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Critical power (CP) is a fundamental parameter defining high-intensity exercise tolerance and is related to the time constant of phase II pulmonary oxygen uptake kinetics (τVO2). To test the hypothesis that this relationship is causal we determined the impact of prior exercise (“priming”) on CP and τVO2 in the upright and supine positions. 17 healthy men were assigned to either upright or supine exercise groups, whereby CP, τVO2 and muscle deoxyhaemoglobin kinetics (τ[HHb]) were determined via constant-power tests to exhaustion at four work-rates with (primed) and without (control) priming exercise at ∼31%Δ. During supine exercise, priming reduced τVO2 (control: 54 ± 18 vs. primed: 39 ± 11 s; P < 0.001), increased τ[HHb] (control: 8 ± 4 vs. primed: 12 ± 4 s; P = 0.003) and increased CP (control: 177 ± 31 vs. primed: 185 ± 30 W, P = 0.006) compared to control. However, priming exercise had no effect on τVO2 (control: 37 ± 12 vs. primed: 35 ± 8 s; P = 0.82), τ[HHb] (CON: 10 ± 5 s vs. PRI: 14 ± 10; P = 0.10), or CP (control: 235 ± 42 vs. primed: 232 ± 35 W; P = 0.57) during upright exercise. The concomitant reduction of τVO2 and increased CP following priming in the supine group, effects that were absent in the upright group, provides the first experimental evidence that τVO2 is mechanistically related to critical power. The increased τ[HHb] suggests that this effect was mediated, at least in part, by improved oxygen availability.

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 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.

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.

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 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.

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.

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.

1. At work rates which do not result in a sustained increase in blood lactate ([L-]), oxygen uptake (VO2) approaches the steady state with first-order kinetics. However, when [L-] is increased, at least two kinetic components are required to characterize the VO2 response dynamics. The purpose of the present investigation was to determine whether these more-complex kinetics are best represented as: (a) two components which operate throughout the exercise or (b) a delayed slow component which is consequent to the lactic acidaemia and which does not influence the early development of the O2 deficit. 2. Six healthy subjects underwent an incremental ramp test on a cycle ergometer, to the limit of tolerance, for determination of the maximum VO2 (micro VO2) and and estimation [symbol: see text] of the threshold for lactic acidaemia (theta L) non-invasively. Subjects then performed, on different days, two to four repetitions of square-wave exercise from a baseline of unloaded pedalling ('O' Watts (W)) to work rates (WR) less than theta L (90% theta L) and greater than theta L (half-way between theta L and micro VO2). Ventilatory and pulmonary gas exchange variables were determined breath-by-breath. For each subject, the VO2 transitions were averaged prior to fitting a least-squares algorithm to the on- and off-transient responses. 3. The less than theta L test resulted in a mono-exponential VO2 response, with a time constant of 31.3 and 31.5 s for the on- and off-transients, respectively. 4. The VO2 responses to the greater than theta L test were fitted to three competing models: (a) a single exponential for the entire period; (b) a double exponential for the entire period; and (c) an initial single exponential with a subsequent phase of delayed onset. Model (c) yielded a significantly lower residual mean-squares error than methods (a) and (b), with a time constant for the initial component of 40.2 s for the on-transient and 32.9 s for the off-transient and a subsequent phase of VO2 increase for the on-transient which averaged 230 ml min-1. The delta VO2/delta WR for the early kinetics of the greater than theta L test were not different from the less than theta L test (9.6 and 9.5 ml min-1 W-1, respectively). 5. These data suggest that the slow phase of the greater than theta L VO2 kinetics is a delayed-onset process. This being the case, the O2 deficit during heavy exercise, as conventionally estimated, would be overestimated.

Novel time-resolved near-infrared spectroscopy (TR-NIRS), with adipose tissue thickness correction, was used to test the hypotheses that heavy priming exercise reduces the (V˙O2) slow component (V˙O2SC) (1) by elevating microvascular [Hb] volume at multiple sites within the quadriceps femoris (2) rather than reducing the heterogeneity of muscle deoxygenation kinetics. Twelve subjects completed two 6-min bouts of heavy work rate exercise, separated by 6 min of unloaded cycling. Priming exercise induced faster overall (V˙O2) kinetics consequent to a substantial reduction in the (V˙O2SC)(0.27 ± 0.12 vs. 0.11 ± 0.09 L·min(-1), P < 0.05) with an unchanged primary (V˙O2) time constant. An increased baseline for the primed bout [total (Hb + Mb)] (197.5 ± 21.6 vs. 210.7 ± 22.5 μmol L-1, P < 0.01), reflecting increased microvascular [Hb] volume, correlated significantly with the (V˙O2SC) reduction. At multiple sites within the quadriceps femoris, priming exercise reduced the baseline and slowed the increase in [deoxy (Hb + Mb)]. Changes in the intersite coefficient of variation in the time delay and time constant of [deoxy (Hb + Mb)] during the second bout were not correlated with the (V˙O2SC) reduction. These results support a mechanistic link between priming exercise-induced increase in muscle [Hb] volume and the reduced (V˙O2SC) that serves to speed overall (V˙O2) kinetics. However, reduction in the heterogeneity of muscle deoxygenation kinetics does not appear to be an obligatory feature of the priming response.