The rate of oxygen uptake (V˙O2) increases with exponential kinetics after the onset of exercise (40). The rate of muscle ATP turnover, on the other hand, increases instantaneously at exercise onset, with the energetic equivalent of the incurred "O2 deficit" compensated by an increased rate of ATP resynthesis through phosphocreatine (PCr) degradation and anaerobic glycolysis. The tolerable duration of high-intensity exercise increases hyperbolically as power output declines, with the power asymptote of the power-duration curve termed the critical power (CP) (22,27,29). The curvature constant of this power-duration relationship, W′, represents a finite amount of work that can be performed above CP and is related to the potential for ATP yield from substrate-level phosphorylation and/or the accumulation of fatigue-related metabolites (e.g., H+, Pi, H2PO4 −, extracellular K+) (16,24,27-29,36). For the same work rate, increasing the initial rate of oxidative energy production would be expected to reduce the depletion of the finite anaerobic energy reserves and the accumulation of fatiguing metabolites, thereby preserving W′ and improving exercise performance (10,21). Accordingly, interventions that result in faster V˙O2 dynamics tend to result in improved performance during high-intensity exercise (5,6,25).
The pacing strategy adopted during an exercise bout, through determining the pattern of work rate distribution, has important implications for the activation and proportional contribution of oxidative metabolism to energy turnover. The total oxidative energy yield and the speed with which oxidative metabolism rises after the onset of exercise is increased when using all-out or fast-start (FS) pacing strategies compared with even-start (ES) or slow-start (SS) pacing strategies (2,3,8,19,25). The pacing strategy adopted during exercise therefore has important implications for exercise performance. During continuous athletic events of up to approximately 2-3 min in duration, the literature indicates that optimal performance is typically achieved with an all-out or positive pacing strategy (1,8,12,15,17,37). As the event duration is increased beyond 2-3 min, however, the optimal pacing strategy to enhance athletic performance becomes less clear with better performance having been reported after ES (15,32), all-out (2), FS (3), and FS followed by even pace (12) pacing strategies. Thus, information on the extent to which event duration and pacing strategy interact to determine V˙O2 kinetics and exercise performance is presently limited.
In a recent study (25), we reported that the time to exhaustion during high-intensity exercise was significantly extended when subjects used an FS compared with an ES or SS pacing strategy. The V˙O2 kinetics was significantly faster in the FS condition compared with the ES and SS conditions. We interpreted these data to indicate that the FS pacing strategy enhanced high-intensity exercise performance by sparing the nonoxidative energy contribution to energy turnover across the rest-to-exercise transition, such that this energy equivalent was available for utilization later in the exercise bout (25). However, time-to-exhaustion trials do not adequately reflect the physiological demands or pacing strategy adopted in competition. For example, middle-to-long distance events are commonly terminated with and are often decided by performance during an "end sprint" (4,14,17,31). An investigation into the interaction of changes in V˙O2 kinetics and changes in exercise performance should therefore involve different initial pacing strategies (FS, ES, and SS) followed by a return to the same constant work rate and then an end-sprint phase in which subjects attempt to maximize the work done.
The purpose of this investigation was to assess how pacing strategy (FS, ES, and SS) and exercise duration (3 and 6 min) interact to determine end-sprint and hence overall high-intensity exercise performance. We hypothesized that an FS strategy would result in faster V˙O2 kinetics and an SS strategy would result in slower V˙O2 kinetics relative to ES for both exercise durations. To provide insight into the physiological bases of possible differences in V˙O2 kinetics between pacing conditions, we used near-infrared spectroscopy (NIRS) to assess differences in muscle oxygenation and estimated muscle fractional O2 extraction (13,18). We also hypothesized that faster V˙O2 kinetics would be associated with improved end-sprint performance during both the 3- and the 6-min exercise trials.
Seven healthy males (mean ± SD: age = 21 ± 2 yr, stature = 1.80 ± 0.06 m, body mass = 80 ± 8 kg) volunteered to participate in this study. The subjects participated in exercise at a recreational level but were not highly trained and were familiar with laboratory exercise testing procedures, having previously participated in studies using similar procedures in our laboratory. The study was approved by the University of Exeter Research Ethics Committee. All subjects were required to give their written informed consent before the commencement of the study after the experimental procedures, associated risks, and potential benefits of participation had been explained. Subjects were instructed to arrive at the laboratory in a rested and fully hydrated state, at least 3 h postprandial, and to avoid strenuous exercise in the 24 h preceding each testing session. Each subject was also asked to refrain from caffeine and alcohol for 6 and 24 h before each test, respectively. All tests were performed at the same time of day (±2 h) at sea level in an air conditioned laboratory at 20°C.
The subjects were required to report to the laboratory on eight occasions over a 3- to 4-wk period with the eight visits being separated by at least 24 h. After the completion of a ramp incremental test (visit 1) and a 3-min all-out test ((9,34); visit 2), all subjects completed six paced exercise trials during which pulmonary V˙O2, heart rate (HR), blood [lactate], muscle oxygenation (by NIRS), and exercise performance (peak work rate and mean work rate achieved during the end sprint) were assessed. To assess the interactive influence of pacing strategy and exercise duration on exercise performance, we used a paradigm comprising three different pacing strategies (FS, ES, and SS) and two different exercise durations (3 and 6 min).
On the first laboratory visit, the subjects completed a ramp incremental exercise test for determination of the V˙O2max and gas exchange threshold (GET). All cycle tests were performed on an electrically braked cycle ergometer (Lode Excalibur Sport, Groningen, The Netherlands). Initially, subjects performed 3 min of baseline cycling at "0 W," after which the work rate was increased by 30 W·min−1 until the limit of tolerance. The subjects cycled at a constant self-selected pedal rate (between 70 and 90 rpm), and the chosen pedal rate along with saddle and handle bar height and configuration was recorded and reproduced in subsequent tests. Breath-by-breath pulmonary gas exchange data were collected continuously during the incremental tests and averaged over consecutive 10-s periods. The V˙O2max was taken as the highest 30-s mean value attained before the subject's volitional exhaustion in the test. The GET was determined from a cluster of measurements including 1) the first disproportionate increase in CO2 production (V˙CO2) from visual inspection of individual plots of V˙CO2 versus V˙O2, 2) an increase in expired ventilation (V˙E)/V˙O2 with no increase in V˙E/V˙CO2, and 3) an increase in end-tidal O2 tension with no fall in end-tidal CO2 tension. The work rate that would require 50%Δ (GET plus 50% of the difference between the work rate at the GET and V˙O2max) was subsequently calculated.
The 3-min all-out test
To estimate the parameters of the power-duration relationship (CP and W′), we used a 3-min all-out CP test (9,34). Before the test, subjects performed a 5-min warm-up at 90% GET, followed by 5 min of rest. The test then began with 3 min of unloaded baseline pedaling, followed by a 3-min all-out effort against a fixed resistance. Subjects were asked to accelerate to 110-120 rpm over the last 5 s of the baseline period. The resistance on the pedals during the 3-min all-out effort was set for each individual using the linear mode of the Lode ergometer so that the subject would attain the power output calculated to be 50%Δ on reaching their preferred cadence (linear factor = power/preferred cadence2). Strong verbal encouragement was provided throughout the test, but subjects were not informed of the elapsed time to prevent pacing. To ensure an all-out effort, subjects were instructed to attain their peak power output as quickly as possible from the start of the test and to maintain the cadence as high as possible at all times throughout the 3 min. The CP was estimated as the mean power output over the final 30 s of the test and W′ as the power-time integral above CP. The work rate that would be expected to lead to exhaustion in 3 min (3-tlim-WR) and 6 min (6-tlim-WR) was then calculated from the equation:
where P is the target work rate, TE is the time to exhaustion, CP is the critical power, and W′ is the finite work capacity >CP in Joules. For example, the work rate estimated to elicit a time to exhaustion of 180 s in a subject with W′ of 20,000 J and CP of 250 W would be as follows: (20,000/180) + 250 = 361 W.
The six experimental conditions were administered in a randomized order. Three of these exercise trials were of 3 min duration, and three were of 6 min duration. For each exercise duration, subjects completed the trial using ES, FS, and SS pacing strategies (Fig. 1). Each trial was preceded by 4 min of baseline cycling at 20 W before an abrupt step increment to the target work rate. The final minute of each trial required subjects to complete an all-out sprint against a fixed resistance, using the same linear factor as used in the 3-min all-out test, to determine the influence of the respective pacing strategy on exercise performance. In the 3-ES trial, subjects completed 2 min of constant work rate exercise at the 3-tlim-WR before the sprint, whereas in the 6-ES condition, the sprint was preceded by 5 min of constant work rate exercise at the 6-tlim-WR. In the FS and SS conditions, however, the work rate was initially not constant but rather decreased or increased with time, respectively, followed by a constant work rate "stabilization" phase before the all-out sprint (Fig. 1). In the 3-FS trial, the imposed work rate was initially 10% above the 3-tlim-WR, and this decreased linearly over 90 s to 10% below the 3-tlim-WR; conversely, in the 3-SS trial, the work rate increased from 10% below to 10% above the 3-tlim-WR over the first 90 s of the test. After this "pacing" phase, a step increment (3-FS) or decrement (3-SS) was used to restore the work rate to the 3-tlim-WR, at which subjects completed 30 s of constant work rate cycling before initiation of the all-out sprint. A similar pattern of work rate imposition, relative to the test duration, was used in the 6-min trials (Fig. 1). Each subject completed an equal amount of work over the first 2 min of the 3-min trials and over the first 5 min of the 6-min trials, irrespective of the pacing strategy used. The pacing phase was used for one-half of the total exercise duration in the FS and SS conditions for both the 3- and the 6-min trials, and the final sprint was initiated from the same absolute work rate for the 3-min (∼368 W) and the 6-min (∼311 W) trials. Subjects were provided with a 5-s countdown before the sprint and were instructed to attain the peak power as quickly as possible and to continue exercising maximally for the duration of the sprint. No time feedback was given to the subjects at any point during the sprint.
During all tests, pulmonary gas exchange and ventilation were measured breath by breath, with subjects wearing a nose clip and breathing through a low dead space, low-resistance mouthpiece, and an impeller turbine assembly (Jaeger Triple V). The inspired and the expired gas volume and gas concentration signals were continuously sampled at 100 Hz, the latter using paramagnetic (O2) and infrared (CO2) analyzers (Jaeger Oxycon Pro, Hoechberg, Germany) via a capillary line connected to the mouthpiece. The gas analyzers were calibrated before each test with gases of known concentration, and the turbine volume transducer was calibrated with a 3-L syringe (Hans Rudolph, Kansas City, MO). The volume and the concentration signals were time aligned by accounting for the delay in the capillary gas transit and the analyzer rise time relative to the volume signal. Pulmonary gas exchange and ventilation were calculated and displayed breath by breath. HR was measured during all tests using short-range radiotelemetry (Polar S610; Polar Electro Oy, Kempele, Finland).
During the exercise trials, a blood sample was collected from a fingertip into a capillary tube over the 20 s preceding the step transition in work rate, the 20 s preceding the sprint, and also immediately after the sprint. These whole blood samples were subsequently analyzed to determine blood [lactate] (YSI 1500; Yellow Springs Instruments, Yellow Springs, OH) within 30 s of collection.
The oxygenation status of the musculus vastus lateralis of the right leg was monitored using a commercially available NIRS system (model NIRO 300; Hamamatsu Photonics KK, Hiugashi-ku, Japan). The system consisted of an emission probe that radiates laser beams and a detection probe. Four different wavelength laser diodes provided the light source (776, 826, 845, and 905 nm) and the light returning from the tissue was detected by a photomultiplier tube in the spectrometer. The intensity of incident and transmitted light was recorded continuously at 2 Hz and used to estimate concentration changes from the resting baseline for oxygenated, deoxygenated, and total tissue hemoglobin/myoglobin. Therefore, the NIRS data represent a relative change based on the optical density measured in the first datum collected. The deoxygenated hemoglobin/myoglobin oncentration ([HHb]) signal was assumed to provide an estimate of changes in fractional O2 extraction in the field of interrogation (5,13,18). The leg was initially cleaned and shaved around the belly of the muscle, and the optodes were placed in the holder that was secured to the skin with adhesive at 20 cm above the fibular head. To secure the holder and wires in place and to minimize the possibility that extraneous light could influence the signal, an elastic bandage was wrapped around the subject's leg. Indelible pen marks were made around the holder to enable precise reproduction of the placement in subsequent tests. The probe gain was set with the subject at rest in a seated position with the leg extended at down stroke on the cycle ergometer before the first exercise bout, and NIRS data were collected continuously throughout the exercise protocols. The data were subsequently downloaded onto a personal computer, and the resulting text files were stored on disk for later analysis.
Data analysis procedures.
The breath-by-breath V˙O2 data from each test were initially examined to exclude errant breaths caused by coughing, swallowing, sighing, and so forth, and those values lying more than 4 SD from the local mean were removed. The breath-by-breath data were subsequently linearly interpolated to provide second-by-second values and time aligned to the start of exercise, and a nonlinear least square algorithm was used to fit the data thereafter. Given that the subjects only completed one trial in each condition, we did not consider it was justified to use a biexponential model to characterize the V˙O2 kinetics because statistical confidence in the derived parameters would be low. Therefore, a single-exponential model without time delay, with the fitting window commencing at t = 0 s (equivalent to the mean response time [MRT]), was used to characterize the kinetics of the overall V˙O2 response during the pacing trials as described in the following equation:
where V˙O2 (t) represents the absolute V˙O2 at a given time t, V˙O2baseline represents the mean V˙O2 measured over the final 90 s of baseline pedaling, and A and τ represent the amplitude and time constant, respectively, describing the overall increase in V˙O2 above baseline. In addition, the same model was applied to the data between 20 and 120 s for all exercise bouts to provide an estimate of phase II τ. An iterative process was used to minimize the sum of the squared errors between the fitted function and the observed values. We quantified the MRT and also the absolute V˙O2 at the end of the pacing (±5 s), stabilization (±5 s), and sprint (average over final 10 s) phases of the trials. The oxygen deficit was also calculated at these time points by multiplying the MRT and the Δ V˙O2 at the specified time. The total O2 consumed (in liters) was also computed at these same time points, and the oxidative energy yield was estimated with the assumption that 1 L of O2 consumed was equivalent to 20.9 kJ of energy expended (38).
To provide information on muscle oxygenation, we also modeled the [HHb] response to exercise. The [HHb] kinetics during the exercise was determined by fitting a monoexponential model from the first data point, which was 1 SD above the baseline mean through the entire response. The [HHb] TD and the τ values were summed to provide information on the overall [HHb] response dynamics. The [O2Hb] and the [Hbtot] responses do not approximate an exponential (18) and were not modeled. Rather, we assessed changes in these variables by determining the [O2Hb] and the [Hbtot] at baseline and after the pacing, stabilization, and sprint phases for both exercise durations. Pacing-induced changes in HR were assessed through comparing the HR at baseline and after the pacing, stabilization, and sprint phases for both exercise durations.
Performance during the end sprint was evaluated using the peak power output, time to peak power output, mean power output, and total sprint work done. The work done above the CP and the total work done in the 3- and 6-min tests were also calculated.
A one-way repeated-measures ANOVA was used to determine the effects on the relevant physiological and performance variables elicited by the pacing permutations for the 3- and 6-min trials. Where the analysis revealed a significant difference, individual paired t-tests were used with a Fisher's LSD to determine the origin of such effects. The influence of pacing strategy and event duration on the total work done above CP was explored by a two-way (pacing strategy × duration) repeated-measures ANOVA. All data are presented as mean ± SD. Statistical significance was accepted when P < 0.05.
During the ramp incremental test, subjects attained a peak work rate of 390 ± 66 W and a V˙O2max of 4.17 ± 0.60 L·min−1. The CP and the W′ estimated from the 3-min all-out test were 253 ± 60 W and 20.7 ± 4.5 kJ, respectively, such that the 3-tlim-WR and the 6-tlim-WR were calculated to be 368 ± 67 and 311 ± 62 W, respectively (Fig. 1).
The parameters of V˙O2 dynamics during the variously paced 3- and 6-min exercise trials are shown in Table 1 and illustrated as group mean responses in Figure 2. The overall V˙O2 kinetics during the 3-min trials when the fitting window was constrained to the end of the pacing phase (90 s) was fastest in the 3-FS condition, slowest in the 3-SS condition, and intermediate in the 3-ES condition, with the trials being significantly different from one another (Table 1, Fig. 2). When the fitting window was extended to the onset of the sprint (120 s), the MRT was reduced in the 3-FS versus the 3-SS condition (Table 1). The total O2 consumed over the first 90 s of the 3-min trials was significantly greater in 3-FS and 3-ES compared with 3-SS, whereas the total O2 consumed over the first 120 s of the 3-min trials was greater in 3-FS compared with 3-SS (Table 1).
The overall V˙O2 kinetics during the 6-min trials when the fitting window was constrained to the end of the pacing phase (180 s) was significantly faster in the 6-FS and 6-ES conditions compared with the 6-SS condition (P < 0.05), but there was no significant difference between 6-FS and 6-ES (P = 0.09) (Table 1, Fig. 2). However, V˙O2 kinetics was significantly different between all conditions, being fastest in the 6-FS and slowest in the 6-SS, when the fitting window was extended to the start of the sprint (300 s; Table 1, Fig. 2). The total O2 consumed over the first 180 s of the 6-min trials was significantly greater in the 6-FS than that in the 6-SS but not in the 6-ES (Table 1). However, the total O2 consumed in the first 300 s of exercise was not influenced by the pacing strategy in the 6-min trials.
NIRS, HR, and blood [lactate] responses.
The absolute [O2Hb] and [Hbtot] were not significantly different during the baseline or throughout exercise for any of the pacing strategies and exercise durations investigated. The [HHb] responses during the pacing trials are reported in Table 2 and illustrated in SDC 1 (Influence of pacing strategy and event duration on [HHb] response dynamics; http://links.lww.com/MSS/A48). During the 3-min pacing trials, the [HHb] τ + TD was significantly shorter in the 3-FS and 3-ES conditions compared with the 3-SS condition (Table 2). The [HHb] τ + TD was not significantly different during the 6-min trials irrespective of the pacing strategy or fitting procedures used. The absolute HR was not significantly different during the baseline or throughout exercise across all the pacing permutations investigated (Table 2). The blood [lactate] was not significantly different at any point during the 3-min pacing trials. However, the blood [lactate] before the sprint was significantly greater in the 6-SS compared with the 6-ES condition (Table 2).
The exercise performance parameters during the various pacing conditions are reported in Table 3, and the group mean power profile during the 60-s all-out sprint is shown in Figure 3. The peak power output attained in the sprint was significantly (∼16%) greater in 3-FS compared with 3-ES and 3-SS, and the time to attain the peak work rate was significantly (∼33%) shorter in 3-FS compared with 3-ES (Fig. 3). In addition, the mean power output during the sprint was significantly (∼7%) greater in the 3-FS compared with the 3-ES and 3-SS conditions. Therefore, over the entire 3 min of exercise, the total work done was significantly greater in 3-FS compared with 3-ES and 3-SS (Table 3). In contrast, none of the parameters of exercise performance were enhanced during the 6-FS condition, with the values being similar to those observed in the 6-ES and 6-SS conditions (Table 3).
Comparison of the 3- and 6-min trials.
The end-exercise V˙O2 in 3-FS, 6-ES, 6-FS, and 6-SS were not significantly different from one another or from the V˙O2max attained in the ramp incremental test (P > 0.05; Table 1). However, the end-exercise V˙O2 in 3-ES and 3-SS was significantly lower than the V˙O2max (P < 0.05). The total work done above the CP was not significantly different from the W′ estimated in the 3-min all-out test for any of the six trials. However, the total work done above CP was significantly greater in the 6-min than the 3-min exercise trials (P < 0.05). Follow-up analyses revealed that the total work done above the CP in 3-FS (20.8 ± 5.4 kJ), 6-ES (22.1 ± 7.4 kJ), 6-FS (22.1 ± 7.9 kJ), and 6-SS (21.9 ± 6.9 kJ) was not significantly different from one another. However, the total work done above the CP was significantly lower in 3-ES (19.2 ± 5.7 kJ) and 3-SS (19.0 ± 5.8 kJ) compared with the other conditions (P < 0.05).
The principal original finding of the present investigation was that an FS pacing strategy enhanced performance during the shorter (3 min) but not longer (6 min) exercise bouts, an effect that was linked to alterations in V˙O2 dynamics. The V˙O2 kinetics (and thus the magnitude of the O2 deficit incurred over the initial transient phase) was influenced by the pacing strategy used during high-intensity exercise. Overall, an FS strategy resulted in faster V˙O2 kinetics than ES, with ES in turn resulting in faster V˙O2 kinetics than SS.
During the 3-min exercise bouts, an FS strategy significantly enhanced performance: compared with the ES condition, the peak power output attained in the end-sprint phase was 16% higher and the mean power output over the final 60 s was 7% higher. These results might be interpreted to indicate that the initial "sparing" of the W′ due to the faster V˙O2 kinetics meant that a greater nonoxidative energy reserve was available later in exercise. However, although V˙O2 kinetics was slower in SS compared with ES in the 3-min exercise bouts, exercise performance was not impaired. Also, despite differences in V˙O2 kinetics between the three pacing conditions during the 6-min exercise bouts, there were no significant differences in exercise performance. The end-exercise V˙O2 was not significantly different from the V˙O2max for 3-FS or for any of the 6-min exercise bouts but was significantly lower than the V˙O2max in 3-ES and 3-SS. Similarly, the total work done above the CP was not different for 3-FS or for any of the 6-min exercise bouts but was significantly lower in 3-ES and 3-SS. These results therefore imply that FS resulted in an enhanced performance during short-term high-intensity exercise by enabling the attainment of V˙O2max that, in turn, permitted more work to be done above the CP or vice versa.
Influence of pacing strategy on V˙O2 kinetics
The overall V˙O2 kinetics was fastest in FS, slowest in SS, and intermediate for ES in both the 3- and the 6-min exercise trials. This is consistent with previous research, which has indicated that faster starting strategies can increase V˙O2 across the transition from rest to high-intensity exercise (2,3,8,19,25). However, these previous studies did not characterize the dynamics with which oxidative metabolism rose toward the projected steady state in the differently paced conditions.
Jones et al. (25) assessed the influence of pacing strategy on the dynamics of V˙O2 using exponential curve fitting and found that V˙O2 kinetics was fastest with an FS strategy, slowest with an SS strategy, and intermediate for an ES strategy. The results of the present study support these findings. As has been suggested previously (8,25), the greater initial rate of muscle ATP hydrolysis with an FS strategy would be expected to increase the "error signal" between the instantaneous supply and the required rates of oxidative phosphorylation (39). The muscle ATP turnover rate is proportional to the change in muscle PCr concentration per unit change in time (Δ[PCr]/Δt), and therefore a greater rate of change of [PCr] at and after the onset of exercise should be associated with a more rapid increase in V˙O2 (30,39). Compared with ES, an FS pacing strategy would be expected to increased the Δ[PCr]/Δt and to increase the concentrations of ADP, Pi, and Ca2+, thus augmenting several of the stimuli believed to be responsible for an acceleration of oxidative phosphorylation (7,11,30). Conversely, compared with ES, an SS pacing strategy would be expected to reduce the initial error signal and result in a blunting of the V˙O2 response dynamics.
To elucidate the mechanistic bases for the faster V˙O2 kinetics with faster starting strategies, we measured [Hbtot] and [HbO2] to provide information on total blood volume and oxygenation within the NIRS area of interrogation and [HHb] kinetics to estimate muscle O2 extraction dynamics (13,18). The faster V˙O2 kinetics in the FS and ES compared with the SS condition during the 3-min trials was accompanied by a shorter [HHb] τ + TD, but there were no differences in [Hbtot], [HbO2], or HR between the conditions. These results suggest that the improved V˙O2 dynamics that are evident with faster starting strategies may be linked to increased muscle O2 extraction. However, although the V˙O2 kinetics was altered in a similar fashion under the three pacing strategies when the exercise duration was extended to 6 min, the mechanisms that governed these adjustments were less clear. That is, the [Hbtot], the [HbO2], and the [HHb] were all similar across the various pacing conditions. For the 6-min exercise bouts, the unchanged [HHb] kinetics imply that the faster V˙O2 kinetics was linked to improvements in both muscle O2 supply and utilization.
During high-intensity exercise of short duration (≤3 min), exhaustion often ensues before the V˙O2max is attained (20,41). Consistent with this, in the present study, the end-exercise V˙O2 for 3-ES and 3-SS was significantly lower than the V˙O2max measured in the ramp incremental test. However, in 3-FS and in all three of the 6-min pacing conditions, the end-exercise V˙O2 was not significantly different from the V˙O2max. Therefore, one consequence of the faster V˙O2 kinetics that attend the adoption of an FS pacing strategy is that it permits the attainment of V˙O2max during "extreme" exercise bouts when this is ordinarily not possible (20,41).
To investigate the influence of pacing strategy and event duration on exercise performance, we had subjects perform 3- and 6-min exercise trials initiated with FS, ES, and SS pacing strategies, with all trials culminating in an all-out sprint over the final minute of the bout. After the pacing phase, the work rate returned to a constant work rate (ES work rate), which was maintained until the onset of the sprint so that all sprints were initiated from the same absolute work rates and the total work done before the sprint was matched between conditions. It was therefore expected that the same fixed amount of work could be achieved during the end-sprint phase for all conditions, unless one or more of the initial pacing conditions predisposed to improved exercise performance.
Of all the pacing permutations investigated, exercise performance was only enhanced in the 3-FS condition. Specifically, the peak and the mean power outputs during the end sprint were higher, the time to reach the peak power output was reduced, and the total work done during the end sprint and over the entire bout was increased. Intriguingly, however, performance was not impaired in the SS condition compared with the ES condition. These data are consistent with a previous report (25) and suggest the existence of an "asymmetry" in the physiological consequences of FS and SS pacing strategies during short-term high-intensity exercise; that is, relative to ES, an FS strategy is clearly ergogenic, whereas an SS strategy is not necessarily ergolytic. Exercise performance was not different between the pacing strategies during the 6-min trials, indicating that the potential for an FS pacing strategy to enhance exercise performance recedes as the event duration is extended (14).
In the present study, V˙O2 kinetics was faster and exercise performance was superior in 3-FS compared with 3-ES and 3-SS. These data might suggest that exercise performance was enhanced in the 3-FS condition consequent to the faster V˙O2 kinetics sparing the W′ over the transient region; this additional nonoxidative energy would then be available for utilization at the commencement of the end-sprint phase, enabling a greater total work output. Indeed, the additional oxidative energy yield associated with the greater O2 consumed in the first 90 s of exercise in 3-FS compared with 3-ES (equivalent to 2.0 kJ on average; Table 1) was not significantly different from the greater work done over the end-sprint phase (1.5 kJ on average; Table 3). This supports the suggestion that V˙O2 kinetics and the W′ are inherently linked in the determination of exercise tolerance (10,21). In contrast, the greater oxidative energy yield in the first 90 s of exercise in 3-ES compared with 3-SS (4.0 kJ on average; Table 1) was significantly greater than the increased work done over the end-sprint phase in 3-ES compared with 3-SS (0.2 kJ on average; Table 3). With the assumptions that the total ATP requirement and muscle efficiency were identical for the first 120 s of exercise in all three conditions (cf. (26)), these data indicate complex interrelationships between oxidative and nonoxidative metabolic contributions to energy turnover during high-intensity exercise, which are sensitive to the pattern of work rate imposition (for discussion, see Jones et al. (25)).
Exercise performance was not different across the 6-min trials, irrespective of the imposed pacing strategy. The FS strategy, through increasing the initial ATP turnover rate, would be expected to increase both oxidative and nonoxidative energy turnover. The key difference between the influence of an FS strategy on performance during shorter-term (∼3 min) compared with longer-term (∼6 min) high-intensity exercise, at least in the present study, might be the duration that the higher-than-average work rate is sustained. For example, the work rate during FS was higher than that during ES and SS for 90 s in the 6-min trials compared with 45 s in the 3-min trials. It is possible that the greater oxidative energy yield in the 6-FS condition was offset by an increased nonoxidative energy turnover such that W′ was not significantly spared before the commencement of the end sprint. In particular, it is likely that anaerobic glycolysis was activated to a greater extent during the FS phase of the 6-min compared with the 3-min exercise bouts. In this regard, an FS that is of short duration relative to the event duration might be considered optimal in both shorter and longer duration high-intensity exercise bouts because it would increase Δ[PCr]/Δt and drive a rapid increase in mitochondrial respiration without risking a precipitous drop in pH early in the event. Overall, the data suggest that pacing strategy, at least in the forms administered herein, has little effect on exercise performance during maximal exercise of around 6 min duration.
An alternative, but attractive, interpretation of the performance data in the present study requires a reconsideration of the physiological meaning of the parameters derived from the power-duration relationship (i.e., CP and W′). It is noteworthy that, despite differences in the MRT, the V˙O2 attained at the end of each of the 6-min pacing trials was not different from the preestablished V˙O2max, and there was no difference in the amount of work done above CP or in overall performance between the conditions. In contrast, for the ES and SS conditions in the 3-min trials, the end-exercise V˙O2 was significantly lower than the V˙O2max, and both the work done above the CP and the overall performance were significantly reduced compared with the FS condition. If the attainment of V˙O2max is a major determinant of W′ (10,33,35), then it is possible that the pacing strategy chosen will not significantly impact on high-intensity exercise performance, provided that the V˙O2max is attained, as was the case for the 6-min exercise trials. However, for shorter duration high-intensity exercise bouts in which the V˙O2max cannot be attained when an ES strategy is used, the W′ will not be fully manifested such that performance might be "suboptimal." In such a situation, an intervention such as the adoption of an FS strategy, which speeds V˙O2 kinetics and enables the attainment of V˙O2max, would enable a more complete utilization of the W′ and consequently better overall performance. This interpretation is supported by other lines of evidence. For example, Jones et al. (23) compared the V˙O2 response and the time to exhaustion during extreme exercise (120% V˙O2max) with and without a preceding "priming" bout of heavy exercise. Without priming, the end-exercise V˙O2 reached ∼89% V˙O2max (significantly lower than V˙O2max), and the time to exhaustion was 139 ± 18 s; after priming, V˙O2 kinetics were faster, the end-exercise V˙O2 was increased to 98% V˙O2max (not significantly different from the V˙O2max), and the time to exhaustion was extended to 180 ± 29 s.
In both the 3- and 6-min trials, V˙O2 kinetics was fastest in FS, slowest in SS, and intermediate in ES. These findings indicate that the rate at which V˙O2 increases after the onset of exercise is sensitive to the pattern of work rate imposition, even when the mean work rate is identical. A higher initial work rate and thus muscle ATP turnover rate would result in a greater initial Δ[PCr]/Δt and a more rapid accumulation of metabolites that stimulate oxidative phosphorylation. In 3-FS, the energy equivalent of the additional O2 consumed across the transient was subsequently expended in the end-sprint phase, such that performance was significantly enhanced. Conversely, the relatively slow V˙O2 kinetics across the transient phase in 3-SS did not impair end-sprint or overall exercise performance relative to 3-ES. Alongside an earlier report (25), this indicates the existence of an asymmetry in the bioenergetic response to the pattern of work rate allocation during short-term high-intensity exercise. Although differences in V˙O2 kinetics between the three pacing strategies persisted during the 6-min exercise bouts, there were no differences in performance indices. During short-term "extreme" exercise, an FS pacing strategy might enhance performance by enabling the attainment of V˙O2max when this is not ordinarily possible and by permitting a more complete utilization of the W′. However, during longer-term "severe" exercise in which the V˙O2max is normally attained and the W′ is fully expended, differences in pacing strategy have a relatively small effect on performance outcomes.
This research was not supported by external funding.
The results of the present study do not constitute an endorsement by the American College of Sports Medicine.
1. Abbiss CR, Laursen PB. Describing and understanding pacing strategies during athletic competition. Sports Med
2. Aisbett B, Lerossignol P, McConell GK, Abbiss CR, Snow R. Influence of all-out and fast start on 5-min cycling time trial performance. Med Sci Sports Exerc
3. Aisbett B, Lerossignol P, McConell GK, Abbiss CR, Snow R. Effects of starting strategy on 5-min cycling time-trial performance. J Sports Sci
4. Ansley L, Schabort E, St Clair Gibson A, Lambert MI, Noakes TD. Regulation of pacing strategies during successive 4-km time trials. Med Sci Sports Exerc
5. Bailey SJ, Vanhatalo A, Wilkerson DP, DiMenna FJ, Jones AM. Optimizing the "priming" effect: influence of prior exercise intensity and recovery duration on O2
uptake kinetics and severe-intensity exercise tolerance
. J Appl Physiol
6. Bailey SJ, Wilkerson DP, DiMenna FJ, Jones AM. Influence of repeated sprint training on pulmonary O2
uptake and muscle deoxygenation kinetics in humans. J Appl Physiol
7. Balaban RS. The role of Ca2+
signalling in the coordination of mitochondrial ATP production with cardiac work. Biochim Biophys Acta
8. Bishop D, Bonetti D, Dawson B. The influence of pacing strategy on O2
and supramaximal kayak performance. Med Sci Sports Exerc
9. Burnley M, Doust JH, Vanhatalo A. A 3-min all-out test to determine peak oxygen uptake and the maximal steady state. Med Sci Sports Exerc
10. Burnley M, Jones AM. Oxygen uptake kinetics as a determinant of sports performance. Eur J Sports Sci
11. Chance B, Williams GR. Respiratory enzymes in oxidative phosphorylation. I. Kinetics of oxygen utilization. J Biol Chem
12. De Koning JJ, Bobbert MF, Foster C. Determination of optimal pacing strategy in track cycling with an energy flow model. J Sci Med Sport
13. DeLorey DS, Kowalchuk JM, Heenan AP, duManoir GR, Paterson DH. Prior exercise speeds pulmonary O2
uptake kinetics by increases in both local muscle O2
availability and O2
utilization. J Appl Physiol
14. Foster C, deKoning JJ, Hettinga F, et al. Effect of competitive distance on energy expenditure during simulated competition. Int J Sports Med
15. Foster C, Snyder AC, Thompson NN, Green MA, Foley M, Schrager M. Effect of pacing strategy on cycle time trial performance. Med Sci Sports Exerc
16. Fukuba Y, Miura A, Endo M, Kan A, Yanagawa K, Whipp BJ. The curvature constant parameter of the power-duration curve for varied-power exercise. Med Sci Sports Exerc
17. Garland SW. An analysis of the pacing strategy adopted by elite competitors in 2000 m rowing. Br J Sports Med
18. Grassi B, Pogliaghi S, Rampichini S, et al. Muscle oxygenation and pulmonary gas exchange kinetics during cycle exercise on-transitions in humans. J Appl Physiol
19. Hettinga FJ, de Koning JJ, Foster C. V˙O2
response in supramaximal cycling time trial exercise of 750 to 4000 m. Med Sci Sports Exerc
20. Hill DW, Poole DC, Smith JC. The relationship between power and the time to achieve V˙O2max
. Med Sci Sports Exerc
21. Jones AM, Burnley M. Oxygen uptake kinetics: an underappreciated determinant of exercise performance. Int J Sports Physiol Perform
22. Jones AM, Vanhatalo A, Burnley M, Morton RH, Poole DC. Critical power
: implications for the determination of V˙O2max
and exercise tolerance
. Med Sci Sports Exerc
23. Jones AM, Wilkerson DP, Burnley M, Koppo K. Prior heavy exercise enhances performance during subsequent perimaximal exercise. Med Sci Sports Exerc
24. Jones AM, Wilkerson DP, DiMenna F, Fulford J, Poole DC. Muscle metabolic responses to exercise above and below the "critical power
" assessed using 31P-MRS. Am J Physiol Regul Integr Comp Physiol
25. Jones AM, Wilkerson DP, Vanhatalo A, Burnley M. Influence of pacing strategy on O2
uptake and exercise tolerance
. Scand J Med Sci Sports
26. Krustrup P, Ferguson RA, Kjaer M, Bangsbo J. ATP and heat production in human skeletal muscle during dynamic exercise: higher efficiency of anaerobic than aerobic ATP resynthesis. J Physiol
27. Monod H, Scherrer J. The work capacity of a synergic muscular group. Ergonomics
28. Moritani T, Nagata A, deVries HA, Muro M. Critical power
as a measure of physical work capacity and anaerobic threshold. Ergonomics
29. Poole DC, Ward SA, Gardner GW, Whipp BJ. Metabolic and respiratory profile of the upper limit for prolonged exercise in man. Ergonomics
30. Rossiter HB, Ward SA, Kowalchuk JM, Howe FA, Griffiths JR, Whipp BJ. Dynamic asymmetry of phosphocreatine concentration and O2
uptake between the on- and off-transients of moderate- and high-intensity exercise in humans. J Physiol
31. St Clair Gibson A, Schabort EJ, Noakes TD. Reduced neuromuscular activity and force generation during prolonged cycling. Am J Physiol
32. Thompson KG, MacLaren DPM, Lees A, Atkinson G. The effect of even, positive and negative pacing on metabolic, kinematic and temporal variables during breaststroke swimming. Eur J Appl Physiol
33. Vanhatalo A, Doust JH, Burnley M. A 3-min all-out cycling test is sensitive to a change in critical power
. Med Sci Sports Exerc
34. Vanhatalo A, Doust JH, Burnley M. Determination of critical power
using a 3-min all-out cycling test. Med Sci Sports Exerc
35. Vanhatalo A, Fulford J, Dimenna F, Jones AM. Influence of hyperoxia on muscle metabolic responses and the power-duration relationship during severe-intensity exercise in humans: a 31P-MRS study. Exp Physiol
36. Vanhatalo A, Jones AM. Influence of prior sprint exercise on the parameters of the "all-out critical power
test" in men. Exp Physiol
37. van Ingen Schenau GJ, de Koning JJ, de Groot G. The distribution of anaerobic energy in 1000 and 4000 meter cycling bouts. Int J Sports Med
38. Weir JBdcV. New methods for calculating metabolic rate with special reference to protein metabolism. J Physiol
39. Whipp BJ, Mahler M. Dynamics of gas exchange during exercise. In: West JB, editor. Pulmonary Gas Exchange
. Vol II. New York: Academic Press; 1980. p. 33-96.
40. Whipp BJ, Ward SA, Lamarra N, Davis JA, Wasserman K. Parameters of ventilatory and gas exchange dynamics during exercise. J Appl Physiol
41. Wilkerson DP, Koppo K, Barstow TJ, Jones AM. Effect of work rate on the functional `gain' of Phase II pulmonary O2
uptake response to exercise. Respir Physiol Neurobiol
Keywords:©2011The American College of Sports Medicine
V˙O2 DYNAMICS; CRITICAL POWER; ANAEROBIC CAPACITY; EXERCISE TOLERANCE