Explaining sports performance is complicated, even in comparatively simple "pursuit" sports where power output and power losses are the primary performance-related variables. Due to the complexity of sports performance and the difficulty in experimentally controlling the behavior of athletes, mathematical models are attractive devices for exploring effects attributable to training, ergogenic aids, equipment, and tactics. We have performed several studies using an energy balance model developed in our laboratory (10,11,32), where both expressions for biomechanical factors and energy supply have been manipulated to predict performance (25). To model sports performance, it is necessary to make several assumptions involving the parameters of energy supply and energy losses. We have demonstrated a time- or distance-dependent pattern of anaerobic energy use (10,13,14,20), and a recent report from our laboratory has demonstrated the relative constancy of the anaerobic capacity in response to different patterns of total power output (e.g., pacing strategy) (18). An untested assumption in our model is the pattern of V˙O2 response during supramaximal exercise intensity, typical of speed skating, athletics, swimming, and track cycling competitions. A fast start strategy appears to accelerate the V˙O2 response (4,21). However, to our knowledge, there are few data regarding V˙O2 response during supramaximal exercise intensities (9,19,34,37), particularly when the power output is free to vary rather than the square wave manipulations of power output that are traditionally used in studies on V˙O2 kinetics (1-3,6-9,12,15,19,22,23,26-31,33-37).
Numerous studies have been performed investigating V˙O2 response. It has been shown that V˙O2 kinetics are affected by different warm-up protocols potentially leading to subsequent performance benefits (5,7,8,12,15,16) and are influenced by training status (6,23,24). Also, several studies have investigated the influence of exercise intensity on V˙O2 response but have shown different outcomes (1,2,9,19,21,23,26,27,31). Relatively little research has been performed at work rates exceeding peak V˙O2. Because the aerobic system is maximally stressed in the supramaximal domain, changes in the V˙O2 response to exercise have great implications on the use of the anaerobic capacity and are thus relevant for sports performance. Additionally, although the V˙O2 response to exercise has mostly been modeled in square-wave exercise bouts (1-3,6-9,12,15,19,22,23,26-31,33-37), sports performance is often characterized by a large short-duration burst of power output at the commencement of exercise (10,13,14). To address this gap in our understanding about how to construct models of high-intensity exercise performance, the present study was designed to measure and model the V˙O2 response to exercise during supramaximal time trial exercise representative of that undertaken during competition. Time trials of maximal effort were performed, and the V˙O2 response was hypothesized to be invariant with starting intensity in the supramaximal domain.
Nine well-trained male cyclists participated in this study (Table 1). All subjects gave written informed consent before entering the study. The experiment was approved by the ethics committee of the Faculty of Human Movement Sciences at the VU University Amsterdam (The Netherlands). The subjects were requested to follow their usual diets and to lessen physical activities the day before each trial, just as they would before a competition.
Four maximal effort time trials (mean power output > 100% P V˙O2max) were completed by each subject: 750, 1500, 2500, and 4000 m. All tests were done on separate days and at the same time of the day. All time trials commenced after a 10-min submaximal warm-up protocol was completed, including two 5-s all-out sprints and followed by a cooling down period as described by Hettinga et al. (18). The warm-up protocol was standardized so that results could not be attributed to differences in prior exercise (5,7,8,12,15,16). Between warm-up and the beginning of the time trial, 3 min of rest was allowed. For the time trial, the subjects were instructed to finish as fast as possible. Athletes were provided with distance and velocity feedback, as they would be in competition. Subjects performed all trials on a custom-made electronically braked laboratory cycle ergometer (FBW-MTO, Amsterdam, The Netherlands) designed to simulate competition. Torque and crank rotational velocity were measured directly. Pedaling cadence, power output, virtual velocity, and virtual distance were calculated based on these measurements and gear ratio. The ergometer was linked to a computer, which continually measured and stored mechanical power output (P tot), pedaling cadence, and torque at 20 Hz. Handlebars and saddle height were adjusted to the preferences of the subject and were kept constant for each trial. All subjects first completed a maximal incremental test to measure maximal rate of oxygen consumption (V˙O2max) and maximal power output (P V˙O2max). On a second day, the subjects cycled 1500- and 4000-m habituation time trials at maximal intensity, with a 30-min rest between trials. Subsequently, the experimental time trials were performed in random order, with 48-96 h between trials.
Respiratory gas exchange was measured breath-by-breath using open circuit spirometry (Oxycon alpha, Mijnhardt, The Netherlands) and afterward interpolated to 1-s values. The flow meter and gas analyzer were calibrated before each test using a 3-L syringe (Jaeger, Germany), room air, and a standard gas mixture. Blood lactate concentration (BLC) was measured 3 min after finishing each time trial from a fingertip and was analyzed using dry chemistry (Lactate Pro; Arkray Inc, Kyoto, Japan). Conforming to our procedures in other modeling studies (10,11), V˙O2 response was fit by a least-squares monoexponential model (1,3), minimizing the sum of squared error, and was modeled monoexponentially according to equation 1, with an error defined as the sum of squared errors per number of samples. For 750 m, V˙O2 response was fit over 54 s (duration of fastest 750 m). For 1500, 2500, and 4000 m, V˙O2 response was fit over 114 s (duration of the fastest 1500 m).
V˙O2rest is the average over 1 min of V˙O2 immediately before exercise, t is the time, A is the asymptotic amplitude, τ is the time constant, and td is the time delay of the V˙O2 response. Because the cardiodynamic component does not directly represent active muscle O2 utilization (26), the V˙O2 response was calculated from the first point after the cardiodynamic phase based on visual inspection for each trial. Depending on this point, the first 10 to 20 s was omitted from the fitting field. For 1500, 2500, and 4000 m, the value of A at 114 s (duration of the fastest 1500-m time trial) was calculated (A end) to allow comparison of amplitudes at the same moment in time. Because the 750-m time trial was of shorter duration, A end was calculated at 54 s (based on the shortest 750-m time trial). To characterize and to compare the V˙O2 responses, mean V˙O2 over the first part of the race was calculated, and mean response time (MRT) was calculated as MRT = td + τ.
V˙O2 responses were compared using a one-way repeated-measures ANOVA. To reveal significant differences between trials in case of a significant main effect, paired sample t-tests were performed. The significance level was set at P < 0.05.
All subjects completed the time trials without problems. Mean P tot profiles are shown together with standard deviations in Figure 1. Power output was normalized to P V˙O2max as determined in the incremental test. In Table 2, final time and mean values for P tot and V˙O2 were shown. Mean V˙O2 and P tot were calculated over the first 114 s. For 750 m, mean V˙O2 and P tot were averaged over the first 54 s (duration of the fastest 750-m time trial). Mean V˙O2 was also calculated over the first 15 s (V˙O215), the first 30 s (V˙O230), and from 15 to 30 s (V˙O21530).
Mean V˙O2 during the time trials is shown in Figure 2, together with standard deviations. V˙O2 response was fit through these mean data. Results are shown in equations 2 to 5 and plotted in Figure 3.
Also, individual V˙O2 data were fit per subject to make statistical analysis and comparisons possible. Parameters of the V˙O2 response are shown in Table 3 as well as a typical example of the V˙O2 response and the residuals in a 1500-m time trial in Figure 4. Comparing A end + V˙O2rest (L·min−1) values with V˙O2max (4.5 ± 0.2 L·min−1) attained at the incremental test, differences were significant with all but the 1500-m time trial.
The present study was designed to observe the V˙O2 response in maximal effort competitive simulations. All time trials were characterized by an initial burst of power output during the first 15 s, which is an important difference between the competitive exercise and the square wave exercise that is ordinarily used in studies of V˙O2 kinetics. In 750 m, the initial burst in power output was larger than that in all other trials. Simultaneously, the V˙O2 response was accelerated in the 750-m time trial, as shown by a significant reduction in MRT compared with all other trials (see also Fig. 3). It seems that the initial burst of power output, which is so characteristic for sports performance and was apparent in all exercise conditions, is of fundamental importance in terms of defining V˙O2 response. When the mean V˙O2 over the first 30 s of exercise, was studied no differences were found, mainly because V˙O2 over the first 15 s, a period corresponding with the time delay (11.6-13.8 s), was not differing. From seconds 15 to 30, a significant higher mean V˙O2 was found for 750 m and also 1500 m compared with 4000 m. Accordingly, our experimental hypothesis was not supported. Jones et al. (21) also found that a fast start strategy resulted in a more rapid increase in V˙O2 during high-intensity exercise (exhaustion in 120 s) compared with a slower start strategy. Also, an initial burst in power output over the first 15 s of 500-m kayaking has been shown to result in a faster V˙O2 response over the first 30-45 s of exercise, resulting in a significant increase in mean power output (4). A possible explanation for the faster V˙O2 response in the time trial with the higher initial burst might be linked to the phosphocreatine (PCr) response to exercise. It has been shown that the time constants of decreases in [PCr] are identical with simultaneously measured V˙O2 on-kinetics of the primary component (29). This equality was also present at high-intensity exercise (30), supporting the concept that V˙O2 kinetics are determined by intramuscular mechanisms. The higher initial burst in peak power could be a signal to accelerate oxidative phosphorylation and apparently lead to a faster increase in V˙O2 on response, as is shown by the present data.
Although the high-intensity domain has received attention in literature, exercise intensities that substantially exceed P V˙O2max have not been studied extensively. It has been found that nitric oxide-dependent metabolic inertia represents an important limitation to V˙O2 kinetics after the onset of high-intensity cycle exercise (37), where O2 transport limitations were shown not to constrain V˙O2 response (36). Further, the gain of V˙O2 response was reduced at intensities above critical power (26,31,34). This was suggested to be caused by a direct effect of acid pH on mitochondrial respiration. Also, at higher intensities, anaerobic metabolism is becoming of increasing importance, and V˙O2 will be constrained by the attainment of V˙O2 peak. A lower response amplitude is reached than the one predicted by the V˙O2-workrate relation, and the V˙O2 response in supramaximal exercise is thus truncated, resulting in relatively higher τ values (19,33) compared with submaximal intensities. A semilog model takes (19) this into account and assumes a predicted V˙O2 beyond the upper limit of V˙O2, resulting in a slower τ (9,33). Because this predicted V˙O2 cannot be attained in real life, as also noted by Carter et al. (9), it is not suitable for modeling the V˙O2 response to describe athletic performance in competitive exercise, where we are mainly interested in describing the actual V˙O2 response during time trial exercise. MRT shows that the response is clearly fastest at 750 m (Fig. 4).
For the present results, the main intention was to describe V˙O2 response in competitive exercise to test assumptions necessary for modeling sports performance as has been previously done in studies from our lab (10,11,32) and elsewhere (25). For 1000 m (∼1 min) and 4000 m (∼6 min) cycling (10,25) and 1500 m (∼2 min) speed skating (11), modeling studies have led to accurate predictions of performance and excellent fits of V˙O2 response with a monoexponential model, with correlation coefficients ranging from 0.94 to 0.98 (25). As discussed, the initial burst of 10-15 s seems to be of fundamental importance in speeding V˙O2 kinetics. Additionally, at 114 s, V˙O2 values were only about 0.1 L·min−1 lower than the V˙O2max attained at the incremental test, and in ∼20 s from start, 63% of the final amplitude was already reached. Apparently, values close to maximum V˙O2 can be reached well within 2 min of strenuous exercise, at least in well-trained (23) and warmed-up (12,15) athletes. A end of the 1500-, 2500-, and 4000-m time trials did not differ largely. Only during the 750-m time trials did athletes reach a lower maximum during exercise from baseline, which was probably caused by the shorter endurance of the event. Looking at the absolute amplitude, differences were found between 1500 m and all other trials but were within a range of ∼0.2 L·min−1. It thus seems that for middle-distance exercise, about the same pattern of V˙O2 response was found, as was already observed in a previous study (17), where different pacing strategies were mainly determined by differences in distribution of anaerobic energy, whereas aerobic energy contribution globally followed the same profile for differently paced supramaximal 4000-m cycling time trials.
A remaining question is how much the V˙O2 response is influenced by the nature of the athlete and the nature of the sport. In the present study, we used very well-trained subelite athletes, with an MRT of 18.8 s on a 1500-m cycling. In an earlier report from our laboratory (11), we noted an even faster V˙O2 response with an MRT of 15.2 s during simulated speed skating competition of a 1500-m time trial in elite junior speed skaters (including the Junior World Champions and holders of 7 of 11 recognized Junior World Records). MRT for a fast start cycling time trial of ∼120 s (but not with the characteristic burst in peak power) in recreationally but not highly trained cyclists was 37-40 s (21). In submaximal exercise, where truncation of the V˙O2 response does not influence time constants, fastest τ values were 8-10 s, observed in well-trained athletes (23). Training status has been shown to increase speed of muscle V˙O2 kinetics (24), and trained individuals exhibit a faster V˙O2 response compared with untrained individuals (23). Although the influence of training on V˙O2 response has been well documented, it is still uncertain what the best actual type of training is to optimize V˙O2 response (22). On the basis of the present results, it might be favorable to train the V˙O2 response not only by aerobic training but also by intensive interval training. In terms of modeling, there is understandably an interest in modeling the behavior of elite athletes. It may be that even if the relative intensity of the start has little effect on the V˙O2 response to exercise, these individuals still have remarkably fast V˙O2 kinetics. Likewise, at the other end of the performance continuum, sedentary individuals or patients with cardiorespiratory pathologies have slow V˙O2 kinetics (28) that need to be taken into account when modeling human locomotor activities.
The higher initial burst in peak power output in 750 m was accompanied by a faster V˙O2 response. To make optimal use of the aerobic system, the initial burst of power output that is characteristic for time trial exercise of maximal effort seems to be of high importance.
The results of the present study do not constitute endorsement by ACSM. The authors would like to acknowledge the efforts of Lennart Teunissen, Emiel Meijer, Wim Groen, and Luuk Goede in the process of collecting data for this experiment.
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Keywords:© 2009 American College of Sports Medicine
PERFORMANCE; COMPETITION; OXYGEN UPTAKE KINETICS; MODELING; POWER OUTPUT; AEROBIC POWER