Prior exercise, or "warm-up", is almost universally accepted as a precompetition regimen to enhance performance. Although physiological mechanisms underlying the prior exercise effect have received particular attention (7,21,25,29-31,39), the impact on performance per se is less clear. Studies have provided conflicting results and few have directly addressed the performance implications using ecologically valid protocols. To date, warm-up in some form has been shown to improve (2,10,13,27), worsen (13), or have no effect on performance (1,13,28). Studies specifically addressing cycling performance have shown no change in performance (28) or improved (8,10,27) performance.
For exercise in the moderate-intensity domain, a reduced rate of oxygen consumption (V˙O2) during exercise is considered beneficial because it indicates improved economy (37). In the heavy and severe exercise domains, where some of the net energy transfer is from anaerobic pathways, a greater aerobic contribution is considered beneficial for a given absolute intensity as the reliance on anaerobic pathways is reduced, thereby improving exercise tolerance (40). A reduced reliance on the anaerobic pathways, particularly during early stages of an exercise bout, could spare the finite anaerobic capacity, reduce metabolic disturbance, and possibly enhance performance.
Prior heavy exercise has been shown to increase aerobic responses to subsequent exercise and improve performance (8,10,27). Prior heavy exercise seems to increase the primary amplitude and reduce the slow component of subsequent exercise without a speeding of the primary time constant (9). Prior heavy exercise could therefore have important performance implications during subsequent exercise by increasing aerobic contribution. It is unknown, however, how prior exercise affects the anaerobic response to the same bout of exercise and/or pace selection. Moreover, the effect of altering the energy system contribution on pacing and performance has not been determined because most studies use constant-intensity performance tasks (6-8). No data are available on the effects of prior exercise on performance or energy system contribution using externally valid cycling performance tests. Such a model could provide valuable insight into how changes in aerobic versus anaerobic contributions affect pace selection and performance.
Relative contributions of aerobic and anaerobic mechanisms of energy provision to exercise have been reported previously for exercise of various durations (18,40,41), modes (15), training status (20,35), and standard of athlete (17). Although changes in pacing strategy seem to have a limited effect on the overall aerobic and anaerobic response to exercise (19,22), it is not known how other acute interventions, such as prior heavy exercise, which is known to increase the aerobic response to exercise, affect the overall energy system contribution to exercise in the severe domain during ecologically valid cycling time trials. Furthermore, the performance implications and impact on pace selection remain to be determined.
The efficacy of various prior exercise regimens has been examined in the laboratory, in particular prior heavy exercise. Although the nature of prior heavy exercise regimens and its subsequent impact on performance are becoming clearer, there seem to be limited data on the typical "warm-up" practices of highly trained athletes. Moreover, it is uncertain whether highly trained athletes should adopt prior exercise regimens that resemble the prior "heavy" exercise regimens used in the literature.
The purpose of this study was to determine the effects of prior heavy exercise on performance, pacing strategy, and energy system contributions in a laboratory-based 4000-m time trial. It was hypothesized that compared with no prior exercise, prior heavy exercise would increase the aerobic contribution to subsequent exercise and improve performance while the anaerobic contribution would remain unchanged. An additional purpose of this study was to quantify the nature of prior exercise regimens typically used by well-trained athletes and the energetic and performance effects of such regimens.
Eight national-standard cyclists provided written informed consent to participate in this study. All participants were training in preparation for regional and national track cycling competitions. Prior ethics approval was obtained from the University of Otago Human Research Ethics Committee. The participant characteristics were as follows (mean ± SD): age = 30 ± 8 yr, body mass = 78.7 ± 8.6 kg, stature = 181 ± 5 cm, V˙O2peak = 63.7 ± 6.7 mL·kg−1·min−1, and 4000-m personal best time = 297.1 ± 17.0 s. Participants were required to attend each session in a hydrated and rested state (no intense exercise the day before). Each session was performed at the same time of day and on the same weekday to control for variations in participants' training programs and competition schedules. Participants were also requested to maintain normal eating habits and a consistent pattern of training across the study. All testing was performed in a well-ventilated room maintained at ∼20°C.
Participants visited the laboratory on four occasions. The first visit was used to establish an individual relationship between V˙O2 and intensity of exercise in addition to V˙O2peak. Participants performed one familiarization time trial 3-7 d before performing three testing sessions (each 1 wk apart) in a pseudorandomized order. Each testing session consisted of a 4000-m laboratory-based time trial preceded by one of three prior exercise protocols, namely, no prior exercise, prior heavy exercise, and self-selected prior exercise.
All testing was performed on an electromagnetically braked ergometer (Velotron; Racermate, Seattle, WA). For all sessions, the ergometer was adjusted to fit each participant on the basis of their normal bike measurements including fitting of their own pedals and a racing saddle. All measurements were replicated during subsequent tests. The ergometer was also fitted with handlebar extensions ("aerobars") as would typically be used during a 4000-m track time trial. Upon arriving at the laboratory, participants had their stature and body mass recorded before being fitted with a heart rate transmitter belt (Polar™, Kemplele, Finland).
The first test was used to establish the linear relationship between V˙O2 and power output and also maximal aerobic power. The test was continuous in nature, whereby the intensity was increased by 25 W at 5-min intervals. Participants typically performed 8 to 10 exercise intensities between approximately 40% and 90% V˙O2peak (32). Cadence was self-selected (typically 90-100 rpm). Oxygen consumption was measured breath-by-breath as described below between minutes 2 and 5 of each bout (16). Lactate was sampled via a finger prick and analyzed for blood lactate concentration (blood [lactate]) using an automated lactate analyzer (Model 27 Analyzer; YSI, Yellow Springs, OH) during the final seconds of each stage to determine the lactate threshold according to the method of Bourdon (4). Heart rate was also recorded during the final 10 s of each stage. After 20 min of passive rest, participants performed a ramp protocol (25 W·min−1) to exhaustion starting at 150 W. The highest V˙O2 over a 30-s period was defined as V˙O2peak. Volitional exhaustion and a respiratory exchange ratio greater than 1.15 were used to ensure that V˙O2peak had been obtained.
The control condition involved no prior exercise. The prior heavy exercise protocol consisted of 5 min of very easy cycling exercise (100 W) immediately followed by 5 min of exercise in the heavy domain (50% difference between lactate threshold and V˙O2peak). Participants completed the prior heavy exercise protocol by riding at a low intensity (<80 W) for 60 s before resting passively for 12 min to replicate typical competition. For the self-selected prior exercise protocol, participants were requested to perform their typical prerace regimen. The recovery duration between the prior exercise regimen and the performance trial for the self-selected regimen was determined by the participant as would also be the case under typical race conditions. Before each 4000-m time trial, participants were given the instruction to perform the test as quickly as possible using whatever pacing strategy they deemed appropriate and would typically adopt during competition. Knowledge of elapsed time and distance covered was provided throughout the test, but power output was not. All participants were verbally encouraged to provide a maximal effort during the final stages of all maximal tests. Before the test, participants were permitted to select an appropriate gear ratio within the Velotron software. This allowed the participant to cycle at their preferred cadence for their physical ability, i.e., a fitter athlete would probably select a larger gear ratio allowing him/her to generate more power despite a similar cadence range to a less fit athlete. The same gear ratio was used across all three time trials. This procedure is also performed by cyclists before a track-based time trial because track bikes permit only a single gear ratio throughout a given trial.
During the 4000-m time trial, power output and heart rate were recorded at 33 Hz and subsequently interpolated to 2 Hz. Oxygen consumption was measured breath-by-breath (Metalyser; Cortex, Leipzig, Germany). Expiratory flows were measured using the system's turbine connected to the end of a mouthpiece, while expiration was sampled via a capillary tube inserted into the mouthpiece. The flow turbine and gas sensors were calibrated before each test using a 3-L syringe and gases of known concentrations (β-Standard, 16.0% O2 and 4.3% CO2), respectively. The calibration gas was passed through the turbine and gas sensor before and after each test to check for any drift in calibration. Blood lactate was sampled via a finger prick for subsequent determination of [lactate] before and immediately after prior exercise interventions, 60 s before the start of each 4000-m time trial, and finally 60 s after each trial.
Energy system contribution.
The V˙O2 data were filtered and interpolated to values at 1 Hz. The overall aerobic response (V˙O2; L) associated with each 4000-m time trial was then calculated as the area under the V˙O2-power curve. Calculation of the total anaerobic energy contribution for each 4000-m trial was based on the maximal accumulated oxygen deficit (MAOD) technique (33). This involves extrapolating an individualized V˙O2-power output relationship to calculate the O2 demand at intensities associated with a maximal 4000-m time trial. The total anaerobic energy contribution (MAOD; mL O2·kg−1) was calculated as the sum of the differences between the O2 demand and the measured V˙O2. The aerobic and anaerobic contributions were expressed as percentages of the total estimated energy system contribution. It was assumed that the measured V˙O2 reflected the total rate of energy expenditure and that the previously established V˙O2-intensity of exercise relationship remained valid throughout the time trial. The power output (W) associated with the aerobic and anaerobic contributions was also calculated by extrapolating the individualized V˙O2-power relationship.
Outcome measures (V˙O2 and power output) were interpolated and adjusted to the same distance scale (as opposed to time) to allow direct comparison between trials of different durations. The distributions of data were checked to ensure that the use of parametric statistics was appropriate. Differences in dependent variables that were not time-dependent were assessed using one-way repeated-measures ANOVA, whereas a fully repeated two-way ANOVA was used to compare means and examine the main effects for blood [lactate] and pacing strategy across prior exercise trials. Subsequent Sidak-corrected pairwise comparisons were performed to identify the source of differences from main effects and interactions. Statistical significance was accepted at P < 0.05 and adjusted for sphericity (Huynh-Feldt). The overall contribution from aerobic sources was calculated as the area under the V˙O2-distance curve. Results are presented as means ±SD, with 95% confidence intervals for principal comparisons.
The participants' V˙O2peak (63.7 ± 6.7 mL·kg−1·min−1; 5.0 ± 0.5 L·min−1) and peak aerobic power output (366 ± 39 W) were reflective of their well-trained status and are typical of category 1 cyclists in New Zealand. The individual V˙O2-power relationships were linear (mean R2 = 0.9967) in the range of 40-94% PPO. Cyclists also adopted a wide range of self-selected prior exercise regimens (Table 1). Performance time differed with prior exercise condition (F[1.09, 7.60] = 6.85, P = 0.031), yet Sidak-controlled comparisons did not reveal the source(s) of this difference (Table 2). The mean difference between the control and self-selected priming condition was 7.7 s or 2.2 ± 1.9% (95% CI −0.3 to 15.7 s faster than the control), whereas the difference between the control and heavy priming condition was 7.2 s or 2.0 ± 2.3% (95% CI −2.2 to 16.7 s faster than the control).
Mean power output across the 4000-m time trial differed according to prior exercise condition (F[1.15, 8.06] = 8.50, P= 0.017). Specifically, mean power for the control condition was 21 W or 6.0 ± 5.8% lower than that for the self-selected prior exercise condition (95% CI 1.3-39.6 W; P = 0.037). Although the mean power for the heavy prior exercise condition was similarly higher than that in the control condition (18 W or 5.4 ± 3.6%), this difference was not significant (95% CI −3.2 to 39.1; Table 2 and Fig. 1).
Baseline V˙O2 was not different between conditions; however, pre-time trial V˙O2 for the two interventions was higher than baseline (F[2, 14] = 7.13, P = 0.007; Table 3). Furthermore, V˙O2 just before the time trial was higher for the self-selected condition than the heavy (8.2 ± 2.3 vs 6.2 ± 1.1 mL·kg−1·min−1; F[1, 7] = 7.85, P = 0.026) and control conditions (8.2 ± 2.3 vs 5.8 ± 0.6 mL·kg−1·min−1; F[1, 7] = 10.19, P = 0.015), whereas V˙O2 for the heavy condition was not different from the control. The overall aerobic contribution (area under the V˙O2 curve) during the 4000 m was not different between conditions (∼323 mL·kg−1) nor was the oxygen deficit (∼64 mL·kg−1; Table 3). However, when examined at matched distances (400-m intervals), V˙O2 was higher throughout the first half of the trial for the prior heavy and self-selected prior exercise conditions than the control condition (F[18, 126] = 5.53, P < 0.001; Fig. 2). Power output associated with the aerobic contribution (Fig. 3) was higher for both the prior heavy and self-selected conditions than the control (F[2, 14] = 6.69, P = 0.009). The power associated with the aerobic contribution also differed across time (F[9, 63] = 161.4, P < 0.001), but no condition-by-distance interaction was evident. The proportion of the power output attributed to the anaerobic energy contribution was lower during the initial 800 m of the prior heavy condition (by 22-32 W) than the control and self-selected conditions (by 7-8 W). Nevertheless, the power output attributed to the anaerobic energy contribution was higher for both the prior heavy (by 25-27 W) and self-selected (by 6-18 W) conditions during the final stages of the time trial (F[18, 126] = 3.81, P < 0.001). Typical V˙O2 and aerobic demand data for one participant are shown in Figure 4.
Blood [lactate] did not differ between conditions at baseline (1.1-1.2 mmol·L−1) but responded differently to the prior exercise regimens (F[6, 42] = 12.30, P = 0.001; Table 4 and Fig. 5). Prior exercise raised the blood [lactate] for the heavy condition (by 4.8 mmol·L−1; F[1, 7] = 36.21, 95% CI 2.9-6.6, P = 0.001) and for the self-selected condition (by 2.2 mmol·L−1; F[1, 7] = 10.61, 95% CI 0.6-3.8, P = 0.014). Blood [lactate] after the prior exercise for the heavy condition was also higher than for the self-selected condition (by 2.6 mmol·L−1; F[1, 7] = 18.38, 95% CI 1.2-4.0, P = 0.004). Just before the performance trial, blood [lactate] was higher in the heavy condition than baseline (by 2.5 mmol·L−1; 95% CI 1.0-4.1, P = 0.006) and in self-selected than baseline (by 1.4 mmol·L−1; 95% CI 0.2-2.7, P = 0.03), but these preperformance levels were not necessarily related to performance outcome (Fig. 5). The 4000-m trial raised blood [lactate] equally across the three conditions.
Pacing strategy was examined using mean power for each kilometer. Pacing differed between prior exercise conditions (F[1.18, 8.24] = 8.96, P = 0.014) and across the 4000 m (F[1.29, 8.99] = 4.41, P = 0.05), but there was no interaction of condition and distance on pacing (Fig. 6). Pairwise comparisons revealed that participants paced ∼20 W higher throughout the self-selected than the control condition (95% CI 1.8-37.7, P = 0.032), although the difference between the control and heavy protocol showed a similar pattern with respect to distance but was not statistically higher than in the control condition (P = 0.085). Pairwise comparisons did not reveal the source of the significant distance-related pacing effect.
The main new finding of this study was that a self-selected prior exercise (warm-up or priming) protocol improved overall mean power output (by 6%) and increased V˙O2 (initial 2000 m) during a 4000-m laboratory-based time trial and was equivalent to an imposed heavy-exercise protocol. This was in spite of widely varying self-selected protocols, none of which resembled the heavy priming protocol. Two additional contributions of this study are in supporting recent evidence that (i) prior exercise sufficient to raise blood [lactate] modestly is associated with greater oxygen consumption and improved performance during subsequent severe-intensity exercise and that (ii) total anaerobic energy contribution is unchanged in response to such priming exercise.
The effect of warm-up on performance and energy supply has been studied previously. No change in the overall aerobic component and oxygen deficit with either improved (2) or unchanged performance (1) has been reported during 2 min of all-out kayak ergometry. To our knowledge, the present data are among the first to evaluate the energy demands of simulated cycling competition in response to warm-up. Our data are similar to those of other studies (1,2) in that we also found no difference in the overall aerobic and anaerobic contribution when the entire trial was considered despite improved performance with prior exercise. Although prior exercise was associated with a higher aerobic contribution early in the trials, the total O2 consumed between the conditions was the same, possibly due to the exercise time being less in the prior exercise conditions. Although there was a trend toward higher overall aerobic contribution in response to warm-up, the temporal changes in energy supply could provide more information about performance potential.
The mean power output across the intervention trials was ∼400 W. Previously reported power outputs for Olympic standard pursuit cyclists include 495 W for a male pursuit cyclist competing at a UCI World Cup event (11), although Broker et al. (5) estimated that the current world pursuit record of 251.11 s would have required a mean power output of 520 W for the entire race. Therefore, the population in the present study represents well-trained but not world-class competitive cyclists.
The mean power output across the two intervention trials excluding the rapid acceleration associated with the start was 397 W, which corresponds to 108% of estimated peak aerobic power output determined from the incremental test to exhaustion. The end trial V˙O2 (mean over final 400 m) was ∼61.7 mL·kg−1·min−1 (∼97% of V˙O2peak) and was not statistically different from V˙O2peak. The contributions from the aerobic and anaerobic energy systems when expressed relatively across the full duration of the intervention trials were 84% and 16%, respectively. These data compare favorably with previously reported studies (24) where the aerobic contribution was estimated to be 85% for the current men's 4000-m individual pursuit world record (251 s). The oxygen deficit values also compare favorably with those reported previously for track endurance cyclists. Craig et al. (12) calculated oxygen deficits in highly trained cyclists of 62.1 mL·kg−1 during a 300-s all-out test, compared with 64.0 mL·kg−1 for the current study over a mean duration of 340 s.
It has been suggested that a minor increase in blood [lactate] improves subsequent performance in the heavy (10) and severe domains (8,39). Direct comparisons between studies have been difficult because of variations in the protocols used, particularly the recovery durations. The present study used 5 min of prior heavy exercise with 12 min of passive recovery. Performance time was improved by 2.0 ± 2.3% (95% CI 2.2-16.7 s) and 2.2 ± 1.9% (95% CI −0.3 top 15.7 s) for the prior heavy (P > 0.05) and self-selected conditions (P > 0.05), respectively, whereas mean power output was improved by 5.4% (P > 0.05) and 6.0% (P < 0.05), respectively, which is consistent with previous studies (2,10,13,27). Although there was marked interindividual variation in the nature of the self-selected prior exercise, there was no difference in performance between the two interventions. Furthermore, the difference in the pretrial blood [lactate] between the intervention trials was only ∼1 mmol·L−1, which might indicate that a slight metabolic perturbation is more important than the nature of the prior exercise regimen.
For the self-selected prior exercise condition, participants were instructed to perform a warm-up routine as they would for their most important competition. Typical warm-up routines of national-standard cyclists have not been reported previously; therefore, it is not possible to conclude whether the observed warm-up regimens in the present study are in fact typical. Warm-up durations varied from 11 to 80 min, with a recovery of between 2 and 11 min. The intensity also varied as indicated by the observed work profiles and end warm-up blood [lactate] of 3.3 mmol·L−1, but ranged from 0.9 to 6.6 mmol·L−1. There was also variation in the pretrial blood [lactate], which ranged from 0.9 to 5.1 mmol·L−1. When the pretrial blood [lactate] was expressed in relation to the performance improvement, there was no clear indication of an optimal pretrial blood [lactate], unlike previous data during constant intensity exercise (39).
The characteristics of self-selected prior exercise regimens varied between participants; however, there were some common elements. All participants performed a sustained bout of exercise lasting between 4 and 20 min (one participant 40 min), the relative intensity of which was once again varied but always was low enough so as not to perturb blood [lactate] (i.e., ∼45% PPO). All participants also performed one or more bouts of cycling at a power output associated with V˙O2peak or above. The optimal intensity of prior exercise and recovery duration has received attention in the literature, yet the optimal combination of these two variables remains unclear. However, it seemed from this and previous research (26) that an optimal combination of intensity and recovery duration that elicits an elevated pretrial blood [lactate] (whether causally involved or not) might be optimal for performance, although this is presumably only true if the recovery period is sufficient to allow muscle phosphocreatine concentration to be restored. Almost complete recovery (∼85-95%) of phosphocreatine stores after exercise in the severe zone can take at least 6 min with incomplete recovery still present after 12 min (3,23).
It is acknowledged that there are several major sources of error in the calculation of total anaerobic energy contribution including (i) establishing the linear relationship between work and V˙O2, (ii) the extrapolation of this relationship to higher exercise intensities, and (iii) the maintenance of this relationship throughout the time trial. Although it can be anticipated that the linear relationship would be violated during the early stages of the trials as the ergometer flywheel is accelerated to the desired speed, there was no difference in the mean power between conditions during the first 400-m, and therefore, any violation of the linear relationship during this phase would be consistent between trials. Typically, the trials were not characterized by rapid changes in power output, which would further violate the linear relationship; rather, subtle changes in power were coupled with expected changes in V˙O2. Furthermore, body position was controlled throughout the trials to prevent a shift in the major muscles used.
Several studies have examined the effect of enforced pacing strategies on energy supply using either modeling techniques (14,38) or through the measurement of V˙O2 (17,22). Although pacing strategy was not enforced in the present study (e.g., as a constant intensity), the prior exercise conditions led to no consistent change in pacing strategy other than a higher power throughout exercise (at least for self-selected regimen) in conjunction with higher V˙O2. In contrast, major changes in pacing strategy induced in previous studies have led to either no change in energy supply (19) or no change in overall contribution and minor changes in the time course for the aerobic and anaerobic response (22). Together, these data indicate that pacing strategy per se does not explain the differences in energy system use; rather, the enhanced performance is likely to be associated with higher use of available energy (achieved through an enhanced oxidative contribution to energy turnover).
As expected, the anaerobic contribution increased rapidly during the early stages of the time trial, remaining as high as 7-10% during the midsection and 12-14% during the final 400 m. Foster et al. (18) reported higher values of 20-25% during the midsection and 30-35% during the final 400 m of a 3000-m time trial (mean duration = 296 s). During the present 4000-m trial, an anaerobic contribution was always present, unlike reports from 2000-m time trials (17,19). Furthermore, we observed an increase in power output during the final 400 m of the intervention trials, which was associated with an increased anaerobic contribution. It seems that the terminal increase in anaerobic contribution and, therefore, power output was achieved via less reliance on anaerobic energy from earlier during the trial (Fig. 4). Foster et al. (18) also reported a terminal increase in power output during a laboratory-based 3000-m cycling time trial. As in the present study, the terminal increase in power output was achieved via anaerobic pathways because the measured V˙O2 remained unchanged. Therefore, present and previous (18) data indicate that available anaerobic resources are distributed over an exercise bout regardless of minor variations in pacing strategy or changes in energy system contribution. These results are also consistent with the predictions of the critical power model of exercise tolerance whereby individuals possess a finite exercise capacity at intensities above critical power (34,36).
In summary, prior exercise improves performance during a laboratory-based 4000-m cycling time trial, with there being no difference in performance after either a self-selected prior exercise (warm-up) regimen or an imposed heavy exercise regimen. To optimize performance, athletes are advised to perform a bout of heavy exercise as part of their prior exercise regimen. The prior exercise-mediated performance improvement was not associated with any changes in the overall aerobic contribution or the oxygen deficit, but rather an increased aerobic contribution from the onset of exercise. Athletes seem to manage their energy potential so that both the aerobic and anaerobic reserves contribute throughout the performance bout and to exploit the available anaerobic capacity.
This study was supported by a research grant from Sport and Recreation New Zealand (SPARC). The authors also thank the technical team at the School of Physical Education for their assistance with data collection, in particular Mr. Dene Irvine. Results of the present study do not constitute endorsement by ACSM.
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Keywords:© 2009 American College of Sports Medicine
WARM-UP; ENERGY DISTRIBUTION; O2 DEFICIT; AEROBIC CONTRIBUTION