%) was not correlated with muscle or blood lactate levels. PHE eliminated the slow increase in and reduced gross exercise efficiency during AC. It is concluded that the slow component cannot be explained by a progressive acidosis because both muscle and blood lactate levels remained stable during CON. We suggest that both the slow component during CON and the reduced gross efficiency during AC are related to impaired contractility of the working fibres and the necessity to recruit additional motor units. Despite a pronounced stockpiling of ACn during AC, initial kinetics were not affected by PHE and PCr concentration decreased to a lower plateau. The discrepancy with previous studies, where initial oxidative ATP generation appears to be limited by acetyl group availability, might relate to remaining fatiguing effects of PHE.

The effect of prior heavy-intensity warm-up exercise on subsequent moderate-intensity phase 2 pulmonary O2 uptake kinetics (τV̇o2) was examined in young adults exhibiting relatively fast (FK; τV̇o2 < 30 s; n = 6) and slow (SK; τV̇o2 > 30 s; n = 6) V̇o2 kinetics in moderate-intensity exercise without prior warm up. Subjects performed four repetitions of a moderate (Mod1)-heavy-moderate (Mod2) protocol on a cycle ergometer with work rates corresponding to 80% estimated lactate threshold (moderate intensity) and 50% difference between lactate threshold and peak V̇o2 (heavy intensity); each transition lasted 6 min, and each was preceded by 6 min of cycling at 20 W. V̇o2 and heart rate (HR) were measured breath-by-breath and beat-by-beat, respectively; concentration changes of muscle deoxyhemoglobin (HHb), oxyhemoglobin, and total hemoglobin were measured by near-infrared spectroscopy (Hamamatsu NIRO 300). τV̇o2 was lower ( P < 0.05) in Mod2 than in Mod1 in both FK (20 ± 5 s vs. 26 ± 5 s, respectively) and SK (30 ± 8 s vs. 45 ± 11 s, respectively); linear regression analysis showed a greater “speeding” of V̇o2 kinetics in subjects exhibiting a greater Mod1 τV̇o2. HR, oxyhemoglobin, and total hemoglobin were elevated ( P < 0.05) in Mod2 compared with Mod1. The delay before the increase in HHb was reduced ( P < 0.05) in Mod2, whereas the HHb mean response time was reduced ( P < 0.05) in FK (Mod2, 22 ± 3 s; Mod1, 32 ± 11 s) but not different in SK (Mod2, 36 ± 13 s; Mod1, 34 ± 15 s). We conclude that improved muscle perfusion in Mod2 may have contributed to the faster adaptation of V̇o2, especially in SK; however, a possible role for metabolic inertia in some subjects cannot be overlooked.

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 (V̇o2) kinetics during subsequent perimaximal-intensity constant work rate exercise, if O2 availability represented a limitation to V̇o2 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 ∼105% of the predetermined V̇o2 peak, separated by 3 × 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 V̇o2 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 V̇o2 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 V̇o2 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 V̇o2 response but does increase the amplitude to which V̇o2 may rise following the onset of perimaximal-intensity cycle exercise.

Pulmonary O2 uptake (V̇o2p) and muscle deoxygenation kinetics were examined during moderate-intensity cycling (80% lactate threshold) without warm-up and after heavy-intensity warm-up exercise in young ( n = 6; 25 ± 3 yr) and older ( n = 5; 68 ± 3 yr) adults. We hypothesized that heavy warm-up would speed V̇o2p kinetics in older adults consequent to an improved intramuscular oxygenation. Subjects performed step transitions ( n = 4; 6 min) from 20 W to moderate-intensity exercise preceded by either no warm-up or heavy-intensity warm-up (6 min). V̇o2p was measured breath by breath. Oxy-, deoxy-(HHb), and total hemoglobin and myoglobin (Hbtot) of the vastus lateralis muscle were measured continuously by near-infrared spectroscopy (NIRS). V̇o2p (phase 2; τ) and HHb data were fit with a monoexponential model. After heavy-intensity warm-up, oxyhemoglobin (older subjects: 13 ± 9 μM; young subjects: 9 ± 8 μM) and Hbtot (older subjects: 12 ± 8 μM; young subjects: 14 ± 10 μM) were elevated ( P < 0.05) relative to the no warm-up pretransition baseline. In older adults, τV̇o2p adapted at a faster rate ( P < 0.05) after heavy warm-up (30 ± 7 s) than no warm-up (38 ± 5 s), whereas in young subjects, τV̇o2p was similar in no warm-up (26 ± 7 s) and heavy warm-up (25 ± 5 s). HHb adapted at a similar rate in older and young adults after no warm-up; however, in older adults after heavy warm-up, the adaptation of HHb was slower ( P < 0.01) compared with young and no warm-up. These data suggest that, in older adults, V̇o2p kinetics may be limited by a slow adaptation of muscle blood flow and O2 delivery.

Single muscle fibre metabolites and pulmonary oxygen uptake (VO2) were measured during moderate and intense, sub-maximal exercise to test the hypothesis that additional fibre recruitment is associated with the slow component of VO2. Seven healthy, male subjects performed 20 min moderate (MOD, approximately 50% of VO(2,max)) and intense (INT, approximately 80% VO(2,max)) cycling at 70 rpm. Glycogen content decreased significantly in type I and IIa fibres during INT, but only in type I fibres during MOD. During INT, creatine phosphate (CP) content decreased significantly both in types I and II fibres in the first 3 min (DeltaCP: 16.0+/-2.7 and 16.8+/-4.7 mmol kg(-1) d.w., respectively) and in the next 3 min (DeltaCP: 16.2+/-4.9 and 25.7+/-6.7 mmol kg(-1) d.w., respectively) with no further change from 6-20 min. CP content was below the pre-exercise level (mean-1 SD) in 11, 37, 70 and 74% of the type I fibres after 0, 3, 6 and 20 min of INT, respectively, and in 13, 45, 83 and 74% of the type II fibres. During INT, VO2 increased significantly by 6+/-1 and 4+/-1% in the periods 3-6 and 6-20 min, respectively (Delta VO(2,(6-3 min)): 0.14+/-0.02 l min(-1)), whereas VO2 was unchanged from 3 to 20 min of MOD. Exponential fitting revealed a slow component of VO2 during INT that appeared after approximately 2.6 min and amounted to 0.24 l min(-1). The present study demonstrates that additional type I and II fibres are recruited with time during intense sub-maximal exercise in temporal association with a significant slow component of VO2.

The temporal relationship between the kinetics of phase 2 pulmonary O2 uptake (V̇o2p) and deoxygenation of the vastus lateralis muscle was examined during moderate-intensity leg-cycling exercise. Young adults (5 men, 6 women; 23 ± 3 yr; mean ± SD) performed repeated transitions on 3 separate days from 20 W to a constant work rate corresponding to 80% of lactate threshold. Breath-by-breath V̇o2p was measured by mass spectrometer and volume turbine. Deoxyhemoglobin (HHb), oxyhemoglobin, and total hemoglobin and myoglobin were sampled each second by near-infrared spectroscopy (Hamamatsu NIRO-300). V̇o2p data were filtered, interpolated to 1 s, and averaged to 5-s bins; HHb data were averaged to 5-s bins. Phase 2 V̇o2p data were fit with a monoexponential model. For HHb, a time delay (TDHHb) from exercise onset to an increase in HHb was determined, and thereafter data were fit with a monoexponential model. The time constant for V̇o2p (30 ± 8 s) was slower ( P < 0.01) than that for HHb (10 ± 3 s). The TDHHb before an increase in HHb was 13 ± 2 s. The possible mechanisms of the TDHHb are discussed with reference to metabolic activation and matching of local muscle O2 delivery and O2 utilization. After this initial TDHHb, the kinetics of local muscle deoxygenation were faster than those of phase 2 V̇o2p (and presumably muscle O2 consumption), reflecting increased O2 extraction and a mismatch between local muscle O2 consumption and perfusion.

We tested the hypothesis that O2 uptake (V˙o 2) kinetics at the onset of heavy exercise would be altered in a state of muscle fatigue and prior metabolic acidosis. Eight well-trained cyclists completed two identical bouts of 6-min cycling exercise at >85% of peak V˙o 2 separated by three successive bouts of 30 s of sprint cycling. Not only was baselineV˙o 2 elevated after prior sprint exercises but also the time constant of phase IIV˙o 2 kinetics was faster (28.9 ± 2.4 vs. 22.2 ± 1.7 s; P < 0.05). CO2 output (V˙co 2) was significantly reduced throughout the second exercise bout. SubsequentlyV˙o 2 was greater at 3 min and increased less after this after prior sprint exercise. Cardiac output, estimated by impedance cardiography, was significantly higher in the first 2 min of the second heavy exercise bout. Normalized integrated surface electromyography of four leg muscles and normalized mean power frequency were not different between exercise bouts.V˙o 2 andV˙co 2 kinetic responses to heavy exercise were markedly altered by prior multiple sprint exercises.

We hypothesized that the elevated primary O2 uptake (V˙o 2) amplitude during the second of two bouts of heavy cycle exercise would be accompanied by an increase in the integrated electromyogram (iEMG) measured from three leg muscles (gluteus maximus, vastus lateralis, and vastus medialis). Eight healthy men performed two 6-min bouts of heavy leg cycling (at 70% of the difference between the lactate threshold and peakV˙o 2) separated by 12 min of recovery. The iEMG was measured throughout each exercise bout. The amplitude of the primary V˙o 2 response was increased after prior heavy leg exercise (from mean ± SE 2.11 ± 0.12 to 2.44 ± 0.10 l/min, P < 0.05) with no change in the time constant of the primary response (from 21.7 ± 2.3 to 25.2 ± 3.3 s), and the amplitude of theV˙o 2 slow component was reduced (from 0.79 ± 0.08 to 0.40 ± 0.08 l/min, P < 0.05). The elevated primary V˙o 2 amplitude after leg cycling was accompanied by a 19% increase in the averaged iEMG of the three muscles in the first 2 min of exercise (491 ± 108 vs. 604 ± 151% increase above baseline values, P < 0.05), whereas mean power frequency was unchanged (80.1 ± 0.9 vs. 80.6 ± 1.0 Hz). The results of the present study indicate that the increased primaryV˙o 2 amplitude observed during the second of two bouts of heavy exercise is related to a greater recruitment of motor units at the onset of exercise.

The on- and off-transient (i.e. phase II) responses of pulmonary oxygen uptake (V(O(2))) to moderate-intensity exercise (i.e. below the lactate threshold, theta;(L)) in humans has been shown to conform to both mono-exponentiality and 'on-off' symmetry, consistent with a system manifesting linear control dynamics. However above theta;(L) the V(O(2)) kinetics have been shown to be more complex: during high-intensity exercise neither mono-exponentiality nor 'on-off' symmetry have been shown to appropriately characterise the V(O(2)) response. Muscle [phosphocreatine] ([PCr]) responses to exercise, however, have been proposed to be dynamically linear with respect to work rate, and to demonstrate 'on-off' symmetry at all work intenisties. We were therefore interested in examining the kinetic characteristics of the V(O(2)) and [PCr] responses to moderate- and high-intensity knee-extensor exercise in order to improve our understanding of the factors involved in the putative phosphate-linked control of muscle oxygen consumption. We estimated the dynamics of intramuscular [PCr] simultaneously with those of V(O(2)) in nine healthy males who performed repeated bouts of both moderate- and high-intensity square-wave, knee-extension exercise for 6 min, inside a whole-body magnetic resonance spectroscopy (MRS) system. A transmit-receive surface coil placed under the right quadriceps muscle allowed estimation of intramuscular [PCr]; V(O(2)) was measured breath-by-breath using a custom-designed turbine and a mass spectrometer system. For moderate exercise, the kinetics were well described by a simple mono-exponential function (following a short cardiodynamic phase for V(O(2))), with time constants (tau) averaging: tauV(O(2))(,on) 35 +/- 14 s (+/- S.D.), tau[PCr](on) 33 +/- 12 s, tauV(O(2))(,off) 50 +/- 13 s and tau[PCr](off) 51 +/- 13 s. The kinetics for both V(O(2)) and [PCr] were more complex for high-intensity exercise. The fundamental phase expressing average tau values of tauV(O(2))(,on) 39 +/- 4 s, tau[PCr](on) 38 +/- 11 s, tauV(O(2))(,off) 51 +/- 6 s and tau[PCr](off) 47 +/- 11 s. An associated slow component was expressed in the on-transient only for both V(O(2)) and [PCr], and averaged 15.3 +/- 5.4 and 13.9 +/- 9.1 % of the fundamental amplitudes for V(O(2)) and [PCr], respectively. In conclusion, the tau values of the fundamental component of [PCr] and V(O(2)) dynamics cohere to within 10 %, during both the on- and off-transients to a constant-load work rate of both moderate- and high-intensity exercise. On average, approximately 90 % of the magnitude of the V(O(2)) slow component during high-intensity exercise is reflected within the exercising muscle by its [PCr] response.

In humans, pulmonary oxygen uptake (.V(O2)) kinetics may be speeded by prior exercise in the heavy domain. This "speeding" arises potentially as the result of an increased muscle O(2) delivery (.Q(O2)) and/or a more rapid elevation of oxidative phosphorylation. We adapted phosphorescence quenching techniques to determine the.Q(O2)-to-O(2) utilization (.Q(O2)/.V(O2)) characteristics via microvascular O(2) pressure (P(O2,m)) measurements across sequential bouts of contractions in rat spinotrapezius muscle. Spinotrapezius muscles from female Sprague-Dawley rats (n = 6) were electrically stimulated (1 Hz twitch, 3-5 V) for two 3 min bouts (ST(1) and ST(2)) separated by 10 min rest. P(O2,m) responses were analysed using an exponential + time delay (TD) model. There was no significant difference in baseline and DeltaP(O2,m) between ST(1) and ST(2) (28.5 +/- 2.6 vs. 27.9 +/- 2.4 mmHg, and 13.9 +/- 1.8 vs. 14.1 +/- 1.3 mmHg, respectively). The TD was reduced significantly in the second contraction bout (ST(1), 12.2 +/- 1.9; ST(2), 5.7 +/- 2.2 s, P0.05), whereas the time constant of the exponential P(O2,m) decrease was unchanged (ST(1), 16.3 +/- 2.6; ST(2), 17.6 +/- 2.7 s, P0.1). The shortened TD found in ST(2) led to a reduced time to reach 63 % of the final response of ST(2) compared to ST(1) (ST(1), 28.3 +/- 3.0; ST(2), 20.2 +/- 1.8 s, P0.05). The speeding of the overall response in the absence of an elevated P(O2,m) baseline (which had it occurred would indicate an elevated.Q(O2)/.V(O2) or muscle blood flow suggests that some intracellular process(es) (e.g. more rapid increase in oxidative phosphorylation) may be responsible for the increased speed of P(O2,m) kinetics after prior contractions under these conditions.

We undertook this study to determine whether low intensity exercise (55 % (O2,max) would significantly alter the metabolic and ventilatory responses observed during 10 min of subsequent moderate intensity exercise (75 % (O2,max). By executing this work, we hoped to further our understanding of the mechanisms that limit mitochondrial ATP production at the onset of exercise. Seven healthy human subjects performed 10 min of moderate intensity exercise in the presence and absence of 10 min of low intensity exercise, which preceded the moderate intensity exercise by 3 min. Muscle biopsy samples were obtained from the vastus lateralis at pre-determined time points and oxygen consumption kinetics were determined at rest and during low and moderate intensity exercise. Following low intensity exercise and 3 min of passive recovery, muscle lactate and acetylcarnitine concentrations were elevated above basal levels, but (O2) had returned to the resting rate. When moderate intensity exercise was preceded by low intensity exercise, there was a significant sparing of phosphocreatine (PCr, approximately 25 %, P0.05) and reductions in glucose 6-phosphate (G-6-P, approximately 50 %, P0.05) and lactate (approximately 50 %, P0.05) accumulation during the first minute of moderate intensity exercise. No differences were observed after 10 min of moderate intensity exercise. The (O2) on-kinetic response over the first minute of moderate intensity exercise was accelerated when preceded by low intensity exercise. Collectively, our results suggest the lag in the oxidative ATP delivery at the onset of moderate intensity exercise can be overcome by prior low intensity exercise. Furthermore, our findings support the view that this lag is at least in part attributable to a limitation in acetyl group delivery/availability at the onset of exercise, rather than delayed oxygen supply.

Prior heavy exercise (above the lactate threshold, Th(la)) increases the amplitude of the primary oxygen uptake (VVO(2)) response and reduces the amplitude of the VO(2) slow component during subsequent heavy exercise. The purpose of this study was to determine whether these effects required the prior performance of an identical bout of heavy exercise, or if prior short-duration sprint exercise could cause similar effects. A secondary purpose of this study was to determine the effect of elevating muscle temperature (through passive warming) on VO(2) kinetics during heavy exercise. Nine male subjects performed a 6-min bout of heavy exercise on a cycle ergometer 6 min after: (1) an identical bout of heavy exercise; (2) a 30-s bout of maximal sprint cycling; (3) a 40-min period of leg warming in a hot water bath at 42 degrees C. Prior sprint exercise elevated blood [lactate] prior to the onset of heavy exercise (by aproximately 5.6 mM) with only a minor increase in muscle temperature (of approximately 0.7 degrees C). In contrast, prior warming had no effect on baseline blood lactate concentration, but elevated muscle temperature by approximately 2.6 degrees C. Both prior heavy exercise and prior sprint exercise significantly increased the absolute primary VO(2) amplitude (by approximately 230 ml x min(-1) and 260 ml x min(-1), respectively) and reduced the amplitude of the VO(2) slow component (by approximately 280 ml x min(-1) and 200 ml x min(-1), respectively) during heavy exercise, whereas prior warming had no significant effect on the VO(2) response. We conclude that the VO(2) response to heavy exercise can be markedly altered by both sustained heavy-intensity submaximal exercise and by short-duration sprint exercise that induces a residual acidosis. In contrast, passive warming elevated muscle temperature but had no effect on the VO(2) response.

Made available in DSpace on 2014-12-03T13:07:08Z (GMT). No. of bitstreams: 0 Previous issue date: 2014-04-16Bitstream added on 2014-12-03T13:24:31Z : No. of bitstreams: 1 WOS000336863900115.pdf: 772021 bytes, checksum: 15bdb430fd0805ff5085fad9dff4acb9 (MD5) Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) The purpose of this study was to determine both the independent and additive effects of prior heavy-intensity exercise and pacing strategies on the VO2 kinetics and performance during high-intensity exercise. Fourteen endurance cyclists (VO(2)max -62.8 +/- 8.5 mL.kg(-1).min(-1)) volunteered to participate in the present study with the following protocols: 1) incremental test to determine lactate threshold and VO(2)max; 2) four maximal constant-load tests to estimate critical power; 3) six bouts of exercise, using a fast-start (FS), even-start (ES) or slow-start (SS) pacing strategy, with and without a preceding heavy-intensity exercise session (i.e., 90% critical power). In all conditions, the subjects completed an all-out sprint during the final 60 s of the test as a measure of the performance. For the control condition, the mean response time was significantly shorter (p

1. A prior bout of high-intensity square-wave exercise can increase the temporal adaptation of pulmonary oxygen uptake (.V(O2)) to a subsequent bout of high-intensity exercise. The mechanisms controlling this adaptation, however, are poorly understood. 2. We therefore determined the dynamics of intramuscular [phosphocreatine] ([PCr]) simultaneously with those of .V(O2) in seven males who performed two consecutive bouts of high-intensity square-wave, knee-extensor exercise in the prone position for 6 min with a 6 min rest interval. A magnetic resonance spectroscopy (MRS) transmit-receive surface coil under the quadriceps muscle allowed estimation of [PCr]; .V(O2) was measured breath-by-breath using a custom-designed turbine and a mass spectrometer system. 3. The .V(O2) kinetics of the second exercise bout were altered compared with the first such that (a) not only was the instantaneous rate of .V(O2) change (at a given level of .V(O2)) greater but the phase II tau was also reduced - averaging 46.6 +/- 6.0 s (bout 1) and 40.7 +/- 8.4 s (bout 2) (mean +/- S.D.) and (b) the magnitude of the later slow component was reduced. 4. This was associated with a reduction of, on average, 16.1% in the total exercise-induced [PCr] decrement over the 6 min of the exercise, of which 4.0% was due to a reduction in the slow component of [PCr]. There was no discernable alteration in the initial rate of [PCr] change. The prior exercise, therefore, changed the multi-compartment behaviour towards that of functionally first-order dynamics. 5. These observations demonstrate that the .V(O2) responses relative to the work rate input for high-intensity exercise are non-linear, as are, it appears, the putative phosphate-linked controllers for which [PCr] serves as a surrogate.

Increased aerobic production of ATP at the onset of exercise could be limited by availability of metabolic substrates independent of O2, or interaction between O2 and metabolic substrates. We point out the importance of feedback control to match O2 supply to demand and discuss metabolic control at the onset of exercise.

We used an exercise paradigm with repeated bouts of heavy forearm exercise to test the hypothesis that alterations in local acid-base environment that remain after the first exercise result in greater blood flow and O2 delivery at the onset of the second bout of exercise. Two bouts of handgrip exercise at 75% peak workload were performed for 5 min, separated by 5 min of recovery. We continuously measured blood flow using Doppler ultrasound and sampled venous blood for O2 content, Pco 2, pH, and lactate and potassium concentrations, and we calculated muscle O2uptake (V˙o 2). Forearm blood flow was elevated before the second exercise compared with the first and remained higher during the first 30 s of exercise (234 ± 18 vs. 187 ± 4 ml/min, P < 0.05). Flow was not different at 5 min. Arteriovenous O2 content difference was lower before the second bout (4.6 ± 0.9 vs. 7.2 ± 0.7 ml O2/dl) and higher by 30 s of exercise (11.2 ± 0.7 vs. 10.8 ± 0.7 ml O2/dl, P < 0.05). Muscle V˙o 2was unchanged before the start of exercise but was elevated during the first 30 s of the transition to the second exercise bout (26.0 ± 2.1 vs. 20.0 ± 0.9 ml/min, P < 0.05). Changes in venous blood Pco 2, pH, and lactate concentration were consistent with reduced reliance on anaerobic glycolysis at the onset of the second exercise bout. These data show that limitations of muscle blood flow can restrict the adaptation of oxidative metabolism at the onset of heavy muscular exertion.

The present study examined the onset and the rate of rise of muscle oxidation during intense exercise in humans and whether oxygen availability limits muscle oxygen uptake in the initial phase of intense exercise. Six subjects performed 3 min of intense one-legged knee-extensor exercise [65.3 ± 3.7 (means ± SE) W]. The femoral arteriovenous blood mean transit time (MTT) and time from femoral artery to muscle microcirculation was determined to allow for an examination of the oxygen uptake at capillary level. MTT was 15.3 ± 1.8 s immediately before exercise, 10.4 ± 0.7 s after 6 s of exercise, and 4.7 ± 0.5 s at the end of exercise. Arterial venous O2difference (a-vdiffO2) of 18 ± 5 ml/l before the exercise was unchanged after 2 s, but it increased ( P < 0.05) after 6 s of exercise to 43 ± 10 ml/l and reached 146 ± 4 ml/l at the end of exercise. Thigh oxygen uptake increased ( P < 0.05) from 32 ± 8 to 102 ± 28 ml/min after 6 s of exercise and to 789 ± 88 ml/min at the end of exercise. The time to reach half-peak a-vdiffO2and thigh oxygen uptake was 13 ± 2 and 25 ± 3 s, respectively. The difference between thigh oxygen delivery (blood flow × arterial oxygen content) and thigh oxygen uptake increased ( P < 0.05) after 6 s and returned to preexercise level after 14 s. The present data suggest that, at the onset of exercise, oxygen uptake of the exercising muscles increases after a delay of only a few seconds, and oxygen extraction peaks after ∼50 s of exercise. The limited oxygen utilization in the initial phase of intense exercise is not caused by insufficient oxygen availability.

Considerable debate surrounds the issue of whether the rate of adaptation of skeletal muscle O2consumption (Q˙o2) at the onset of exercise is limited by 1) the inertia of intrinsic cellular metabolic signals and enzyme activation or 2) the availability of O2to the mitochondria, as determined by an extrinsic inertia of convective and diffusive O2transport mechanisms. This review critically examines evidence for both hypotheses and clarifies important limitations in the experimental and theoretical approaches to this issue. A review of biochemical evidence suggests that a given respiratory rate is a function of the net drive of phosphorylation potential and redox potential and cellular mitochondrial[Formula: see text](Pmitoo2). Changes in both phosphorylation and redox potential are determined by intrinsic metabolic inertia. Pmitoo2is determined by the extrinsic inertia of both convective and diffusive O2transport mechanisms during the adaptation to exercise and the rate of mitochondrial O2utilization. In a number of exercise conditions, Pmitoo2appears to be within a range capable of modulating muscle metabolism. Within this context, adjustments in the phosphate energy state of the cell would serve as a cytosolic “transducer,” linking ATP consumption with mitochondrial ATP production and, therefore, O2consumption. The availability of reducing equivalents and O2would modulate the rate of adaptation ofQ˙o2.

For moderate work rates (i.e. below the lactate threshold, theta), oxygen uptake (Vo2) approaches the steady state mono-exponentially. At higher work rates, the Vo2 kinetics are more complex, reflecting the delayed superimposition of an additional, slow component. The mechanisms of this 'slow' component are poorly understood. It has been demonstrated, however, that while a prior bout of supra theta L cycling (with a 6 min recovery) does not significantly affect the V02 time course for a subsequent sub-theta L bout, it significantly speeds the V02 response to a subsequent supra-theta L bout (Gausche, Harmon, Lamarra & Whipp, 1989; Gerbino, Ward & Whipp, 1996). These investigators proposed that this speeding was a result of improved muscle perfusion during the exercise transient, possibly related to the residual metabolic acidaemia still present at the start of the subsequent exercise bout. To determine whether speeding of the V02 kinetics could also be induced by a bout of prior high-intensity exercise performed at a remote site (e.g. the arms), subjects each performed two 6 min bouts of high-intensity cycling (leg exercise: LE) at a work rate equivalent to 50% of lambda le' (the difference between maximum V02,LE and theta L,LE). On one occasion this was preceded by a 6 min period of cycling at 50% lambda LE and, on another, by a similar period of arm-crank exercise (arm exercise: AE) at 50% lambda LE in each case, the work bouts were separated by 6 min of unloaded pedalling. Pulmonary gas exchange variables were derived breath-by-breath. During unloaded pedalling and at minute 6 of each work bout, arterialized venous blood samples were drawn from the dorsum of the heated hand or at the wrist for analysis of PH, lactate, pyruvate, noradrenaline (NAdr), adrenaline (Adr), and potassium (K+). The difference in V02 between minute 6 and 3 of each work bout (lambda V02 ?6-3] and the 'partial' O2 deficit (O2 Def) provided indices of the slow phase of V02 kinetics. The initial AE and LE bouts resulted in similar degrees of metabolic (lactic) acidaemia; the residual acidaemia at the end of the subsequent 6 min recovery phase was also similar for the two protocols, as were [K+], [Adr? and [NAdr]. The subsequent LE bouts were associated with reductions in both lambda V02[6-3] and O2 Def, relative to control, with the effect being more marked when the work was preceded by a prior LE bout than a prior AE bout: lambda V02[6-3] averaging 32 and 56% of control, respectively, and O2 Def 71 and 81%. Consequently, the increase in [lactate] and decrease in PH induced in this second LE bout were smaller when preceded by prior leg exercise than prior arm exercise. It is therefore concluded that while metabolic acidaemia induced at a site remote from the legs is associated with a less prominent slow phase of the V02 kinetics for high-intensity leg exercise, a component specific to the involved contractile units appears to exert the dominant effect. The mechanisms underlying this response are, however, presently uncertain.

MacDonald, Maureen, Preben K. Pedersen, and Richard L. Hughson. Acceleration ofV˙o 2 kinetics in heavy submaximal exercise by hyperoxia and prior high-intensity exercise. J. Appl. Physiol. 83(4): 1318–1325, 1997.—We examined the hypothesis that O2 uptake (V˙o 2) would change more rapidly at the onset of step work rate transitions in exercise with hyperoxic gas breathing and after prior high-intensity exercise. The kinetics ofV˙o 2 were determined from the mean response time (MRT; time to 63% of total change inV˙o 2) and calculations of O2 deficit and slow component during normoxic and hyperoxic gas breathing in one group of seven subjects during exercise below and above ventilatory threshold (VT) and in another group of seven subjects during exercise above VT with and without prior high-intensity exercise. In exercise transitions below VT, hyperoxic gas breathing did not affect the kinetic response of V˙o 2 at the onset or end of exercise. At work rates above VT, hyperoxic gas breathing accelerated both the on- and off-transient MRT, reduced the O2 deficit, and decreased theV˙o 2 slow component from minute 3 to minute 6 of exercise, compared with normoxia. Prior exercise above VT accelerated the on-transient MRT and reduced theV˙o 2 slow component from minute 3 to minute 6 of exercise in a second bout of exercise with both normoxic and hyperoxic gas breathing. However, the summated O2 deficit in the second normoxic and hyperoxic steps was not different from that of the first steps in the same gas condition. Faster on-transient responses in exercise above, but not below, VT with hyperoxia and, to a lesser degree, after prior high-intensity exercise above VT support the theory of an O2 transport limitation at the onset of exercise for workloads >VT.

Objectives To determine the effects of “strides” with a weighted-vest during a warm-up on endurance performance and its potential neuromuscular and metabolic mediators. A bout of resistance exercise can enhance subsequent high-intensity performance, but little is known about such priming exercise for endurance performance. Design A crossover with 5–7 days between an experimental and control trial was performed by 11 well-trained distance runners. Methods Each trial was preceded by a warm-up consisting of a 10-min self-paced jog, a 5-min submaximal run to determine running economy, and six 10-s strides with or without a weighted-vest (20% of body mass). After a 10-min recovery period, runners performed a series of jumps to determine leg stiffness and other neuromuscular characteristics, another 5-min submaximal run, and an incremental treadmill test to determine peak running speed. Clinical and non-clinical forms of magnitude-based inference were used to assess outcomes. Correlations and linear regression were used to assess relationships between performance and underlying measures. Results The weighted-vest condition resulted in a very-large enhancement of peak running speed (2.9%; 90% confidence limits ±0.8%), a moderate increase in leg stiffness (20.4%; ±4.2%) and a large improvement in running economy (6.0%; ±1.6%); there were also small-moderate clear reductions in cardiorespiratory measures. Relationships between change scores showed that changes in leg stiffness could explain all the improvements in performance and economy. Conclusions Strides with a weighted-vest have a priming effect on leg stiffness and running economy. It is postulated the associated major effect on peak treadmill running speed will translate into enhancement of competitive endurance performance.

This study examines the effects of recovery duration following heavy-intensity “priming” exercise (Hvy) on pulmonary oxygen (O2) uptake (V̇O2p) during subsequent prolonged moderate-intensity exercise (Mod). Nine participants (6 men and 3 women) (27 ± 7 years) each completed 3 repetitions of 2 continuous Mod 1-Hvy-Mod 2 leg-cycling protocols in which Mod 2 lasted 30 min, but was preceded by a recovery duration of either 6 (R6) or 20 (R20) min at 20 W following Hvy; in each case, Mod 1 and Hvy lasted 6 min and were preceded by 6 min at 20 W. V̇O2p, heart rate (HR), and near-infrared spectroscopy (NIRS)–derived muscle deoxygenation ([HHb]) responses were modeled as a monoexponential; additionally, 60-s averages were computed every 6 min in Mod 1 and Mod 2. V̇O2p was elevated (p < 0.05) throughout Mod 2 compared with Mod 1 in both R6 and R20 (by −82 mL·min−1 or ∼5.0%); this occurred despite a complete recovery of baseline V̇O2p (V̇O2pBsln) following R20. HR and minute ventilation (V̇E), but not [HHb], were also elevated throughout Mod 2. The phase II time constant for V̇O2p (τV̇O2p) was reduced in Mod 2 (22 s (Mod 1), 19 s (Mod 2); p < 0.05), as was the “overshoot” in the normalized [HHb]/O2 uptake ratio (p < 0.05). This study shows that V̇O2p was elevated during Mod following Hvy, regardless of recovery duration; however, a determining role for V̇O2pBsln is precluded. Furthermore, neither V̇O2p, HR, nor V̇E showed any evidence of a readjustment back to no-Hvy conditions during prolonged Mod (p > 0.05). Lastly, regardless of recovery duration, τV̇O2p was reduced to a similar extent with Hvy, likely resulting from an improved matching of local muscle O2 delivery to O2 utilization.

Engelen, Marielle, Janos Porszasz, Marshall Riley, Karlman Wasserman, Kazuhira Maehara, and Thomas J. Barstow. Effects of hypoxic hypoxia on O2 uptake and heart rate kinetics during heavy exercise. J. Appl. Physiol. 81(6): 2500–2508, 1996.—It is unclear whether hypoxia alters the kinetics of O2 uptake (V˙o 2) during heavy exercise [above the lactic acidosis threshold (LAT)] and how these alterations might be linked to the rise in blood lactate. Eight healthy volunteers performed transitions from unloaded cycling to the same absolute heavy work rate for 8 min while breathing one of three inspired O2 concentrations: 21% (room air), 15% (mild hypoxia), and 12% (moderate hypoxia). Breathing 12% O2 slowed the time constant but did not affect the amplitude of the primary rise inV˙o 2 (period of first 2–3 min of exercise) and had no significant effect on either the time constant or the amplitude of the slowV˙o 2 component (beginning 2–3 min into exercise). Baseline heart rate was elevated in proportion to the severity of the hypoxia, but the amplitude and kinetics of increase during exercise and in recovery were unaffected by level of inspired O2. We conclude that the predominant effect of hypoxia during heavy exercise is on the early energetics as a slowed time constant forV˙o 2 and an additional anaerobic contribution. However, the sum total of the processes representing the slow component ofV˙o 2 is unaffected.

Aging is associated with a functional decline of the oxidative metabolism due to progressive limitations of both O2 delivery and utilization. Priming exercise (PE) increases the speed of adjustment of oxidative metabolism during successive moderate-intensity transitions. We tested the hypothesis that such improvement is due to a better matching of O2 delivery to utilization within the working muscles. In 21 healthy older adults (65.7 ± 5 yr), we measured contemporaneously noninvasive indexes of the overall speed of adjustment of the oxidative metabolism (i.e., pulmonary V̇o2 kinetics), of the bulk O2 delivery (i.e., cardiac output), and of the rate of muscle deoxygenation (i.e., deoxygenated hemoglobin, HHb) during moderate-intensity step transitions, either with (ModB) or without (ModA) prior PE. The local matching of O2 delivery to utilization was evaluated by the ΔHHb/ΔV̇o2 ratio index. The overall speed of adjustment of the V̇o2 kinetics was significantly increased in ModB compared with ModA ( P < 0.05). On the contrary, the kinetics of cardiac output was unaffected by PE. At the muscle level, ModB was associated with a significant reduction of the “overshoot” in the ΔHHb/ΔV̇o2 ratio compared with ModA ( P < 0.05), suggesting an improved O2 delivery. Our data are compatible with the hypothesis that, in older adults, PE, prior to moderate-intensity exercise, beneficially affects the speed of adjustment of oxidative metabolism due to an acute improvement of the local matching of O2 delivery to utilization.

The V·O₂ slow component, a slowly developing increase in V·O₂ during constant-work-rate exercise performed above the lactate threshold, represents a progressive loss of skeletal muscle contractile efficiency and is associated with the fatigue process. This brief review outlines the current state of knowledge concerning the mechanistic bases of the V·O₂ slow component and describes practical interventions that can attenuate the slow component and thus enhance exercise tolerance. There is strong evidence that, during constant-work-rate exercise, the development of the V·O₂ slow component is associated with the progressive recruitment of additional (type II) muscle fibers that are presumed to have lower efficiency. Recent studies, however, indicate that muscle efficiency is also lowered (resulting in a "mirror-image" V·O₂ slow component) during fatiguing, high-intensity exercise in which additional fiber recruitment is unlikely or impossible. Therefore, it seems that muscle fatigue underpins the V·O₂ slow component, although the greater fatigue sensitivity of recruited type II fibers might still play a crucial role in the loss of muscle efficiency in both situations. Several interventions can reduce the magnitude of the V·O₂ slow component, and these are typically associated with an enhanced exercise tolerance. These include endurance training, inspiratory muscle training, priming exercise, dietary nitrate supplementation, and the inspiration of hyperoxic gas. All of these interventions reduce muscle fatigue development either by improving muscle oxidative capacity and thus metabolic stability or by enhancing bulk muscle O2 delivery or local Q·O₂-to-V·O₂ matching. Future honing of these interventions to maximize their impact on the V·O₂ slow component might improve sports performance in athletes and exercise tolerance in the elderly or in patient populations.

This study aimed to investigate the influence of prior heavy- and severe-intensity exercise on the oxygen uptake (V·O₂) kinetics and the power-duration relationship.Ten cyclists performed 13 exercise tests during a 4-wk period, consisting of a ramp test to determine the gas exchange threshold (GET) and the peak V·O₂, followed by a series of square-wave tests to exhaustion under three conditions: no prior exercise (control), prior heavy exercise (6 min at a work rate above GET but below critical power [CP)], and prior severe exercise (6 min at a work rate above the CP). Pulmonary gas exchange was measured throughout the exhaustive exercise bouts and the parameters of the power-duration relationship (CP and the curvature constant, W') were determined from the linear work-time model.Prior heavy exercise increased the amplitude of the primary V·O₂ response (by ∼ 0.19 ± 0.28 L·min(-1), P = 0.001), reduced the V·O₂ slow component trajectory (by 0.04 ± 0.09 L·min(-2), P = 0.002), and increased the time to exhaustion (by ∼ 52 ± 92 s, P = 0.005). The CP was unchanged (control vs prior heavy: 284 ± 47 vs 283 ± 44 W; 95% confidence interval, -7 to 5 W), whereas the W' was increased by heavy-intensity priming (16.0 ± 4.8 vs 18.7 ± 4.8 kJ; 95% confidence interval, 0.3-5.2 kJ). Severe-intensity exercise had a similar effect on the V·O₂ kinetics but had no effect on the time to exhaustion, the CP (275 ± 45 W), or the W' (16.7 ± 4.7 kJ).Prior heavy-intensity exercise primes the V·O₂ kinetics and increases the amount of work that can be performed above the CP.

The aim of the present study was to gain better insight into the mechanisms underpinning the sigmoid pattern of deoxy[Hb + Mb] during incremental exercise by assessing the changes in the profile following prior high-intensity exercise. Ten physically active students performed two incremental ramp (25 W min(-1)) exercises (AL and LL, respectively) preceded on one occasion by incremental arm (10 W min(-1)) and on another occasion by incremental leg exercise (25 W min(-1)), which served as the reference test (RT). Deoxy[Hb + Mb] was measured by means of near-infrared spectroscopy and surface EMG was recorded at the Vastus Lateralis throughout the exercises. Deoxy[Hb + Mb], integrated EMG and Median Power Frequency (MdPF) were expressed as a function of work rate (W) and compared between the exercises. During RT and AL deoxy[Hb + Mb] followed a sigmoid increase as a function of work rate. However, during LL deoxy[Hb + Mb] increased immediately from the onset of the ramp exercise and thus no longer followed a sigmoid pattern. This different pattern in deoxy[Hb + Mb] was accompanied by a steeper slope of the iEMG/W-relationship below the GET (LL: 0.89 ± 0.11% W(-1); RT: 0.74 ± 0.08% W(-1); AL: 0.72 ± 0.10% W(-1)) and a more pronounced decrease in MdPF in LL (17.2 ± 4.5%) compared to RT (5.0 ± 2.1%) and AL (3.9 ± 3.2%). It was observed that the sigmoid pattern of deoxy[Hb + Mb] was disturbed when the ramp exercise was preceded by priming leg exercise. Since the differences in deoxy[Hb + Mb] were accompanied by differences in EMG it can be suggested that muscle fibre recruitment is an important underlying mechanism for the pattern of deoxy[Hb + Mb] during ramp exercise.

The dynamic responses of O2 uptake (VO2) to a range of constant power output levels were related to exercise intensity [as percent maximal VO2 and as below vs. above lactic acid threshold (LAT)] and to the associated end-exercise lactate in three groups of subjects: group I, untrained subjects performing leg cycle ergometer exercise; group II, the same subjects performing arm cycle exercise; and group III, trained cyclists performing leg cycle ergometer exercise. Responses were described by a double-exponential equation, with each component having an independent time delay, which reduced to a monoexponential description for moderate (below-LAT) exercise. When a second exponential component to the VO2 response was present, it did not become evident until approximately 80–100 s into exercise. An overall time constant (tau T, determined as O2 deficit for the total response divided by net end-exercise VO2) and a primary time constant (tau P, determined from the O2 deficit and the amplitude for the early primary VO2 response) were compared. The tau T rose with power output and end-exercise lactate levels, but tau P was virtually invariant, even at high end-exercise lactate levels. Moreover the gain of the primary exponential component (as delta VO2/delta W) was constant across power outputs and blood lactate levels, suggesting that the primary VO2 response reflects a linear system, even at higher power outputs. These results suggest that elevated end-exercise lactate is not associated with any discernible slowing of the primary rise in VO2.(ABSTRACT TRUNCATED AT 250 WORDS)

The mechanical power (Wtot, W·kg−1) developed during ten revolutions of all-out periods of cycle ergometer exercise (4–9 s) was measured every 5–6 min in six subjects from rest or from a baseline of constant aerobic exercise [50%–80% of maximal oxygen uptake (VO2max)] of 20–40 min duration. The oxygen uptake [VO2 (W·kg−1, 1 ml O2 = 20.9 J)] and venous blood lactate concentration ([la]b, mM) were also measured every 15 s and 2 min, respectively. During the first all-out period, Wtot decreased linearly with the intensity of the priming exercise (Wtot = 11.9−0.25·VO2). After the first all-out period (i greater than 5–6 min), and if the exercise intensity was less than 60% VO2max, Wtot, VO2 and [la]b remained constant until the end of the exercise. For exercise intensities greater than 60% VO2max, VO2 and [la]b showed continuous upward drifts and Wtot continued decreasing. Under these conditions, the rate of decrease of Wtot was linearly related to the rate of increase of V [(d Wtot/dt) (W·kg−1·s−1) = 5.0·10−5 −0.20·(d VO2/dt) (W·kg−1·s−1)] and this was linearly related to the rate of increase of [la]b [(d VO2/dt) (W·kg−1·s−1) = 2.310−4 + 5.910−5·(d [la]b/dt) (mM·s−1)]. These findings would suggest that the decrease of Wtot during the first all-out period was due to the decay of phosphocreatine concentration in the exercising muscles occurring at the onset of exercise and the slow drifts of VO2 (upwards) and of Wtot (downwards) during intense exercise at constant Wtot could be attributed to the continuous accumulation of lactate in the blood (and in the working muscles).

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 O2 delivery on pulmonary O2 uptake (V̇o2) kinetics during cycle exercise. We hypothesized that phase II V̇o2 kinetics (τp) 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 τp during supine exercise to τp 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. τp 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 τp during moderate- to severe-intensity supine exercise (34 ± 9 s), returning it to a value that was not significantly different from τp in the upright position. This effect occurred in the absence of changes in estimated muscle fractional O2 extraction (from the near-infrared spectroscopy-derived deoxygenated Hb concentration signal), such that the priming-induced facilitation of muscle blood flow matched increased O2 utilization in the recruited fibers, resulting in a speeding of V̇o2 kinetics. These findings suggest that, during supine cycling, priming speeds V̇o2 kinetics by providing an increased driving pressure for O2 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 O2 supply.