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1 17 Journal of Exercise Physiologyonline April 2015 Volume 18 Number 2 Editor-in-Chief Official Research Journal Tommy of the Boone, American PhD, Society MBA of Review Exercise Board Physiologists Todd Astorino, PhD Julien Baker, ISSN PhD Steve Brock, PhD Lance Dalleck, PhD Eric Goulet, PhD Robert Gotshall, PhD Alexander Hutchison, PhD M. Knight-Maloney, PhD Len Kravitz, PhD James Laskin, PhD Yit Aun Lim, PhD Lonnie Lowery, PhD Derek Marks, PhD Cristine Mermier, PhD Robert Robergs, PhD Chantal Vella, PhD Dale Wagner, PhD Frank Wyatt, PhD Ben Zhou, PhD Official Research Journal of the American Society of Exercise Physiologists ISSN JEPonline Pacing at vvo 2 Peak: Metabolic and Performance Profile Elias Zacharogiannis 1, Giorgos Paradisis 1, Theofilos Pilianidis 2, Charis Tsolakis 1, Athanasia Smirniotou 1 1 Department of Track & Field, Faculty of Physical Education and Sports Science, University of Athens, Greece, 2 Democritus University of Thrace, Department of Physical Education and Sport Science, Greece ABSTRACT Zacharogiannis E, Paradisis G, Pilianidis T, Tsolakis C, Smirniotou A. Pacing at vvo 2 peak: Metabolic and Performance Profile. JEPonline 2015;18(2): The aim of this study was to investigate the effect of pacing strategies at peak VO 2 velocity (vvo 2 peak) on performance and selected metabolic parameters. Trained subjects (n = 12) performed an incremental test to determine vvo 2 peak followed by a maximal run at constant vvo 2 peak (even-pace strategy, EPS) at least 48 hrs afterwards. Two days after the vvo 2 peak test, the subjects performed the 2nd or 3rd maximal runs in a random order. The second trial started at a pace 1 km h -1 faster than the vvo 2 peak velocity (fast-start pacing strategy, FPS) for half of the duration of the EPS trial with the rest of the test at a pace 1 km h -1 slower than the vvo 2 peak velocity. The third pacing trial started at a pace 1 km h -1 slower than vvo 2 peak velocity (slow-start pacing strategy, SPS) for half of the duration of the vvo 2 peak trial with the rest of the test at a pace 1 km h -1 faster than the vvo 2 peak velocity. Repeated measures ANOVA showed that FPS produced a significantly longer distance of 2654 ± 1668 m (P<0.05) compared with the EPS of ± and the SPS of ± The post-exercise blood lactate concentration was lower (P<0.05) after FPS (14.41 ± 3.51 mmol L -1 ) than after SPS (16.16 ± 3.52) or EPS (16.78 ± 3.52). The accumulated oxygen deficit (AOD) was also lower during FPS (30.92 ± 8.39 ml kg -1 ) than during SPS (40.36 ± 10.86). The results indicate that if the duration of maximal effort varies between 4 and 12 min, an uneven fast pace during the initial stages of exercise will produce better performance (longer distances and exercising time). There are also indications that an early, slightly fast pace produces less overall stress on anaerobic metabolism and that decreased metabolic acidosis may explain the improved performance. Key Words: Pacing, Peak VO 2 Velocity, Running, Performance

2 18 INTRODUCTION The temporal distribution for utilizing energy reserves, which is relative to the duration of maximal effort and/or the distance (i.e., the pacing strategy athletes adopt), influences the development of fatigue and the race performance (1). The majority of published research efforts have examined the role of physiological factors, such as maximal oxygen uptake (VO 2 max), anaerobic threshold, running economy, mitochondrial density, capillarization and muscle fibers, in endurance running performance (30,37,41). Furthermore, there is sufficient evidence to indicate that some ergogenic aids and practices are effective at improving running ability and decreasing the impact of the environment (6,34). It is surprising, however, that since the initial study of Robinson et al. (38), there have been only a few studies that provide systematic data to determine how various pacing strategies might change the outcome of high-intensity running. Using inconclusive experimental evidence, most athletes and coaches use an even-paced strategy to obtain optimal athletic performance (1,20,38). Moreover, conflicting results have been published from studies that examined the effect of performance level on pacing strategy (21,33). Some pacing strategies have been shown to be better than others, mostly depending on the duration of a running event. For example, an all out pace is preferred for sprinting events, where the duration is short, the acceleration phase is relatively long, and the anaerobic capacity is depleted without the detrimental effects of metabolic acidosis (1). In contrast, long-distance runners adopt a more even pace, as indicated by the split times of the world records for the 5 km, 10 km, and marathon (44). This issue becomes more complicated for middle-distance running events where the duration of maximal effort ranges from 2 to 10 min. There are also data showing that a fast start has more advantages that an even pace (4,9,28,33,43). In contrast, other studies suggest that a fairly even pace can be demonstrated to provide greater protection against premature fatigue (19,38), and some studies did not find a significant difference between pacing strategies (8,31). Despite the fact that there is a trend for middle-distance athletes to run faster during the first half of the race while sustaining the pace as long as possible (1,19), there is little systematic evidence to support this practice. In fact, the studies are not comparable due to differences in the exercise duration and intensity, the training status and level of subjects, and the exercise mode. Furthermore, a variety of dependent variables have been measured to investigate the impact of pacing on endurance performance. These variables include work load, time to exhaustion (3), finish time in a time trial (20), power output, VO 2, O 2 deficit (9), lactate levels, O 2 dept (38), and O 2 kinetics (25). The aim of the present study was to investigate the effect of pacing strategies at a running velocity that corresponds to VO 2 peak (vvo 2 peak) on selected metabolic parameters and running performance. The vvo 2 peak parameter was chosen because of its reproducibility and the known large variability between subjects (36). The duration of the maximal effort at this running speed was expected to range between 1 min:40 sec and 8 min:00 sec close to the duration of maximal effort over distances of 800 to 3000 m (36). METHODS Subjects The subjects were healthy Physical Education students (9 males and 3 females). None of the subjects was highly trained. All subjects provided written informed consent to participate in the study after receiving an explanation of the benefits and risks of participation. The university ethics committee approved all testing procedures used in the study. Each subject s percent body fat was

3 estimated for descriptive purposes using a Harpenden skinfold calliper (model 68875, UK) at the bicep, tricep, subscapular and suprailiac skinfold sites (16). The subject s physical characteristics are presented in Table 1. The subjects visited the exercise physiology laboratory on five occasions. Exercise tests were separated by a minimum of 48 hrs. Testing was performed at the same hour of day ± 2 hrs, and the subjects were instructed to consume a light meal at least 4 hrs before testing and to avoid performing any form of intense exercise for the preceding 24 hrs. 19 Table 1. Subjects Characteristics. Mean ± SD Range Age (yr) ± Height (cm) ± Mass (kg) ± VO 2 Peak (ml kg -1 min -1 ) ± HR Peak (beats min -1 ) ± vvo 2 Peak (km h -1 ) ± Ventilatory Threshold (km h -1 ) ± VO 2 peak, HR peak, vvo 2 peak are peak oxygen uptake, peak heart rate and the running velocity which corresponds with VO 2 peak, respectively, measured during the exhaustive incremental test. Procedures All tests were conducted on a treadmill (Technogym Run Race 1200, Italy) in an air-conditioned laboratory with the temperature set at 19 to 21 C. During the first visit, the subjects were familiarized with the experimental procedures and apparatus. On their 2nd visit, 2 d after the familiarization, the subjects completed an incremental test to exhaustion with a starting velocity (that was set during familiarization) of 7 to 12 km h -1 to determine VO 2 peak, vvo 2 peak, and gas exchange threshold (VT). The treadmill speed was calibrated before the test and while the subject ran at different speeds by counting the time required to complete 30 treadmill revolutions. After a 5-min warm-up, the velocity was increased by 1 km h -1 every 2 min until the subject reached volitional fatigue. This protocol has been validated in other studies for the simultaneous determination of VO 2 peak, VT, and vvo 2 peak in runners (27,37,41). Gas was collected during the last 30-sec period of each 2-min stage to allow the subject to attain a steady-state VO 2 (30). During the 3rd visit, a maximal run at vvo 2 peak with an even-pace start (EPS) was performed to determine the time (tlim) to exhaustion, the total distance covered, and the accumulated oxygen deficit (AOD). Following a 10-min warm-up period at 50 to 60% of VO 2 peak and a 5-min rest, the treadmill speed was adjusted to the individual vvo 2 peak of the subject, and the experimenter initiated a 5 sec countdown when the subject was ready to start the test. For safety reasons, the subject stood beside the motorized treadmill belt, and at the start of the countdown, the subject used the support rails to suspend his/her body above the belt while he/she developed the appropriate cadence in his/her legs. Measurements were initiated when the subject released the support rails and started running on the treadmill belt. A hand-held stopwatch was used to record the time to exhaustion to the nearest second. The time to exhaustion was defined as the point at which the subject could not keep up with the belt speed and had to leave the treadmill by touching the hand rails and placing his/her legs to the side of the moving belt. The subjects were blinded to the time elapsed during exercise, and they received strong verbal encouragement to continue until exhaustion.

4 During visits 4 and 5, subjects completed two exercise tests in random order to the limit of tolerance. During these tests, the work rate was controlled to result in a fast-pace start (FPS) or a slow-pace start (SPS). During FPS, the subjects commenced an exhaustive trial at a pace 1 km h -1 faster than the vvo 2 peak pace for 50% of the EPS tlim and at a pace 1 km h -1 slower than the vvo 2 peak pace for the rest of the time until exhaustion. The SPS exhaustive trial started at a pace 1 km h -1 slower than vvo 2 peak for 50% of the EPS tlim with the rest of the time at a pace 1 km h -1 faster than vvo 2 peak (Figure 1). 20 Figure 1. Schematic Representation of the Experimental Protocol of a Subject. In the even pace start (EPS), the subject ran at vvo 2 peak until exhaustion. For the fast pace start (FPS), the subject ran for 191 sec 50% (382 sec) of the tlim vvo 2 peak at 20 km h -1 (1 km h -1 faster than vvo 2 peak) and for the rest of the duration of maximal effort 1 km h -1 slower than vvo 2 peak. In the slow pace start (SPS), the subject ran for 191 sec 50% (382 sec) of the tlim vvo 2 peak 18 km h -1 (1 km h -1 slower than vvo 2 peak), and for the rest of the duration of maximal effort 1 km h -1 faster than vvo 2 peak. The dotted line indicates the duration of the maximal effort and the time point where the speed was changed abruptly. GAS MEASUREMENTS Oxygen consumption (VO 2 ) was measured using the open-circuit Douglas bag method. The subject breathed through a low-resistance 2-way Hans-Rudolph 2700 B valve. The expired gases passed through a 90-cm length of 340-mm diameter flexible tubing to 150-litre capacity Douglas bags. The concentrations of CO 2 and O 2 in the expired air were measured using a Hitech (GIR 250) combined oxygen and carbon dioxide analyzer. The gas analyzers were calibrated continuously against standardized gases (15.35% O 2, 5.08% CO 2 and 100% N 2 ). The expired volume was measured using a dry gas meter (Harvard, U.S.) that was previously calibrated against a standard air flow using a 3 Liter syringe. The barometric pressure and gas temperature were recorded, and respiratory gas exchange data for each work load (i.e., VO 2, VCO 2, V E, and R) were determined on a locally developed computer program based on the computations described by McArdle, Katch, and Katch (35) when V E atps, FECO 2 and FEO 2 are known. The highest VO 2 value obtained during an incremental exercise test was recorded as the subject's VO 2 peak, which also elicited a heart rate within ±10 beats min -1 of the age-predicted HR max, a respiratory exchange ratio (RER) greater than 1.05, and finally, a score at the completion of the test equal to or greater than 19 on the 15-point Borg scale (10).

5 VENTILATORY THRESHOLD ASSESSMENT Criteria described by others were used for the VT detection (14,46). The VT was primarily determined as the VO 2 or work load at which V E began to increase nonlinearly. To determine the onset of hyperventilation, other secondary criteria were used, including the following: 1) a systematic increase in V E /VO 2, 2) a nonlinear increase in VCO 2 and 3) a systematic decrease in FECO 2. The highest testretest reproducibility (r=0.93) and the closest correlation (r=0.96) with LT have been reported by Sucec (42) and Caiozzo et al. (11) when ventilatory transients such as FEO 2, V E /VO 2 and FECO 2, V E /VCO 2 are used for VT detection. When a 2-min incremental protocol has been employed, the workload before a systematic increase in either V E /VO 2 or V E /VCO 2 with a concomitant decrease in FECO 2 can be easily defined. Yoshida et al. (49) examined the use of the Douglas bag technique for VT assessment and found it to be a valid non-invasive measure of the onset of metabolic acidosis (OMA). ACCUMULATED OXYGEN DEFICIT (AOD) ESTIMATION Expired air was collected during the EPS, FPS, and SPS trials every 20 sec for the first 160 sec because all of the subjects were expected to reach peak VO 2 at that time point (22). The individual relationships between the oxygen cost and running velocity were established during the incremental test. The oxygen cost for the FPS (1 km h -1 above vvo 2 peak speed) trial was determined by extrapolation (22). The oxygen deficit for each 20-sec interval was calculated as the difference between the estimated oxygen cost of the exercise and the actual oxygen uptake. The accumulated oxygen deficit, AOD, for 160 sec gave the AOD160. VELOCITY AT VO 2 PEAK (vvo 2 PEAK) The lowest running speed that elicited a VO 2 equivalent to VO 2 peak during the VO 2 peak test was defined as the vvo 2 peak (7). If the final exercise workload was not completed within 120 sec despite an increase in VO 2, then vvo 2 peak was determined using the following equation (29): vvo 2 peak = last workload completed in 120 sec + [(time of the uncompleted workload/120)*1] BLOOD LACTATE ANALYSIS Blood samples were taken from the fingertip within 5 min of the completion of the EPS, FPS, and SPS experimental conditions to determine the lactate levels. To avoid sweat contamination, the first drop of blood was wiped off, and the second drop was used for analysis. The lactate concentration was measured enzymatically (Dr Lange, Cuvette Test LKM 140) using an LP 20 Plus miniphotometer (Dr Lange, Germany). Blood was taken using 10 μl end-to-end capillaries and was placed in a reagent solution that hemolyzed the blood. Lactate was processed in a reaction that produced quinoneimine in proportion to the amount of lactate in the sample, and the concentration of quinoneimine was measured in an LP 20 Plus apparatus at 540 nm (576 THz) after a 3-min reaction time. HEART RATE Heart rate (HR) was recorded every 5 sec throughout the exercise tests using short-range telemetry (Polar S 710, Polar, Finland). 21 STATISTICAL ANALYSIS Differences in the metabolic response, including the time to exhaustion and the distance run, between the three pacing strategies were assessed using analysis of variance. In the case of a significant F- ratio, a Tukey post hoc test was applied. The 95% level of confidence was chosen in all statistical

6 analysis. The data are presented as the mean ± SD. All statistical analyses were conducted using the SPSS statistical software (version 21, Chicago, USA). 22 RESULTS The subjects mean VO 2 peak, vvo 2 peak, VT, and HR max after the incremental test were ± 8.14 ml kg -1 min -1, ± 2.33 km h -1, ± 2.18 km h -1, and ± 5.88 beats min -1, respectively (Table 1). The total distance (Figure 2) and the duration of maximal effort after FPS (Table 2) were significantly higher ( ± 1668 m and ± sec, respectively) compared with those after EPS ( ± m and ± sec, respectively) and SPS ( ± m and 457 ± sec, respectively) * Total distance (m) EPS FPS SPS Pacing strategies Figure 2. Total Distance Run by the Subjects after EPS, FPS, and SPS (Mean ± SD). *P<0.05 significantly different from EPS and SPS. Table 2. Physiological Responses to Exhaustive Exercise after Using Different Pacing Strategies (Mean ± SD). Even-Pace Strategy (EPS) Fast-Start Pacing Strategy (FPS) Slow-Start Pacing Strategy (SPS) VO 2 Peak (ml kg -1 min -1 ) ± ± 7.71# ± 7.12 Time to Exhaustion (sec) ± ± * 457 ± Peak HR (beats min -1 ) ± ± ± 5.15 Total Distance (m) ± ± 1688* ± AOD 160 (ml kg -1 ) ± 9.32# ± 8.39# ± O Consumed (ml kg -1 ) ± 15.88# ± 16.69# ± Blood Lactate (mmol L -1 ) ± ± 3.51* ± 3.52 *Significantly different from EPS and SPS (P<0.05), #Significantly different from SPS. EPS, FPS, and SPS: even, fast and slow pacing start correspondingly; AOD 160 and O 2 160: accumulated O 2 deficit and measured oxygen consumption during the first 160 sec of the exhaustive trials respectively.

7 The post-maximal effort blood lactate concentration (Figure 3) appeared to be significantly lower (P<0.05) after FPS (14.41 ± 3.51 mmol L -1 ) than after EPS (16.78 ± 3.66 mmol L -1 ) and SPS (16.16 ± 3.52 mmol L -1 ). The mean ± SD peak oxygen uptake value (Table 2) during the first 160 sec after SPS (47.08 ± 7.12 ml kg -1 min -1 ) was lower (Figure 4) than the incremental test VO 2 peak value (54.28 ± 8.14 ml kg -1 min -1 ) and the value after FPS (52.37 ± 7.71 ml kg -1 min -1 ). However, the mean value of the FPS 160VO 2 peak (Table 2) was not different from the incremental VO 2 peak or from the EPS value Blood lactate (mmol.l-1) * EPS FPS SPS Pacing strategies Figure 3. Blood Lactate Levels after EPS, FPS, and SPS (Mean ± SD). *P<0.05 significantly lower from EPS and SPS VO2 ml.kg-1.min * Incremental EPS FPS SPS Figure 4. VO 2 Peak Values for the Incremental Test and during the First 160 sec after EPS, FPS, and SPS (Mean ± SD). *Different from incremental and FPS (P<0.05)

8 The mean AOD (Figure 5) during the first 160 sec (Table 2) was lower in FPS (30.92 ± 8.39 ml kg -1 ) and EPS (33.88 ± 9.32 ml kg -1 ) than in SPS (40.36 ± ml kg -1 ). The mean total O 2 consumption during the first 160 sec also showed similar differences between the groups. It was higher in FPS ( ± ml kg -1 ) and EPS ( ± ml kg -1 ) than in SPS ( ± ml kg -1 ) AOD 160 ( ml.kg-1) * EPS FPS SPS Pacing strategies Figure 5. Accumulated Oxygen Deficit (AOD) Values during the First 160 sec of the Exhaustive Trials (Mean ± SD). *Significant different from EPS and FPS. The mean HR peak values (Table 2) during EPS (198.3), FPS (195.9), and SPS (197 beats min -1 ) were lower than mean HR peak value (Table 1) after the exhaustive incremental trials (203.6 beats min -1 ). DISCUSSION The results of the present study show that a fast-start pacing strategy allowed the subjects to cover more distance and/or resist fatigue for a longer time. To our knowledge, this study is the first to demonstrate the positive effects of fast-start pacing for a maximal running effort lasting 4 to 12 min, which corresponds to approximately 1500 to 3000 m running races. The results that are possibly the most comparable to ours are those of Ariyoshi et al. (1979), where the researchers investigated whether variable pacing during a 1400 m test that lasted 4 min could influence the performance in a subsequent running trial at a standard velocity. Their results indicated that a fast-slow pace during the first test enabled the subjects to cover a longer distance in the second all out 370 m min -1 velocity test. In addition, compared with the slow-fast or even pace, the fast-slow pace during the initial 1400 m run led to faster O 2 kinetics and decreased perception of effort (3). Similarly, Jones et al. (28) demonstrated using a cycle ergometer that relative to an even pace or a slow-start pace, the fast-start strategy increased the total VO 2 and the VO 2 at a discrete time point (120 sec) during the transition from rest to exercise. These authors also reported a lower post-exercise blood lactate level and better performance using a fast-start pacing strategy. They postulated that a fast-start pacing strategy might extend the supramaximal time to exhaustion by

9 enabling a greater contribution of oxidative metabolism to the total energy turnover and thereby extending the time before the finite capacity of the non-oxidative ATP supply is exhausted (28). Another systematic study that supports the adoption of an all out strategy is that of Bissop et al. (9) with kayak paddlers. The results of that study indicated that the 2-min kayak performance was significantly better following an all-out fast-start strategy compared with that after an even-paced strategy. These authors also attributed the increased performance after the fast-start pacing to faster VO 2 kinetics. Gosztyla et al. (22) examined 5 km pacing strategies on a treadmill with female club-level runners. When the first 1.63 km were run at even, fast (3%) and faster (6%) paces, the runners covered the 5 km racing distance in 21:11 (min:sec) ± 29 sec, 20:52 (min:sec) ± 36 sec and 20:39 (min:sec) ± 29 sec, respectively. Despite the improved 5 km performance after the 3% and 6% faster start pacing strategies, however, the metabolic responses did not differ between the pacing strategies. Descriptive data for the world records for the 1500 m and the mile (44) with a maximal effort falling within the range of the maximal effort during the constant load trials of the present work appeared to follow an inverse j shape; the first 400 m section of the race was faster than the second and third sections, and there was a slight speed increase during the final 400 m. Moreover, Garland (20) analyzed the pacing strategy adopted by elite competitors in 2000 m rowing events and revealed that all rowers follow a fast-start pacing strategy independently of the performance level or sex. The athletes usually row faster during the first 500 m of a 2000 m race, and they slow down afterwards (20). Although these descriptive studies have presented the self-selected pacing strategies of elite middle-distance runners and all levels of rowers, they do not provide clear physiological evidence for the advantages of a fast start. Instead, they only hypothesize that the benefit may result from increased blood flow, ventilation, and O 2 uptake (20). Our results do not agree with those of Leger and Ferguson (31). In that study, the effect on the onemile performance of the two pacing strategies have not been published, while the authors also did not notice measurable differences in the metabolic data during the first three quarters of the mile. The lack of a significant difference between the pacing strategies may be attributed to the small difference in speed between the two conditions and the low mean exercise intensity (90% VO 2 max), as the authors note. A later study by Billat et al. (8) confirmed that low variations in running speed do not improve running performance or significantly change the oxygen kinetics and the volume of oxygen consumed. Thus, it can be concluded that larger changes in intensity will result in larger differences in VO 2 and VO 2 kinetics or plasma lactate levels and O 2 deficit (1). In the present study, we chose an even pace near 100% vvo 2 peak, and the ± 7% speed difference made the effects of the fast or slow-start pace more detectable. The studies of Aisbert et al. (2), Chaffin et al. (13), Foster et al. (18) and Liedl et al. (32) present findings that conflict with those of our study concerning the efficacy of pacing strategies on maximal exercise performance. This disagreement may be explained by differences inherent to the mode of exercise, the duration and intensity of the maximal exercise, and the type of tests employed. 25 EFFECT OF PACING STRATEGY ON VO 2 The highest VO 2 attained in the present study during the first 160 sec of the maximal even-start (EPS) and fast-start (FPS) pacing trials was similar to the VO 2 peak measured during the incremental test. At the same discrete time point during SPS, the VO 2 peak value could not reach the corresponding value for the incremental trial. These findings are consistent with the results of previous studies (2,4,19). It seems that the greater total O 2 consumed during FPS resulted from the increased O 2 uptake and the enhanced VO 2 dynamics. As has been mentioned, the absolute rate of

10 change in VO 2 following the onset of exercise is proportional to the imposed work rate and thus, proportional to the muscle ATP turnover rate (47,48). Other running data also elucidate the influence of pacing strategy on the VO 2 response in middledistance events and indicate that an early acceleration or a race-simulation pace results in a higher VO 2 response (4). Furthermore, it seems that for shorter distances (800 vs m), a higher starting velocity evokes faster VO 2 kinetics (15); however, this change has not always been correlated with better performance. The cycling study of Jones et al. (28) also confirmed the greater contribution of aerobic metabolism early in exercise as a result of a fast-slow pacing strategy. In particular, the researchers indicated that this practice provoked a faster adjustment of VO 2 and a conservation of anaerobic reserves. These changes positively affected the performance in a 120 sec task at a pace greater than the critical velocity, as indicated by the longer time to exhaustion and the power output of the subjects. In contrast with these suggestions, the findings of other authors demonstrate that the optimal pace for events that are longer than 2 min is an even pace (17,18). A major argument for this suggestion is the protection against the premature fatigue caused by early metabolic acidosis. Many years ago, Robinson et al. (38) determined that for a fast start, running was less efficient and required more O 2, whereas for a more even pace, the same distance could be covered more economically and with less fatigue. However, evaluating the anaerobic contribution using O 2 dept is now questionable. A review indicated that the theoretical support (1) for an even-pacing strategy for prolonged locomotives events (>2 min) is primarily based on critical power models and mathematical laws of motion, which theorize that speed is the result of the maximal constant force a runner can exert and the resistive forces of the environment (air speed, surface, and temperature). These models also suggest that as a runner accelerates, a greater percentage of energy is spent to overcome the resistance of air than to produce forward motion. In a systematic study, Foster et al. (19) concluded that a 51 to 49% distribution of the total exercise time between the two halves of a 2 km cycling time trial enables subjects to finish faster, but the researchers could not provide a physiological explanation. The decrease in the overall triathlon performance for a starting pace that is 5% faster or 10% slower for the first km than for the 10-km control running speed was also reported in a more recent study using triathletes (26). The discrepancy between these data and those of running studies could be attributed to the different exercise mode. A comparison of the VO 2 kinetics between treadmill and cycle ergometry (12) revealed that for exercise intensities above the anaerobic threshold, the amplitude of the primary component of VO 2 is lower and the amplitude of the slow component is higher in cycling due to differences in fibre recruitment. Therefore, it can be assumed that cycling provokes earlier fatigue; thus, the pace that maximizes performance may not be the same as that for running. However, Hanon et al. (25) investigated the impact of pacing strategies on the O 2 kinetics during a 1500 m track race event and reported a negative correlation between the starting velocity, which was expressed as a % of vvo 2 max, and the final performance. Furthermore, the data showed that the athletes chose to start fast and follow an even pacing velocity while managing to attain VO 2 max in contrast with treadmill studies (40). Finally, the authors suggest that a fast start may help athletes to begin aerobic metabolism earlier, but the metabolism should require the least amount of oxygenindependent glycolysis and should preserve buffering capacity for the later stages of the race. The significance of maintaining exercise intensity within certain critical limits is extensively outlined in the review by Abbiss and Laursen (1). According to the authors, the adoption of a fast pacing strategy depends on the ability of the subjects to resist fatigue. In addition, the self-selected exercise intensity 26

11 is influenced by the rate, the capacity of various physiological systems (aerobic, anaerobic) and even psychological or environmental parameters. In line with these conclusions, a later review (45) analyzed pacing strategy from a more holistic perspective using an anticipatory feedback-rpe model. EFFECT OF PACING STRATEGY ON BLOOD LACTATE LEVEL AND AOD The other significant observations of the present study were the lower blood lactate concentration after FPS compared with that after SPS and EPS and the lower accumulated oxygen deficit (AOD) during FPS and EPS compared with that during SPS. Both are used to evaluate the anaerobic energy release, and AOD in particular is considered to be the most accurate method together with needle biopsy (21). Therefore, it seems that during FPS, the contribution of anaerobic metabolism to the total energy release was lower than that during EPS and SPS. This finding is only confirmed by Jones et al. (28), who reported a possible retardation of the accumulation of fatigue metabolites, such as H +, that increase the AOD. The majority of the studies did not find any difference between the pacing protocols regarding the previous metabolic parameters (8,9,19,31,32), except for one study (4) in which the researchers observed lower blood lactate concentrations and O 2 debt after the completion of a 4-min run following a fast pacing strategy. However, the use of O 2 debt to measure the contribution of anaerobic metabolism has been disputed because O 2 debt has been demonstrated to overestimate the anaerobic energy release (5). The possible attenuated use of anaerobic metabolism could be compensated by the higher contribution of aerobic metabolism. According to this assumption, faster running during the initial stages of the maximal test caused either the cardiorespiratory system or intracellular oxidative metabolism to adapt earlier, resulting in higher VO 2. Ariyoshi and colleagues (3) have also reported a higher VO 2 response during a pacing strategy with a fast start. This higher V O 2 response was particularly noted during the first minute of exercise and did not decrease substantially when the pace became slower. The authors concluded that the greater early mechanical effort forced the ontransient O 2 kinetics by increasing the blood flow of the working muscles and oxidising the detrimental anaerobic by-products, such as lactate. The study of Sandals et al. (40) reported that an accelerated start could induce better perfusion and recruitment of muscle fibres. In addition, a rapid decrease in muscle ph might also increase the O 2 demand and thus result in a rapid O 2 supply. Duffield et al. (15) tried to investigate the differences in the VO 2 response between 800, 1500, and 3000 m races. During those tests, the researchers noted that the acceleration of the VO 2 kinetics in the 800 m event, particularly the higher amplitude of the A1 component, was negatively correlated with AOD, indicating a reduced anaerobic contribution. In the study of Jones et al. (28), the researchers specifically contend that the increased ATP turnover possibly provided a greater stimulus for muscle VO 2, leading to faster VO 2 dynamics and finally, higher exercise tolerance. Compared with that study, where the volunteers cycled above critical velocity for 120 sec, the present study extended the duration of exercise for which a fast pacing strategy may positively affect VO 2 kinetics before the depletion of the anaerobic energy supply and the appearance of premature acidosis. Thus, a plausible explanation for the better performance following the fast pacing protocol is that the higher external mechanical effort and intensity at the start of exercise provoked an accelerated adaptation of aerobic metabolism by increasing the total VO 2, particularly the amplitude of the primary component of VO 2. Regarding the mechanism that regulates the speed of the VO 2 response during the primary phase, there is an assertion that it is linked to intramuscular factors, including the rate of PCr degradation (39). Others have found a proportionality between the products of PCr splitting and VO 2 (22), thus 27

12 providing further confirmation for this suggestions. Bishop and colleagues (9) and Duffield and colleagues (15) also suggest that a fast pace might enhance total V O 2 and that the enhancement could be attributed to increased PCr breakdown. 28 CONCLUSIONS The findings of the present study suggest that if the duration of maximal running effort at VO 2 peak ranges between 4 to 12 min, a fast-start pacing strategy will produce better performance, which is expressed as a longer run distance and exercise time. Furthermore, there are indications of attenuated anaerobic energy release. The slightly faster pace at the initial stages of exercise most likely caused increased PCr degradation and forced the adaptation of either the O 2 delivery system or the intracellular oxidative metabolism, resulting in a higher total VO 2, decreased metabolic acidosis, and better performance. Address for correspondence: Elias Zacharogiannis, PhD, University of Athens, Department of Physical Education and Sports Science, Ethnikis Adistasis 41, Dafni 17237, Athens, Greece, elzach@phed.uoa.gr REFERENCES 1. Abbiss CR, Laursen BP. Describing and understanding pacing strategies during athletic competition. Sports Med. 2008;38: Aisbett B, Rossignol P, Sparrow W. The influence of pacing during 6-minute supramaximal cycle ergometer performance. J Sci Med Sports. 2003;6: Ariyoshi M, Tanaka H, Kanamori K, Obara S, Yoshitake H, Yamaji K, Shephard RJ. Influence of running pace upon performance: Effects upon oxygen intake, blood lactate and ratings of perceived exertion. Can J Appl Sports Sci. 1979;4: Ariyoshi M, Yamaji K, Shephard. R. Influence of running pace upon performance: Effects upon treadmill endurance time and oxygen dept. Eur J Appl Physiol. 1979;41: Bangsbo J, Gollnick P, Graham T. Anaerobic energy production and O 2 deficit-dept relationships during exhaustive exercise in humans. J Physiol. 1990;422: Bell D, McLellan T. Effect of repeated caffeine ingestion on repeated exhaustive exercise endurance. Med Sci Sports Exerc. 2003;35: Billat V, Renoux J, Pinoteau J, Petit B, Koralsztein J. Times to exhaustion at 100% of velocity at V O 2 max and modelling of the time-limit / velocity relationship in elite long-distance runners. Eur J Appl Physiol. 1994;69: Billat V, Slawinski J, Danel M, Koralsztein J. Effect of free versus constant pace on performance and oxygen kinetics in running. Med Sci Sports Exerc. 2001;33:

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