Effect of recovery duration from prior exhaustive exercise on the parameters of the power-duration relationship.

The physiological equivalents of the curvature constant (W') of the high-intensity power-duration (P-t(LIM)) relationship are poorly understood, although they are presumed to reach maxima/minima at exhaustion. In an attempt to improve our understanding of the determinants of W', we therefore aimed to determine its recovery kinetics following exhaustive exercise (which depletes W') concomitantly with those of O(2) uptake (V(O(2)), a proxy for the kinetics of phosphocreatine replenishment) and blood lactate concentration ([L(-)]). Six men performed cycle-ergometer exercise to t(LIM): a ramp and four constant-load tests, at different work rates, for estimation of lactate threshold, W', critical power (CP), and maximum V(O(2)). Three further exhausting tests were performed at different work rates, each preceded by an exhausting "conditioning" bout, with intervening recoveries of 2, 6, and 15 min. Neither prior exhaustion nor recovery duration altered V(O(2)) or [L(-)] at t(LIM). Postconditioning, the P-t(LIM) relationship remained well characterized by a hyperbola, with CP unchanged. However, W' recovered to 37 +/- 5, 65 +/- 6, and 86 +/- 4% of control following 2, 6, and 15 min of intervening recovery, respectively. The W' recovery was curvilinear [interpolated half time (t(1/2)) = 234 +/- 32 s] and appreciably slower than V(O(2)) recovery (t(1/2) = 74 +/- 2 s) but faster than [L(-)] recovery (t(1/2) = 1,366 +/- 799 s). This suggests that W' determines supra-CP exercise tolerance, its restitution kinetics are not a unique function of phosphocreatine concentration or arterial [L(-)], and it is unlikely to simply reflect a finite energy store that becomes depleted at t(LIM).

Quantifying intervention-related improvements in exercise tolerance.

Among the benefits expected to result from a therapeutic intervention in patients with impaired systemic functioning is an increase in exercise tolerance. For this a constant high-intensity work rate has been shown to provide a more sensitive index of improvement than the maximum work rate, or oxygen uptake, on a symptom-limited incremental test. However, the extremely large variability of the improvement in this particular index of tolerance undermines the ability to make general inferences for the underlying functional improvement. We argue that this is a necessary consequence of the particular work rate chosen for the test and the change in the parameters of the subject's hyperbolic power-duration relationship for that form of exercise: its "critical power" and "curvature constant". Without knowledge of these features, any absolute or per cent increase in tolerance time to a single constant-load exercise bout must be interpreted with caution regarding the physiological benefit(s) that have accrued from the intervention.

Thoracic sympathectomy and cardiopulmonary responses to exercise.

The purpose was to study the effect of endoscopic thoracic sympathectomy (ETS) for palmar and/or axillary hyperhidrosis on physiological responses at rest, and during sub-maximal and maximal exercise in ten healthy patients (7 females and 3 males 18-40 years old) with idiopathic palmar and/or axillary hyperhidrosis. T2-T3 thoracoscopic sympathectomy was performed using a simplified one stage bilateral procedure. Physiological variables were recorded at rest and during sub-maximal (steady-state) and maximal treadmill exercise immediately prior to and 70 days (+/-7.5, SD) after bilateral ETS. Exercise performance capacity and peak VO(2) were not found to be different following bilateral ETS than prior to the ETS. However, heart rate was significantly reduced at rest (14%), at sub-maximal exercise (12.3%), and at peak exercise (5.7%), together with a significant increase in oxygen pulse (11.8, 12.7, and 7.8%, respectively). The rate pressure product (RPP) was also significantly reduced following the surgical procedure at all three study stages, while all other physiological variables measured remained unchanged. It is suggested that thoracic-sympathetic denervation affects the heart, sweating, and circulation of the respective denervated region but does not affect exercise performance or mechanical/physiologic efficiency, despite a significant reduction in heart rate (both at rest and during exercise). The latter was, most likely, fully compensated by an increase in stroke volume and less likely by an improved muscle O(2) extraction due to more efficient blood distribution, keeping the work-rate and oxygen uptake unaffected.

Effects of prior very-heavy intensity exercise on indices of aerobic function and high-intensity exercise tolerance.

A recent bout of high-intensity exercise can alter the balance of aerobic and anaerobic energy provision during subsequent exercise above the lactate threshold (theta(L)). However, it remains uncertain whether such "priming" influences the tolerable duration of subsequent exercise through changes in the parameters of aerobic function [e.g., theta(L), maximum oxygen uptake (Vo(2max))] and/or the hyperbolic power-duration (P-t) relationship [critical power (CP) and the curvature constant (W')]. We therefore studied six men performing cycle ergometry to the limit of tolerance; gas exchange was measured breath-by-breath and arterialized capillary blood [lactate] was measured at designated intervals. On different days, each subject completed 1) an incremental test (15 W/min) for estimation of theta(L) and measurement of the functional gain (DeltaVo(2)/DeltaWR) and Vo(2peak) and 2) four constant-load tests at different work rates (WR) for estimation of CP, W', and Vo(2max). All tests were subsequently repeated with a preceding 6-min supra-CP priming bout and an intervening 2-min 20-W recovery. The hyperbolicity of the P-t relationship was retained postpriming, with no significant difference in CP (241 +/- 39 vs. 242 +/- 36 W, post- vs. prepriming), Vo(2max) (3.97 +/- 0.34 vs. 3.93 +/- 0.38 l/min), DeltaVo(2)/DeltaWR (10.7 +/- 0.3 vs. 11.1 +/- 0.4 ml.min(-1).W(-1)), or the fundamental Vo(2) time constant (25.6 +/- 3.5 vs. 28.3 +/- 5.4 s). W' (10.61 +/- 2.07 vs. 16.13 +/- 2.33 kJ) and the tolerable duration of supra-CP exercise (-33 +/- 11%) were each significantly reduced, despite a less-prominent Vo(2) slow component. These results suggest that, following supra-CP priming, there is either a reduced depletable energy resource or a residual fatigue-metabolite level that leads to the tolerable limit before this resource is fully depleted.

Recommendations on the use of exercise testing in clinical practice.

Evidence-based recommendations on the clinical use of cardiopulmonary exercise testing (CPET) in lung and heart disease are presented, with reference to the assessment of exercise intolerance, prognostic assessment and the evaluation of therapeutic interventions (e.g. drugs, supplemental oxygen, exercise training). A commonly used grading system for recommendations in evidence-based guidelines was applied, with the grade of recommendation ranging from A, the highest, to D, the lowest. For symptom-limited incremental exercise, CPET indices, such as peak O(2) uptake (V'O(2)), V'O(2) at lactate threshold, the slope of the ventilation-CO(2) output relationship and the presence of arterial O(2) desaturation, have all been shown to have power in prognostic evaluation. In addition, for assessment of interventions, the tolerable duration of symptom-limited high-intensity constant-load exercise often provides greater sensitivity to discriminate change than the classical incremental test. Field-testing paradigms (e.g. timed and shuttle walking tests) also prove valuable. In turn, these considerations allow the resolution of practical questions that often confront the clinician, such as: 1) "When should an evaluation of exercise intolerance be sought?"; 2) "Which particular form of test should be asked for?"; and 3) "What cluster of variables should be selected when evaluating prognosis for a particular disease or the effect of a particular intervention?"

A test to establish maximum O2 uptake despite no plateau in the O2 uptake response to ramp incremental exercise.

The O2 uptake (Vo2) response to ramp incremental (RI) exercise does not consistently demonstrate plateau-like behavior at the limit of tolerance, and hence the requirements for a maximum Vo2 commonly are not met, despite apparent maximum effort. We sought to determine whether an appended step exercise (SE) test at a work rate greater than that achieved in a preceding ramp test would establish the plateau criterion. Seven healthy male adults performed RI cycle ergometry (20 W/min) to the limit of tolerance, followed by 5-min recovery (20 W) and then an SE test at 105% (RISE-105) of the final work rate (WRpeak) achieved during RI. Five of these subjects also performed an RI test followed by SE at 95% WRpeak (RISE-95). Vo2 was measured breath by breath using a turbine and mass spectrometer. The average of the final 15 s of RI or SE was used to establish respective Vo2 peaks. When Vo2 peak was approached, a constant Vo2 value (e.g., a plateau) was not discernable during any RI or SE component of the tests. Although the WRpeak [mean (SD)] was higher during the SE portion [359 W (SD 31)] than during the RI portion [341 W (SD 29)] of the RISE-105, the peak Vo2 was not different [SE, 4.30 l/min (SD 0.51); RI, 4.33 l/min (SD 0.52); P=0.49; n=7]. Similarly, in the RISE-95 test, WRpeak was 310 W (SD 31) for the SE portion and 326 W (SD 32) for the RI portion, yet the peak Vo2 values were not different [SE, 4.12 l/min (SD 0.53); RI, 4.11 l/min (SD 0.48); P=0.78; n=5]. The lack of notable difference between the Vo2 peaks established at different WRpeak values in our RISE protocols provides the plateau criterion for verification of maximum Vo2 in a single test session, even when the data response profiles do not themselves evidence a plateau.

Overshoot in VO2 following the onset of moderate-intensity cycle exercise in trained cyclists.

We have previously observed that following the onset of moderate intensity cycle ergometry, the pulmonary O2 uptake (VO2) in trained cyclists often does not increase towards its steady-state value with the typical mono-exponential characteristics; rather, there is a transient "overshoot". The purpose of this study was to systematically examine this phenomenon by comparing the VO2 responses to two moderate-intensity work rates and one high-intensity work rate in trained and untrained subjects. Following a ramp exercise test to the limit of tolerance for the determination of the gas exchange threshold (GET) and VO2(peak), seven trained cyclists [mean (SD); VO2(peak) 66.6 (2.5) ml x kg(-1) x min(-1)] and eight sedentary subjects [VO2(peak) 42.9 (5.1) ml x kg(-1) x min(-1)] completed six step transitions from baseline cycling to work rates requiring 60% and 80% GET and three step transitions from baseline cycling to a work rate requiring 50% of the difference between GET and VO2(peak) (50%delta). VO2 was measured breath-by-breath and modelled using standard techniques. The sedentary subjects did not overshoot the steady-state VO2 at any intensity. At 60% GET, six of the seven cyclists overshot the steady-state VO2 [by an integral volume of 164 (44) ml between approximately 45 and 125 s]. At 80% GET, four of the seven cyclists overshot the steady-state VO2 [by an integral volume of 185 (92) ml between approximately 55 and 140 s]. None of the cyclists showed an overshoot at 50%delta. These results indicate that trained cyclists evidence an overshoot in VO2 before steady-state is reached in the transition to moderate-intensity exercise. The mechanism(s) responsible for this effect remains to be elucidated, as does whether the overshoot confers any functional or performance benefit to the trained cyclist.

Serum cortisol reduction and abnormal prolactin and CD4+/CD8+ T-cell response as a result of controlled exercise in patients with rheumatoid arthritis and systemic lupus erythematosus despite unaltered muscle energetics.

OBJECTIVE: To investigate muscle energetics in patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) and measure serum cortisol, prolactin and CD4+/CD8+ T-cell levels during and after controlled exhaustive exercise. METHODS: Patients with RA (n = 7), patients with SLE (n = 6) and healthy individuals (HI) (n = 10) performed incremental cycle ergometry to the limit of tolerance. Ventilation, oxygen uptake (VO2) and carbon dioxide output were measured and the lactate threshold (LT) was estimated. Serum cortisol, prolactin, CD4+ and CD8+ lymphocyte subset levels were determined at baseline, peak exercise and 1 h after exercise. RESULTS: Exercise tolerance was reduced in patients with RA and patients with SLE, as reflected by peak VO2 and LT, but muscle energetics were not altered. In RA and SLE, there was significant reduction in cortisol levels at peak (-10%; P = 0.03) and post-exercise times (-36%; P = 0.05). Prolactin varied significantly at peak exercise in HI only (+60%; P = 0.05). There was a significant reduction in CD4+ T cells at peak exercise in RA (-15%; P = 0.02) and SLE patients (-8%; P = 0.04) and an increase after exercise in SLE patients (+11%; P = 0.03). In HI, CD8+ T cells increased significantly (+47%; P = 0.01) at peak exercise, but this was not found in RA and SLE patients. A significant reduction in CD8+ T cells was noted after exercise in SLE patients (-6%; P = 0.05). CONCLUSION: RA and lupus patients do not have significantly altered muscle energetics, but have abnormal cortisol, prolactin and CD4+/CD8+ T-cell responses to exercise. Further studies need to be carried out to evaluate whether short bouts of strenuous exercise have detrimental clinical effects.

Negative accumulated oxygen deficit during heavy and very heavy intensity cycle ergometry in humans.

The concept of the accumulated O(2) deficit (AOD) assumes that the O(2) deficit increases monotonically with increasing work rate (WR), to plateau at the maximum AOD, and is based on linear extrapolation of the relationship between measured steady-state oxygen uptake ( VO(2)) and WR for moderate exercise. However, for high WRs, the measured VO(2) increases above that expected from such linear extrapolation, reflecting the superimposition of a "slow component" on the fundamental VO(2) mono-exponential kinetics. We were therefore interested in determining the effect of the VO(2) slow component on the computed AOD. Ten subjects [31 (12) years] performed square-wave cycle ergometry of moderate (40%, 60%, 80% and 90% ), heavy (40%Delta), very heavy (80%Delta) and severe (110% VO(2)(peak)) intensities for 10-15 min, theta(L)where is the estimated lactate threshold and Delta is the WR difference between and VO(2)(peak). VO(2) was determined breath-by-breath. Projected "steady-state" VO(2) values were determined from sub- tests. The measured VO(2) exceeded the projected value after approximately 3 min for both heavy and very heavy intensity exercise. This led to the AOD actually becoming negative. Thus, for heavy exercise, while the AOD was positive [0.63 (0.41) l] at 5 min, it was negative by 10 min [-0.61 (1.05) l], and more so by 15 min [-1.70 (1.64) l]. For the very heavy WRs, the AOD was [0.42 (0.67) l] by 5 min and reached -2.68 (2.09) l at exhaustion. For severe exercise, however, the AOD at exhaustion was positive in each case: +1.69 (0.39) l. We therefore conclude that the assumptions underlying the computation of the AOD are invalid for heavy and very heavy cycle ergometry (at least). Physiological inferences, such as the "anaerobic work capacity", are therefore prone to misinterpretation.

The maximally attainable VO2 during exercise in humans: the peak vs. maximum issue.

The quantification of maximum oxygen uptake (V(O2 max)), a parameter characterizing the effective integration of the neural, cardiopulmonary, and metabolic systems, requires oxygen uptake (VO2) to attain a plateau. We were interested in whether a VO2 plateau was consistently manifest during maximal incremental ramp cycle ergometry and also in ascertaining the relationship between this peak VO2 (V(O2 peak)) and that determined from one, or several, maximal constant-load tests. Ventilatory and pulmonary gas-exchange variables were measured breath by breath with a turbine and mass spectrometer. On average, V(O2 peak) [3.51 +/- 0.8 (SD) l/min] for the ramp test did not differ from that extrapolated from the linear phase of the response in 71 subjects. In 12 of these subjects, the V(O2 peak) was less than the extrapolated value by 0.1-0.4 l/min (i.e., a "plateau"), and in 19 subjects, V(O2 peak) was higher by 0.05-0.4 l/min. In the remaining 40 subjects, we could not discriminate a difference. The V(O2 peak) from the incremental test also did not differ from that of a single maximum constant-load test in 38 subjects or from the V(O2 max) in 6 subjects who undertook a range of progressively greater discontinuous constant-load tests. A plateau in the actual VO2 response is therefore not an obligatory consequence of incremental exercise. Because the peak value attained was not different from the plateau in the plot of VO2 vs. work rate (for the constant-load tests), the V(O2 peak) attained on a maximum-effort incremental test is likely to be a valid index of V(O2 max), despite no evidence of a plateau in the data themselves. However, without additional tests, one cannot be certain.

Effects of dichloroacetate on VO2 and intramuscular 31P metabolite kinetics during high-intensity exercise in humans.

Traditional control theories of muscle O2 consumption are based on an "inertial" feedback system operating through features of the ATP splitting (e.g., [ADP] feedback, where brackets denote concentration). More recently, however, it has been suggested that feedforward mechanisms (with respect to ATP utilization) may play an important role by controlling the rate of substrate provision to the electron transport chain. This has been achieved by activation of the pyruvate dehydrogenase complex via dichloroacetate (DCA) infusion before exercise. To investigate these suggestions, six men performed repeated, high-intensity, constant-load quadriceps exercise in the bore of an magnetic resonance spectrometer with each of prior DCA or saline control intravenous infusions. O2 uptake (Vo2) was measured breath by breath (by use of a turbine and mass spectrometer) simultaneously with intramuscular phosphocreatine (PCr) concentration ([PCr]), [Pi], [ATP], and pH (by 31P-MRS) and arterialized-venous blood sampling. DCA had no effect on the time constant (tau) of either Vo2 increase or PCr breakdown [tauVo2 45.5 +/- 7.9 vs. 44.3 +/- 8.2 s (means +/- SD; control vs. DCA); tauPCr 44.8 +/- 6.6 vs. 46.4 +/- 7.5 s; with 95% confidence intervals averaging < +/-2 s]. DCA, however, resulted in significant (P < 0.05) reductions in 1). end-exercise [lactate] (-1.0 +/- 0.9 mM), intramuscular acidification (pH, +0.08 +/- 0.06 units), and [Pi] (-1.7 +/- 2.1 mM); 2). the amplitude of the fundamental components for [PCr] (-1.9 +/- 1.6 mM) and Vo2 (-0.1 +/- 0.07 l/min, or 8%); and 3). the amplitude of the Vo2 slow component. Thus, although the DCA infusion lessened the buildup of potential fatigue metabolites and reduced both the aerobic and anaerobic components of the energy transfer during exercise, it did not enhance either tauVo2 or tau[PCr], suggesting that feedback, rather than feedforward, control mechanisms dominate during high-intensity exercise.

Dynamics of intramuscular 31P-MRS P(i) peak splitting and the slow components of PCr and O2 uptake during exercise.

The dynamics of pulmonary O(2) uptake (Vo(2)) during the on-transient of high-intensity exercise depart from monoexponentiality as a result of a "slow component" whose mechanisms remain conjectural. Progressive recruitment of glycolytic muscle fibers, with slow O(2) utilization kinetics and low efficiency, has, however, been suggested as a mechanism. The demonstration of high- and low-pH components of the exercising skeletal muscle (31)P magnetic resonance (MR) spectrum [inorganic phosphate (P(i)) peak] at high work rates (thought to be reflective of differences between oxidative and glycolytic muscle fibers) is also consistent with this conjecture. We therefore investigated the dynamics of Vo(2) (using a turbine and mass spectrometry) and intramuscular ATP, phosphocreatine (PCr), and P(i) concentrations and pH, estimated from the (31)P MR spectrum. Eleven healthy men performed prone square-wave high-intensity knee extensor exercise in the bore of a whole body MR spectrometer. A Vo(2) slow component of magnitude 15.9 +/- 6.9% of the phase II amplitude was accompanied by a similar response (11.9 +/- 7.1%) in PCr concentration. Only five subjects demonstrated a discernable splitting of the P(i) peak, however, which began from between 35 and 235 s after exercise onset and continued until cessation. As such, the dynamics of the pH distribution in intramuscular compartments did not consistently reflect the temporal features of the Vo(2) slow component, suggesting that P(i) splitting does not uniquely reflect the activity of oxidative or glycolytic muscle fibers per se.

Dynamic asymmetry of phosphocreatine concentration and O(2) uptake between the on- and off-transients of moderate- and high-intensity exercise in humans.

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.

Bioenergetic constraints on tactical decision making in middle distance running.

BACKGROUND: The highest velocity that a runner can sustain during middle distance races is defined by the intersection of the runner's individual velocity-time curve and the distance-time curve. The velocity-time curve is presumably fixed at the onset of a race; however, whereas the race distance is ostensibly fixed, the actual distance-time curve is not. That is, it is possible for a runner to run further than the race distance if he or she runs wide on bends in track races. In this instance, the point of intersection of the individual velocity-time curve and the distance-time curve will move downwards and to the right, reducing the best average velocity that can be sustained for the distance. METHODS: To illustrate this point, the race tactics used by the gold and silver medallists at 800 m and 5000 m in the Sydney Olympics were analysed. The paths taken by the runners were carefully tracked and the total distance they covered during the races and the average velocity they sustained over the distances they actually covered were calculated. RESULTS: In both the Olympic 800 m and 5000 m finals, for example, the winner was not the runner who ran at the highest average velocity in the race. Rather, the winners of these races were able to husband their metabolic resources to better effect by running closer to the actual race distance. CONCLUSIONS: Race results in middle distance running events are dependent not just on the energetic potential of the runners at the start of the race and their strategy for pace allocation, but also on the effect of their tactical approach to positioning on the total distance covered in the race. Middle distance runners should be conscious of minimising the distance covered in races if they wish to optimise their performance.

Reference values for dynamic responses to incremental cycle ergometry in males and females aged 20 to 80.

Interpretation of incremental cardiopulmonary exercise tests (CPET) might be enhanced by considering the simultaneous rates of change of certain key variables, e.g., Delta oxygen uptake/Delta work rate (Delta VO(2)/Delta WR), Delta heart rate/Delta VO(2) (Delta HR/Delta VO(2)), Delta ventilation/Delta carbon dioxide production (Delta VE/Delta VCO(2)), and the linearized Delta tidal volume/Delta VE (Delta VT/Delta lnVE) relationships. However, there are no published age- and sex-dependent reference values for these relationships that were appropriately obtained in randomly selected subjects. We therefore prospectively evaluated 120 sedentary individuals (60 male, 60 female, age 20 to 80 yr) who were randomly selected from more than 8,000 subjects, and submitted to standard ramp-incremental CPET on an electronically braked cycle ergometer. We found that sex and age significantly influenced several of the dynamic relationships, in addition to anthropometric attributes (p < 0.05). A comprehensive set of linear prediction equations is provided; the limits of normality (at the 95% confidence level) differed substantially from previous recommendations based on single discrete values. These data therefore provide a frame of reference for assessing the normalcy of the response profiles of four standard indices of metabolic, cardiovascular, and ventilatory function during rapidly incremental cycle ergometry in sedentary males and females up to 80 yr of age.

Effects of prior exercise on oxygen uptake and phosphocreatine kinetics during high-intensity knee-extension exercise in humans.

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.