Mark Burnley

Oxygen uptake kinetics as a determinant of sports performance.

Abstract It is well known that physiological variables such as maximal oxygen uptake ( ), exercise economy, the lactate threshold, and critical power are highly correlated with endurance exercise performance. In this review, we explore the basis for these relationships by explaining the influence of these “traditional” variables on the dynamic profiles of the response to exercise of different intensities, and how these differences in dynamics are related to exercise tolerance and fatigue. The existence of a “slow component” of during exercise above the lactate threshold reduces exercise efficiency and mandates a greater consumption of endogenous fuel stores (chiefly muscle glycogen) for muscle respiration. For higher exercise intensities (above critical power), steady states in blood acid–base status and pulmonary gas exchange are not attainable and will increase with time until is reached. Here, we show that it is the interaction of the slow component, , and the “anaerobic capacity” that determines the exercise tolerance. Essentially, we take the view that an appreciation of the various exercise intensity “domains” and their characteristic effects on dynamics can be helpful in improving our understanding of the determinants of exercise tolerance and the limitations to endurance sports performance. The reciprocal effects of interventions such as training, prior exercise, and manipulations of muscle oxygen availability on aspects of kinetics and exercise tolerance are consistent with this view.

Effects of Prior Exercise on Metabolic and Gas Exchange Responses to Exercise

Abstract‘Warm-up’ activity is almost universally performed by athletes prior to their participation in training or competition. However, relatively little is known about the optimal intensity and duration for such exercise, or about the potential mechanisms primed by warm-up that might enhance performance. Recent studies demonstrate that vigorous warm-up exercise that normally results in an elevated blood and presumably muscle lactate concentration has the potential to increase the aerobic energy turnover in subsequent high-intensity exercise. The reduced oxygen deficit is associated with a reduction in both the depletion of the intramuscular phosphocreatine stores and the rate at which lactic acid is produced. Furthermore, the oxygen uptake ‘slow component’ that develops during high-intensity, ostensibly submaximal, exercise is attenuated. These factors would be hypothesised to predispose to increased exercise tolerance. Interestingly, the elevation of muscle temperature by prior exercise does not appear to be implicated in the altered metabolic and gas exchange responses observed during subsequent exercise. The physiological mechanism(s) that limit the rate and the extent to which muscle oxygen uptake increases following the onset of exercise, and which are apparently altered by the performance of prior heavy exercise, are debated. However, these mechanisms could include oxygen availability, enzyme activity and/or availability of metabolic substrate, and motor unit recruitment patterns. Irrespective of the nature of the control mechanisms that are influenced, ‘priming’ exercise has the potential to significantly enhance exercise tolerance and athletic performance. The optimal combination of the intensity, duration and mode of ‘warm-up’ exercise, and the recovery period allowed before the criterion exercise challenge, remain to be determined.

Effects of prior exercise and recovery duration on oxygen uptake kinetics during heavy exercise in humans

Prior heavy exercise (above the lactate threshold, LT) reduces the amplitude of the pulmonary oxygen uptake (V̇O2) slow component during heavy exercise, yet the precise effect of prior heavy exercise on the phase II V̇O2 response remains to be established. This study was designed to test the hypotheses that (1) prior heavy exercise increases the amplitude of the phase II V̇O2 response independently of changes in the baseline V̇O2 value and (2) the effect of prior exercise depends on the amount of external work done during prior exercise, irrespective of the intensity of the prior exercise. Nine subjects performed two 6 min bouts of heavy cycling exercise separated by 6 min baseline pedalling recovery (A), two 6 min heavy exercise bouts separated by 12 min recovery (6 min rest and 6 min baseline pedalling, B), and a bout of moderate exercise (below the LT) in which the same amount of external work was performed as during the prior heavy exercise, followed by 6 min heavy exercise (C). In both tests A and B, prior heavy exercise significantly increased the absolute V̇O2 amplitude at the end of phase II (by ∼150 ml min−1), and reduced the amplitude of the V̇O2 slow component by a similar amount. Following 12 min of recovery (B), baseline V̇O2, but not blood [lactate], had returned to pre‐exercise levels, indicating that these effects occurred independently of changes in baseline V̇O2. Prior moderate exercise (C) had no effect on either the V̇O2 or blood [lactate] responses to subsequent heavy exercise. The V̇O2 response to heavy exercise was therefore dependent on the intensity of prior exercise, and the effects on the amplitudes of the phase II and slow V̇O2 components persisted for at least 12 min following prior heavy exercise.

Prior heavy exercise enhances performance during subsequent perimaximal exercise

PURPOSE To test the hypothesis that prior heavy exercise increases the time to exhaustion during subsequent perimaximal exercise. METHODS Seven healthy males (mean +/- SD 27 +/- 3 yr; 78.4 +/- 0.7 kg) completed square-wave transitions from unloaded cycling to work rates equivalent to 100, 110, and 120% of the work rate at VO2peak (W-[VO2peak) after no prior exercise (control, C) and 10 min after a 6-min bout of heavy exercise at 50% Delta (HE; half-way between the gas exchange threshold (GET) and VO2peak), in a counterbalanced design. RESULTS Blood [lactate] was significantly elevated before the onset of the perimaximal exercise bouts after prior HE (approximately 2.5 vs approximately 1.1 mM; P < 0.05). Prior HE increased time to exhaustion at 100% (mean +/- SEM. C: 386 +/- 92 vs HE: 613 +/- 161 s), 110% (C: 218 +/- 26 vs HE: 284 +/- 47 s), and 120% (C: 139 +/- 18 vs HE: 180 +/- 29 s) of W-VO2peak, (all P < 0.01). VO2 was significantly higher at 1 min into exercise after prior HE at 110% W-VO2peak (C: 3.11 +/- 0.14 vs HE: 3.42 +/- 0.16 L x min(-1); P < 0.05), and at 1 min into exercise (C: 3.25 +/- 0.12 vs HE: 3.67 +/- 0.15; P < 0.01) and at exhaustion (C: 3.60 +/- 0.08 vs HE: 3.95 +/- 0.12 L x min(-1); P < 0.01) at 120% of W-VO2peak. CONCLUSIONS This study demonstrate that prior HE, which caused a significant elevation of blood [lactate], resulted in an increased time to exhaustion during subsequent perimaximal exercise presumably by enabling a greater aerobic contribution to the energy requirement of exercise.

Effects of prior warm-up regime on severe-intensity cycling performance.

PURPOSE The purpose of the present study was to determine the effect of three different warm-up regimes on cycling work output during a 7-min performance trial. METHODS After habituation to the experimental methods, 12 well-trained cyclists completed a series of 7-min performance trials, involving 2 min of constant-work rate exercise at approximately 90% VO2max and a further 5 min during which subjects attempted to maximize power output. This trial was performed without prior intervention and 10 min after bouts of moderate, heavy, or sprint exercise in a random order. Pulmonary gas exchange was measured breath by breath during all performance trials. RESULTS At the onset of the performance trial, baseline blood [lactate] was significantly elevated after heavy and sprint but not moderate exercise (mean +/- SD: control, 1.0 +/- 0.3 mM; moderate, 1.0 +/- 0.2 mM; heavy, 3.0 +/- 1.1 mM; sprint, 5.9 +/- 1.5 mM). All three interventions significantly increased the amplitude of the primary VO2 response (control, 2.59 +/- 0.28 L x min(-1); moderate, 2.69 +/- 0.27 L x min(-1); heavy, 2.78 +/- 0.26 L x min(-1); sprint, 2.78 +/- 0.30 L x min(-1)). Mean power output was significantly increased by prior moderate and heavy exercise but not significantly reduced after sprint exercise (control, 330 +/- 42 W; moderate, 338 +/- 39 W; heavy, 339 +/- 42 W; sprint, 324 +/- 45 W). CONCLUSIONS These data indicate that priming exercise performed in the moderate- and heavy-intensity domains can improve severe-intensity cycling performance by ~2-3%, the latter condition doing so despite a mild lactacidosis being present at exercise onset.

Influence of pacing strategy on O2 uptake and exercise tolerance

Seven male subjects completed cycle exercise bouts to the limit of tolerance on three occasions: (1) at a constant work rate (340±57 W; even‐pace strategy; ES); (2) at a work rate that was initially 10% lower than that in the ES trial but which then increased with time such that it was 10% above that in the ES trial after 120 s of exercise (slow‐start strategy; SS); and, (3) at a work rate that was initially 10% higher than that in the ES trial but which then decreased with time such that it was 10% below that in the ES trial after 120 s of exercise (fast‐start strategy; FS). The expected time to exhaustion predicted from the pre‐established power–time relationship was 120 s in all three conditions. However, the time to exhaustion was significantly greater (P<0.05) for the FS (174±56 s) compared with the ES (128±21 s) and SS (128±30 s) conditions. In the FS condition, V̇O2 increased more rapidly toward its peak such that the total O2 consumed in the first 120 s of exercise was greater (ES: 5.15±0.78; SS: 5.07±0.83; FS: 5.36±0.84 L; P<0.05 for FS vs ES and SS). These results suggest that a fast‐start pacing strategy might enhance exercise tolerance by increasing the oxidative contribution to energy turnover and hence “sparing” some of the finite anaerobic capacity across the transition to high‐intensity exercise.

Robustness of a 3 min all-out cycling test to manipulations of power profile and cadence in humans

The purpose of this study was to assess whether end‐test power output (EP, synonymous with ‘critical power’) and the work done above EP (WEP) during a 3 min all‐out cycling test against a fixed resistance were affected by the manipulation of cadence or pacing. Nine subjects performed a ramp test followed, in random order, by three cadence trials (in which flywheel resistance was manipulated to achieve end‐test cadences which varied by ∼20 r.p.m.) and two pacing trials (30 s at 100 or 130% of maximal ramp test power, followed by 2.5 min all‐out effort against standard resistance). End‐test power output was calculated as the mean power output over the final 30 s and the WEP as the power–time integral over 180 s for each trial. End‐test power output was unaffected by reducing cadence below that of the ‘standard test’ but was reduced by ∼10 W on the adoption of a higher cadence [244 ± 41 W for high cadence (at an end‐test cadence of 95 ± 7 r.p.m.), 254 ± 40 W for the standard test (at 88 ± 6 r.p.m.) and 251 ± 38 W for low cadence (at 77 ± 5 r.p.m.)]. Pacing over the initial 30 s of the test had no effect on the EP or WEP estimates in comparison with the standard trial. The WEP was significantly higher in the low cadence trial (16.2 ± 4.4 kJ) and lower in the high cadence trial (12.9 ± 3.6 kJ) than in the standard test (14.2 ± 3.7 kJ). Thus, EP is robust to the manipulation of power profile but is reduced by adopting cadences higher than ‘standard’. While the WEP is robust to initial pacing applied, it is sensitive to even relatively minor changes in cadence.

Estimation of critical torque using intermittent isometric maximal voluntary contractions of the quadriceps in humans

To determine whether the asymptote of the torque-duration relationship (critical torque) could be estimated from the torque measured at the end of a series of maximal voluntary contractions (MVCs) of the quadriceps, eight healthy men performed eight laboratory tests. Following familiarization, subjects performed two tests in which they were required to perform 60 isometric MVCs over a period of 5 min (3 s contraction, 2 s rest), and five tests involving intermittent isometric contractions at approximately 35-60% MVC, each performed to task failure. Critical torque was determined using linear regression of the torque impulse and contraction time during the submaximal tests, and the end-test torque during the MVCs was calculated from the mean of the last six contractions of the test. During the MVCs voluntary torque declined from 263.9 +/- 44.6 to 77.8 +/- 17.8 N x m. The end-test torque was not different from the critical torque (77.9 +/- 15.9 N x m; 95% paired-sample confidence interval, -6.5 to 6.2 N x m). The root mean squared error of the estimation of critical torque from the end-test torque was 7.1 N x m. Twitch interpolation showed that voluntary activation declined from 90.9 +/- 6.5% to 66.9 +/- 13.1% (P < 0.001), and the potentiated doublet response declined from 97.7 +/- 23.0 to 46.9 +/- 6.7 N.m (P < 0.001) during the MVCs, indicating the development of both central and peripheral fatigue. These data indicate that fatigue during 5 min of intermittent isometric MVCs of the quadriceps leads to an end-test torque that closely approximates the critical torque.

Influence of blood donation on O2 uptake on-kinetics, peak O2 uptake and time to exhaustion during severe-intensity cycle exercise in humans

We hypothesized that the reduction of O2‐carrying capacity caused by the withdrawal of ∼450 ml blood would result in slower phase II O2 uptake kinetics, a lower and a reduced time to exhaustion during severe‐intensity cycle exercise. Eleven healthy subjects (mean ±s.d. age 23 ± 6 years, body mass 77.2 ± 11.0 kg) completed ‘step’ exercise tests from unloaded cycling to a severe‐intensity work rate (80% of the difference between the predetermined gas exchange threshold and the ) on two occasions before, and 24 h following, the voluntary donation of ∼450 ml blood. Oxygen uptake was measured breath‐by‐breath, and kinetics estimated using non‐linear regression techniques. The blood withdrawal resulted in a significant reduction in haemoglobin concentration (pre: 15.4 ± 0.9 versus post: 14.7 ± 1.3 g dl−1; 95% confidence limits (CL): −0.04, −1.38) and haematocrit (pre: 44 ± 2 versus post: 41 ± 3%; 95% CL: −1.3, −5.1). Compared to the control condition, blood withdrawal resulted in significant reductions in (pre: 3.79 ± 0.64 versus post: 3.64 ± 0.61 l min−1; 95% CL: −0.04, − 0.27) and time to exhaustion (pre: 375 ± 129 versus post: 321 ± 99 s; 95% CL: −24, −85). However, the kinetic parameters of the fundamental response, including the phase II time constant (pre: 29 ± 8 versus post: 30 ± 6 s; 95% CL: 5, −3), were not altered by blood withdrawal. The magnitude of the slow component was significantly reduced following blood donation owing to the lower attained. We conclude that a reduction in blood O2‐carrying capacity, achieved through the withdrawal of ∼450 ml blood, results in a significant reduction in and exercise tolerance but has no effect on the fundamental phase of the on‐kinetics during severe‐intensity exercise.

Similar metabolic perturbations during all‐out and constant force exhaustive exercise in humans: a 31P magnetic resonance spectroscopy study

It is not possible to attain a metabolic steady state during exercise above the so‐called critical force or critical power. We tested the hypothesis that the muscle metabolic perturbations at the end of a bout of maximal isometric contractions, which yield a stable end‐test force (equal to the critical force), would be similar to that at task failure following submaximal contractions performed above the critical force. Eight healthy subjects (four female) performed isometric single knee‐extension exercise in the bore of a 1.5 T superconducting magnet on two occasions. Following familiarization, subjects performed the following exercises: (1) 60 maximal contractions (3 s contraction, 2 s rest); and (2) submaximal contractions (the same contraction regime performed at 54 ± 8% maximal voluntary contraction) to task failure. Phosphocreatine (PCr), inorganic phosphate (Pi) and diprotonated phosphate (H2PO4−) concentrations and pH were determined using 31P magnetic resonance spectroscopy throughout both tests. During the maximal contractions, force production fell from 213 ± 33 N to reach a plateau in the last 30 s of the test at 100 ± 20 N. The muscle metabolic responses at the end of each test were substantial, but not different between conditions: [PCr] was reduced (to 21 ± 12 and 17 ± 7% of baseline for maximal and submaximal contractions, respectively; P= 0.17), [Pi] was elevated (to 364 ± 98 and 363 ± 135% of baseline, respectively; P= 0.98) and pH reduced (to 6.64 ± 0.16 and 6.69 ± 0.17, respectively; P= 0.43). The [H2PO4−] was also elevated at the end of both tests (to 607 ± 252 and 556 ± 269% of baseline, respectively; P= 0.22). These data suggest that the exercise‐induced metabolic perturbations contributing to force depression in all‐out exercise are the same as those contributing to task failure during submaximal contractions.