17
Journal of Exercise Physiologyonline
April 2015
Volume 18 Number 2
Editor-in-Chief
Official Research Journal
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of theBoone,
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BoardPhysiologists
Exercise
Todd Astorino, PhD
ISSN PhD
1097-9751
Julien Baker,
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
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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 1097-9751
JEPonline
Pacing at vVO2 Peak: Metabolic and Performance
Profile
Elias Zacharogiannis1, Giorgos Paradisis1, Theofilos Pilianidis2,
Charis Tsolakis1, Athanasia Smirniotou1
1
Department of Track & Field, Faculty of Physical Education and Sports
Science, University of Athens, Greece, 2Democritus University of Thrace,
Department of Physical Education and Sport Science, Greece
ABSTRACT
Zacharogiannis E, Paradisis G, Pilianidis T, Tsolakis C, Smirniotou
A. Pacing at vVO2peak: Metabolic and Performance Profile. JEPonline
2015;18(2):17-31. The aim of this study was to investigate the effect of
pacing strategies at peak VO2 velocity (vVO2 peak) on performance and
selected metabolic parameters. Trained subjects (n = 12) performed an
incremental test to determine vVO2 peak followed by a maximal run at
constant vVO2 peak (even-pace strategy, EPS) at least 48 hrs
afterwards. Two days after the vVO2 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 vVO2 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 vVO2 peak velocity. The third
pacing trial started at a pace 1 km·h-1 slower than vVO2 peak velocity
(slow-start pacing strategy, SPS) for half of the duration of the vVO2
peak trial with the rest of the test at a pace 1 km·h-1 faster than the vVO2
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 2001.67 ± 839.63 and the SPS of 1975.83 ± 791.22. 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 VO2 Velocity, Running, Performance
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 (VO2 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, VO2, O2 deficit (9), lactate levels, O2 dept (38), and O2 kinetics (25).
The aim of the present study was to investigate the effect of pacing strategies at a running velocity
that corresponds to VO2 peak (vVO2 peak) on selected metabolic parameters and running
performance. The vVO2 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
19
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.
Table 1. Subjects’ Characteristics.
Age (yr)
Height (cm)
Mean ± SD
Range
22.75 ± 0.97
22-25
176.63 ± 7.22
165-187.5
Mass (kg)
68.87 ± 9.34
48.5-80.5
VO2 Peak (mL·kg-1·min-1)
54.28 ± 8.14
37.68-65.27
HR Peak (beats·min-1)
203.6 ± 5.9
191-211
vVO2 Peak (km·h-1)
15.49 ± 2.33
11.5-19
Ventilatory Threshold (km·h-1)
11.46 ± 2.18
8-15
VO2 peak, HR peak, vVO2 peak are peak oxygen uptake, peak heart rate and the running velocity which corresponds
with VO2 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 VO2 peak, vVO2 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 VO2 peak, VT, and vVO2 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 VO2 (30).
During the 3rd visit, a maximal run at vVO2 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 VO2 peak and a 5-min rest, the
treadmill speed was adjusted to the individual vVO2 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.
20
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 vVO2 peak pace for 50% of the EPS tlim and at a pace 1 km·h-1 slower than the vVO2 peak pace
for the rest of the time until exhaustion. The SPS exhaustive trial started at a pace 1 km·h-1 slower
than vVO2 peak for 50% of the EPS tlim with the rest of the time at a pace 1 km·h-1 faster than vVO2
peak (Figure 1).
Figure 1. Schematic Representation of the Experimental Protocol of a Subject. In the even pace start (EPS),
the subject ran at vVO2 peak until exhaustion. For the fast pace start (FPS), the subject ran for 191 sec 50% (382 sec) of
the tlim vVO2 peak at 20 km·h-1 (1 km·h-1 faster than vVO2 peak) and for the rest of the duration of maximal effort 1 km·h-1
slower than vVO2 peak. In the slow pace start (SPS), the subject ran for 191 sec 50% (382 sec) of the tlim vVO2 peak 18
km·h-1 (1 km·h-1 slower than vVO2 peak), and for the rest of the duration of maximal effort 1 km·h-1 faster than vVO2 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 (VO2) 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 CO2 and O2 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% O2, 5.08% CO2 and 100% N2). 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., VO2, VCO2, VE, and R) were determined on a locally
developed computer program based on the computations described by McArdle, Katch, and Katch
(35) when VEatps, FECO2 and FEO2 are known. The highest VO2 value obtained during an
incremental exercise test was recorded as the subject's VO2 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).
21
VENTILATORY THRESHOLD ASSESSMENT
Criteria described by others were used for the VT detection (14,46). The VT was primarily determined
as the VO2 or work load at which VE began to increase nonlinearly. To determine the onset of
hyperventilation, other secondary criteria were used, including the following: 1) a systematic increase
in VE/VO2, 2) a nonlinear increase in VCO2 and 3) a systematic decrease in FECO2. 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 FEO2, VE/VO2 and FECO2,
VE/VCO2 are used for VT detection. When a 2-min incremental protocol has been employed, the
workload before a systematic increase in either VE/VO2 or VE/VCO2 with a concomitant decrease in
FECO2 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 VO2 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 vVO2 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 VO2 PEAK (vVO2 PEAK)
The lowest running speed that elicited a VO2 equivalent to VO2 peak during the VO2 peak test was
defined as the vVO2 peak (7). If the final exercise workload was not completed within 120 sec despite
an increase in VO2, then vVO2 peak was determined using the following equation (29):
vVO2 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).
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 Fratio, a Tukey post hoc test was applied. The 95% level of confidence was chosen in all statistical
22
analysis. The data are presented as the mean ± SD. All statistical analyses were conducted using the
SPSS statistical software (version 21, Chicago, USA).
RESULTS
The subjects mean VO2 peak, vVO2 peak, VT, and HR max after the incremental test were 54.28 ±
8.14 mL·kg-1·min-1, 15.49 ± 2.33 km·h-1, 11.46 ± 2.18 km·h-1, and 203.67 ± 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 (2654.58 ± 1668 m and 632.75 ± 408.11 sec, respectively)
compared with those after EPS (2001.67 ± 839.63 m and 460.33 ± 186.33 sec, respectively) and SPS
(1975.83 ± 791.22 m and 457 ± 177.17 sec, respectively).
4500
*
3000
2500
1975.8
2654.6
3500
2001.7
Total distance (m)
4000
2000
1500
1000
500
EPS
FPS
Pacing strategies
SPS
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
Fast-Start Pacing
Slow-Start Pacing
Strategy
Strategy
Strategy
(EPS)
(FPS)
(SPS)
VO2 Peak (mL·kg-1·min-1)
50.34 ± 7.56
52.37 ± 7.71#
47.08 ± 7.12
Time to Exhaustion (sec)
Peak HR (beats·min-1)
460.33 ± 186.32
198.3 ± 5.03
632.75 ± 408.11*
195.9 ± 5.11
197.1 ± 5.15
Total Distance (m)
2001.67 ± 839.63
AOD 160 (mL·kg-1)
33.88 ± 9.32#
30.92 ± 8.39#
40.36 ± 10.86
110.86 ± 15.88#
113.27 ± 16.69#
104.13 ± 16.17
16.78 ± 3.66
14.41 ± 3.51*
16.16 ± 3.52
O2 160 Consumed (mL·kg-1)
Blood Lactate (mmol·L-1)
2654.58 ± 1688*
457 ± 177.17
1975.83 ± 791.22
*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 O2 deficit and measured oxygen consumption
during the first 160 sec of the exhaustive trials respectively.
23
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 160VO2 peak (Table 2) was not different from the incremental VO2 peak or
from the EPS value.
*
14.41
18.00
16.16
20.00
16.78
Blood lactate (mmol.L-1)
22.00
16.00
14.00
12.00
10.00
EPS
FPS
Pacing strategies
SPS
Figure 3. Blood Lactate Levels after EPS, FPS, and SPS (Mean ± SD). *P<0.05
significantly lower from EPS and SPS.
65.00
*
FPS
SPS
47.80
50.34
55.00
52.37
54.28
VO2 ml.kg-1.min-1
60.00
50.00
45.00
40.00
Incremental
EPS
Figure 4. VO2 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)
24
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 ± 10.86 mL·kg-1). The mean total O2 consumption
during the first 160 sec also showed similar differences between the groups. It was higher in FPS
(113.27 ± 16.69 mL·kg-1) and EPS (110.86 ± 15.88 mL·kg-1) than in SPS (104.13 ± 16.17 mL·kg-1).
55
*
40.4
45
35
30.9
40
33.9
AOD 160 ( ml.kg-1)
50
30
25
20
EPS
FPS
Pacing strategies
SPS
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 O2 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 VO2 and the VO2 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
25
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
VO2 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 O2 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% VO2 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
VO2 and VO2 kinetics or plasma lactate levels and O2 deficit (1). In the present study, we chose an
even pace near 100% vVO2 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.
EFFECT OF PACING STRATEGY ON VO2
The highest VO2 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 VO2 peak measured during the incremental
test. At the same discrete time point during SPS, the VO2 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 O2 uptake and the enhanced VO2 dynamics. As has been mentioned, the absolute rate of
26
change in VO2 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 VO2 response in middledistance events and indicate that an early acceleration or a race-simulation pace results in a higher
VO2 response (4). Furthermore, it seems that for shorter distances (800 vs. 3000 m), a higher starting
velocity evokes faster VO2 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 VO2 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 VO2 kinetics between treadmill and cycle ergometry (12)
revealed that for exercise intensities above the anaerobic threshold, the amplitude of the primary
component of VO2 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 vVO2 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 VO2 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
27
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 VO2. Ariyoshi and colleagues (3) have also reported a
higher VO2 response during a pacing strategy with a fast start. This higher V̇O2 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 O2 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 O2 supply. Duffield et al. (15) tried to investigate the differences in
the VO2 response between 800, 1500, and 3000 m races. During those tests, the researchers noted
that the acceleration of the VO2 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 VO2, leading to faster VO2 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 VO2 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 VO2,
particularly the amplitude of the primary component of VO2.
Regarding the mechanism that regulates the speed of the VO2 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 VO2 (22), thus
28
providing further confirmation for this suggestions. Bishop and colleagues (9) and Duffield and
colleagues (15) also suggest that a fast pace might enhance total V̇O2 and that the enhancement
could be attributed to increased PCr breakdown.
CONCLUSIONS
The findings of the present study suggest that if the duration of maximal running effort at VO2 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 VO2, 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, Email:
elzach@phed.uoa.gr
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