The on‐ and off‐transient (i.e. phase II) responses of pulmonary oxygen uptake (V̇O2) to moderate‐intensity exercise (i.e. below the lactate threshold, θL) 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 θL the V̇O2 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 V̇O2 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 V̇O2 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 V̇O2 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]; V̇O2 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 V̇O2,), with time constants (τ) averaging: τV̇O2,on 35 ± 14 s (±s.d.), τ[PCr]on 33 ± 12 s, τV̇O2,off 50 ± 13 s and τ[PCr]off 51 ± 13 s. The kinetics for both V̇O2 and [PCr] were more complex for high‐intensity exercise. The fundamental phase expressing average τ values of τV̇O2,on 39 ± 4 s, τ[PCr]on 38 ± 11 s, τV̇O2,off 51 ± 6 s and τ[PCr]off 47 ± 11 s. An associated slow component was expressed in the on‐transient only for both V̇O2 and [PCr], and averaged 15.3 ± 5.4 and 13.9 ± 9.1 % of the fundamental amplitudes for V̇O2 and [PCr], respectively. In conclusion, the τ values of the fundamental component of [PCr] and V̇O2 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, ≈90 % of the magnitude of the V̇O2 slow component during high‐intensity exercise is reflected within the exercising muscle by its [PCr] response.

SUMMARYFor moderate work rates (i.e. below the lactate threshold, OL), 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-OL cycling (with a 6 min recovery) does not significantly affect the VO. time course for a subsequent sub-OL bout, it significantly speeds the VO2 response to a subsequent supra-OL 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 VO2 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 'ALE' (the difference between maximum 1VO2LE and oLLE). On one occasion this was preceded by a 6 min period of cycling at 50 % ALE and, on another, by a similar period of arm-crank exercise (arm exercise: AE) at 50% AAE; 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 (AVO ) and the 'partial' 02 deficit (02 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 A1!02, and 02 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: AV02, averaging 32 and 56 % of control, respectively, and 02 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 V0 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.

The fundamental pulmonary O(2) uptake (.VO(2)) response to moderate, constant-load exercise can be characterized as (d.VO(2)/dt)(tau)+Delta.VO(2) (t)=Delta.VO(2SS) where Delta.VO(2SS) is the steady-state response, and tau is the time constant, with the .VO(2) kinetics reflecting intramuscular O(2) uptake (.QO(2)) kinetics, to within 10%. The role of phosphocreatine (PCr) turnover in .QO(2) control can be explored using (31)P-MR spectroscopy, simultaneously with .VO(2). Although tau.VO(2) and tauPCr vary widely among subjects (approx. 20-65 s), they are not significantly different from each other, either at the on- or off-transient. A caveat to interpreting the "well-fit" exponential is that numerous units of similar Delta.VO(2SS) but with a wide tau distribution can also yield a .VO(2) response with an apparent single tau. This tau is, significantly, inversely correlated with lactate threshold and .VO(2max)(but is poorly predictive; a frail stamen, therefore), consistent with tau not characterizing a compartment with uniform kinetics. At higher intensities, the fundamental kinetics become supplemented with a slowly-developing phase, setting .VO(2)on a trajectory towards maximum .VO(2). This slow component is also demonstrable in Delta[PCr]: the decreased efficiency thereby reflecting a predominantly high phosphate-cost of force production rather than a high O(2)-cost of phosphate production. We also propose that the O(2)-deficit for the slow-component is more likely to reflect shifting Delta.VO(2SS) rather than a single one with a single tau.

The fundamental pulmonary O(2) uptake (.VO(2)) response to moderate, constant-load exercise can be characterized as (d.VO(2)/dt)(tau)+Delta.VO(2) (t)=Delta.VO(2SS) where Delta.VO(2SS) is the steady-state response, and tau is the time constant, with the .VO(2) kinetics reflecting intramuscular O(2) uptake (.QO(2)) kinetics, to within 10%. The role of phosphocreatine (PCr) turnover in .QO(2) control can be explored using (31)P-MR spectroscopy, simultaneously with .VO(2). Although tau.VO(2) and tauPCr vary widely among subjects (approx. 20-65 s), they are not significantly different from each other, either at the on- or off-transient. A caveat to interpreting the "well-fit" exponential is that numerous units of similar Delta.VO(2SS) but with a wide tau distribution can also yield a .VO(2) response with an apparent single tau. This tau is, significantly, inversely correlated with lactate threshold and .VO(2max)(but is poorly predictive; a frail stamen, therefore), consistent with tau not characterizing a compartment with uniform kinetics. At higher intensities, the fundamental kinetics become supplemented with a slowly-developing phase, setting .VO(2)on a trajectory towards maximum .VO(2). This slow component is also demonstrable in Delta[PCr]: the decreased efficiency thereby reflecting a predominantly high phosphate-cost of force production rather than a high O(2)-cost of phosphate production. We also propose that the O(2)-deficit for the slow-component is more likely to reflect shifting Delta.VO(2SS) rather than a single one with a single tau.

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