The Positive Effects of Priming Exercise on Oxygen
Uptake Kinetics and High-Intensity Exercise Performance
Are Not Magnified by a Fast-Start Pacing Strategy in
Trained Cyclists
Renato Aparecido Correˆa Carita´, Camila Coelho Greco*, Benedito Se´rgio Denadai
Human Performance Laboratory, IB – UNESP, Rio Claro, Sa˜o Paulo, Brazil
Abstract
The purpose of this study was to determine both the independent and additive effects of prior heavy-intensity exercise and
pacing strategies on the VO2 kinetics and performance during high-intensity exercise. Fourteen endurance cyclists (VO2max
= 62.868.5 mL.kg21.min21) volunteered to participate in the present study with the following protocols: 1) incremental test
to determine lactate threshold and VO2max; 2) four maximal constant-load tests to estimate critical power; 3) six bouts of
exercise, using a fast-start (FS), even-start (ES) or slow-start (SS) pacing strategy, with and without a preceding heavy-
intensity exercise session (i.e., 90% critical power). In all conditions, the subjects completed an all-out sprint during the final
60 s of the test as a measure of the performance. For the control condition, the mean response time was significantly
shorter (p,0.001) for FS (2764 s) than for ES (3265 s) and SS (3266 s). After the prior exercise, the mean response time
was not significantly different among the paced conditions (FS = 2465 s; ES = 2565 s; SS = 2665 s). The end-sprint
performance (i.e., mean power output) was only improved (,3.2%, p,0.01) by prior exercise. Thus, in trained endurance
cyclists, an FS pacing strategy does not magnify the positive effects of priming exercise on the overall VO2 kinetics and
short-term high-intensity performance.
Citation: Carita´ RAC, Greco CC, Denadai BS (2014) The Positive Effects of Priming Exercise on Oxygen Uptake Kinetics and High-Intensity Exercise Performance
Are Not Magnified by a Fast-Start Pacing Strategy in Trained Cyclists. PLoS ONE 9(4): e95202. doi:10.1371/journal.pone.0095202
Editor: Maria` Alemany, University of Barcelona, Faculty of Biology, Spain
Received February 11, 2014; Accepted March 24, 2014; Published April 16, 2014
Copyright:  2014 Carita´ et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits
unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: This research was supported by grants from Conselho Nacional de Desenvolvimento Cientı´fico e Tecnolo´gico and Fundac¸a˜o de Amparo a` Pesquisa do
Estado de Sa˜o Paulo. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing Interests: The authors have declared that no competing interests exist.
* E-mail: grecocc@rc.unesp.br
Introduction
Exercise intensity domains (i.e., moderate, heavy and severe) are
defined according to the blood lactate and oxygen uptake (VO2)
responses obtained during constant-work-rate exercise [1]. Critical
power (CP – the asymptote of the power-time relationship) is
considered the lower boundary of the severe-intensity domain [2].
Indeed, during constant-work-rate exercise performed within the
severe domain, the VO2 rises inexorably (as the slow component of
the VO2 kinetics increases) to the maximal oxygen uptake
(VO2max). Exercise tolerance within the severe domain can be
predicted and is defined by the curvature constant of the power–
time relationship (W9) [3]. Several lines of evidence indicate that
the interaction between VO2 kinetics, W’ and the attainment of
VO2max can contribute to exercise intolerance during exercise
performed in the severe-intensity domain [4]. Some interventions
(e.g., pacing, priming exercise and nitrate supplementation) that
are used to improve VO2 kinetics (i.e., t – the time taken to reach
63% of the increase in VO2 above baseline and/or the slow
component of VO2 kinetics) can reduce the W’ utilization during
the initial phase of exercise, improving performance [5] and
exercise tolerance [6] during severe-intensity exercise.
Pacing strategy (i.e., the pattern of the rate of energy
expenditure) has important effects on exercise tolerance [7] and
performance [5]. The self-selected pacing strategy adopted during
a time trial is controlled by a complex regulatory system, in which
integrated neural control regulates exercise intensity to prevent
homeostatic disturbances that might cause injury [8]. Factors such
as exercise modality, event duration and performance level can
influence the self-selected pacing strategy [9,10]. Some studies
have demonstrated that a fast-start pacing strategy has a positive
effect on performance during sports events of up to approximately
2–3 min in duration [11,12]; in these events, energy is provided by
both aerobic and anaerobic pathways [13]. In these conditions, the
VO2 kinetics is significantly faster, sparing W’ utilization during
the initial phase of exercise [5,7]. Interestingly, Jones et al. [7]
found that the percentage reduction in the mean response time of
VO2 was significantly correlated (r = 0.85, p,0.05) with the
percentage improvement in exercise tolerance when a fast start
was compared with an even-paced exercise.
Warm-up exercise has been extensively performed by athletes
before their participation in subsequent vigorous exercise. Indeed,
priming exercise performed at heavy or severe intensities domain
can improve exercise tolerance during severe-intensity exercise
(submaximal and perimaximal) [6,14]. These positive alterations
have been attributed, at least in part, to enhancement of the
overall VO2 kinetics [6,15]. Gerbino et al. [16] and MacDonald et
al. [17] demonstrated that prior heavy exercise accelerated the
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monoexponential kinetics (i.e., mean response time) during a
second bout of heavy exercise performed 6 min after the first bout.
Later, studies using a more comprehensive model (two or three
components) to analyze VO2 kinetics [6,18] demonstrated that this
overall acceleration could be attributed to the increased amplitude
of the primary component and the reduced amplitude of the slow
component, with the time constant of the primary component (i.e.,
t) remaining unaffected. A similar response (i.e., increased
amplitude of the primary component and unchanged t) was
found for exercise that was performed at perimaximal intensities
(100%, 110% and 120% of VO2max) after prior heavy exercise
[14].
Thus, the interventions discussed above (i.e., priming exercise
and pacing) seem to have different effects on the VO2 kinetics
during severe-intensity exercise. The mechanism that underpins
these effects is unclear. However, it is possible that different factors
contribute to the VO2 response profile under these conditions
(pacing vs. priming exercise). Priming exercise seems to increase
blood flow, oxygenation, oxidative enzyme activity and electro-
myographic activity, thus accelerating the overall VO2 response to
severe exercise [15]. A positive pacing strategy, which causes a
higher initial rate of muscle ATP hydrolysis, can magnify the VO2
‘‘error signal’’, i.e., the difference between the instantaneous
supply and the required rates of oxidative phosphorylation [5].
The absolute rate at which VO2 increases after the onset of
exercise is a positive function of the ‘‘error signal’’ [19]; therefore,
a fast-start pacing strategy results in faster VO2 kinetics [5,7].
Given this scenario, it is possible that priming exercise can amplify
the positive effect of a fast-start pacing strategy on VO2 kinetics
and exercise tolerance/performance during high-intensity exer-
cise. However, the possible additive effects of priming exercise and
pacing strategy on these variables are unknown.
The purpose of this study was to determine the independent and
additive effects of prior heavy-intensity exercise and pacing
strategies on VO2 kinetics and performance during high-intensity
exercise. The following hypotheses were proposed: 1) A fast-start
pacing strategy would shorten the mean response time, and
increase peak power output and mean power output during short-
term high-intensity exercise; and 2) Priming exercise would
shorten the mean response time, and increase peak power output
and mean power output during short-term high-intensity exercise
irrespectively of the utilized pacing strategy.
Materials and Methods
Ethics statement
The present study was approved by the Ethics Committee of the
Biosciences Institute – Rio Claro of Sa˜o Paulo State University,
and all subjects provided written informed consent prior to
participation. The study was performed in accordance with the
declaration of Helsinki.
Subjects
Fourteen endurance cyclists (2665 years; 7169 kg; 17568 cm)
with at least 5 years of experience in the modality volunteered to
participate in the present study; these athletes were competing in
regional- to national-level meets. The subjects were familiar with
the laboratory testing procedures, as they were previously involved
in similar evaluations. The subjects were instructed to be fully
rested and hydrated at least 3 h postprandially when reporting to
the laboratory and to refrain from using caffeine-containing food
or beverages, drugs, alcohol, cigarette, or any form of nicotine
24 h before testing. Each subject was tested in a climate-controlled
(21–22uC) laboratory at the same time of day (62 h) to minimize
the effects of diurnal biological variation.
Experimental design
The subjects were required to visit the laboratory on 11 different
occasions, separated by at least 24 h, within a period of three
weeks. The first visit to the laboratory was to undergo an
incremental test to determine the lactate threshold, VO2max and
the power output at VO2max (PVO2max). On the following four
visits, the subjects underwent four constant-load tests (75%, 80%,
85% and 100% of PVO2max) to exhaustion, in random order, to
determine the parameters of the power-duration relationship (i.e.,
CP and W9). The CP model was used to estimate the workload
that would be expected to lead to exhaustion in 3 min (P3-min).
From the 6th to the 11th visit, the subjects performed three
different pacing strategies (fast start, even start, and slow start) with
and without a preceding heavy-intensity exercise session.
Incremental protocol
The incremental protocol was performed on a cycle ergometer
(Lode Excalibur Sport, Lode BC, Groningen, Netherlands) with
the subjects pedaling at a constant self-selected pedal rate (between
70 and 90 rpm). The chosen pedal rate along with saddle and
handle bar height and configuration was recorded and reproduced
in subsequent tests. The initial power output was 120 W for 3 min
and was then increased by 20 W every 3 min. Capillary blood
samples were collected within the final 20 s of each stage for the
determination of the blood lactate concentration ([La]). The [La]
were determined (YSI 2300, Yellow Springs, Ohio, USA)
immediately and the test was stopped when the [La] rose above
4 mM. Plots of [La] against the power output were provided by
two independent reviewers, who determined the lactate threshold
as the first sudden and sustained increase in blood lactate above
resting concentrations [20]. After a rest period of 30 min, the
participants performed a fast ramp test. The test began with an
initial 5 min of cycling at 25 W below their previously determined
lactate threshold, and the power was subsequently increased by
5 W every 12 s until voluntary exhaustion. The protocol was
terminated when a drop of more than 5 rpm of their self-selected
cadence occurred for more than 5 seconds despite strong verbal
encouragement. VO2max was defined as the highest average 15-s
VO2 value recorded during the incremental test. Pulmonary gas
exchange was measured continuously using a breath-by-breath
analyzer (Cosmed Quark PFTergo, Rome, Italy). Before each test,
the O2 and CO2 analysis systems were calibrated using ambient
air and a gas of known O2 and CO2 concentration according to
the manufacturer’s instructions, while the gas analyzer turbine
flowmeter was calibrated using a 3-L syringe. The heart rate was
also monitored throughout the tests (Polar, Kempele, Finland).
The PVO2max was defined as the power output at which
VO2max occurred. The work rate that would require 50%D (work
rate at the lactate threshold plus 50% of the difference between the
work rate at the lactate threshold and VO2max) was subsequently
calculated.
Determination of the power–duration relationship
The exercise protocol began with a 10 min warm-up at lactate
threshold, followed by 5 min of rest prior to the commencement of
the exhaustive trial [21]. Thereafter, the subjects exercised for
3 min at 20 W followed by a constant-workload test (75%, 80%,
85% and 100% of PVO2max) to voluntary exhaustion or until the
subject could not maintain the required cadence (i.e., a cadence
,5 rpm of the preferred cadence) despite verbal encouragement
[21]. These tests were conducted at the same cadence as the
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incremental test. During these testing sessions, the participants
were not informed of the imposed work rate, their performance
times or their heart rate. The exercise tolerance (tlim) was
measured to the nearest second. The three equivalents of the 2-
parameter
model
[P = (W9/tlim)+CP;
tlim
= W9/(P-CP);
W = CP?tlim+W9] were used to fit the data and estimate CP and
W9 [22] using an iterative nonlinear regression procedure
(Microcal Origin 7.5; Northampton, MA, USA) for each subject.
The CP and W9 estimates from the 3 equations were compared to
select the best fit using the model associated with the lowest
standard error for CP (SEE) [23,24].
Experimental sessions
The exercise protocol began with a 5 min warm-up at lactate
threshold, followed by 7 min of rest. Thereafter, the subjects
performed 3 min at 20 W before the experimental conditions. In
the even-start (ES) condition, the athletes performed 2 min of
constant-load exercise at P3-min, followed by a 1-min all-out
exercise period. In the fast-start (FS) condition, the first 90 s of
exercise was performed as the work rate was reduced linearly from
110% to 90% of P3-min, followed by a 1-min all-out exercise
period. In the slow-start (SS) condition, the first 90 s of exercise
was performed as the work rate was increased linearly from 90%
to 110% of P3-min, followed by a 1-min all-out exercise period.
The last 30 s of the FS and SS conditions was performed at P3-
min [5]. During the first 2 min of exercise, a hyperbolic mode was
used (fixed power), which was immediately changed to a linear
mode (power dependent on the cadence) during the all-out
exercise. These experimental conditions were performed in
random order with and without previous exercise (Figure 1).
1-min all-out exercise
Following the 2-min pacing exercises, the athletes performed
1 min of all-out exercise. They were required to reach the peak
power as quickly as possible and to exert maximal effort during the
whole test. Throughout the 1-min test, the athletes were given
verbal encouragement but were not informed of time elapsed. The
VO2 was measured breath-by-breath during the exercise, and the
data were reduced to 15-s stationary averages. The resistance to
pedaling was calculated using the preferred cadence obtained
during the incremental test and the workload corresponding to
50%D:
1 min resis tan ce~50%D=preferred cadence2
ð1Þ
The following performance data were obtained from the all-out
test: peak power output, time to peak power output and mean
power output.
Prior exercise
The prior exercise conditions involved participants performing
3 min of baseline cycling at 20 W, followed by a square-wave
transition to a work rate requiring 90% CP (i.e., heavy-intensity
exercise). At 6 min, the subjects were allowed to ‘‘spin down’’
against zero resistance for 1 min and then rested passively for
6 min before remounting the ergometer and pedaling for 3 min at
20 W. After this 3-min period, one of the three pacing conditions
was immediately imposed as described above. One minute before
and immediately after these exercise bouts, a fingertip capillary
blood sample was taken to determine the blood [La]. The subjects
repeated this process on separate days and in a randomized order
until all experimental trials were completed.
VO2 kinetics
The breath-by-breath data from each exercise test were filtered
manually to remove outlying breaths, which were defined as
breaths deviating by more than four standard deviations from the
preceding five breaths. The breath-by-breath data were subse-
quently linearly interpolated to provide second-by-second values
and aligned by time to the start of the exercise, and a nonlinear
least squares algorithm was used to fit the data thereafter. A single-
exponential model without a time delay and with a fitting window
commencing at t = 0 s (equivalent to the mean response time) was
used to characterize the kinetics of the overall VO2 response
during initial phase (i.e., 90 s) of the different pacing strategies for
all subjects. The following equation describes this model:
VO2(t)~VO2baselinezA½1{e{(t=t)
ð2Þ
where VO2(t) represents the absolute VO2 at a given time t,
VO2baseline represents the mean VO2 measured over the final
60 s of baseline pedaling, and A and t represent the amplitude and
time constant, respectively, which describe the overall increase in
VO2 above the baseline. The oxygen deficit was also calculated for
the same time period (i.e., 90 s) by multiplying the mean response
time and the DVO2.
Statistical analysis
The data are reported as the means 6SD. The normality of
data was checked by the Shapiro-Wilk test. The data were
analyzed using two-way ANOVA (prior exercise vs. pacing
strategy), with Fisher’s LSD test where appropriate. For all
statistics, the significance level was set at p#0.05.
Results
During the ramped incremental test, the subjects attained a
peak work rate (i.e., PVO2max) of 411645 W, a VO2max of
4.4360.47 L.min21, a peak [La] of 8.661.6 mM and a maximal
heart rate of 19368 bpm. The CP and the W9 were 283635 W
and 2266 kJ, respectively. The P3-min was calculated to be
407647 W. The goodness-of-fit of the power-time relationship
was R2 = 0.98. The SEE of the CP estimation was 7.066.6 W.
The parameters of the VO2 kinetics during the paced exercise
trials (FS, ES and SS) with and without prior exercise are
presented in table 1. The measurements of VO2 amplitude (i.e., A)
revealed a main effect of prior exercise (F = 37.95; p,0.001), but
no interaction was detected (F = 1.62; p = 0.212). Similarly, the
absolute VO2 (i.e., A+ VO2baseline) of the pacing exercises
revealed a main effect of prior exercise, but no interaction was
detected (F = 0.81; p = 0.452). The analysis of the O2 deficit values
revealed a significant interaction (F = 3.95; p = 0.028), indicating
that the effect from previous exercise occurred only for the ES and
SS conditions. Post hoc analyses revealed a significant reduction in
the O2 deficit only for the SS (p = 0.003) and ES (p,0.001)
conditions after prior exercise. The effect of the pacing strategy
was only significant when comparing SS with FS (p = 0.002) and
ES with FS (p,0.001) during the control condition. The analysis
of the mean response time values revealed a significant interaction
(F = 3.59; p = 0.037), indicating that the effect of previous exercise
occurred only for the ES and SS conditions. Post hoc analyses
revealed a significant reduction in mean response time for the SS
(p,0.001) and ES (p,0.001) conditions after prior exercise. The
effect of the pacing strategy was only significant when comparing
SS with FS (p,0.001) and ES with FS (p,0.001) in the control
condition. Figure 2 shows the VO2 responses during the paced
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exercise trials (FS, ES and SS) with and without prior exercise in a
representative subject.
The VO2peak attained during the sprint for the FS, ES and SS
conditions was significantly lower than VO2max, both with
(FS = 4.1960.35, ES = 4.1460.33 and SS = 4.0360.32 L.min21;
F = 5.678,
p = 0.002)
and
without
(FS = 3.9060.32,
ES = 4.0160.30
and
SS = 3.9960.73 L.min21;
F = 5.678,
p = 0.002) a prior exercise session. The VO2peak attained during
the sprint for the FS, ES and SS conditions was unaffected by the
prior exercise and pacing strategies (p.0.05).
The parameters of exercise performance during the paced
exercise trials (FS, ES and SS) with and without prior exercise are
presented in table 2. The measurements of peak power output
revealed a main effect of prior exercise (F = 61.72; p,0.001), but
no interaction was detected (F = 2.28; p = 0.116). Similarly, the
measurements of mean power output revealed a main effect of
prior exercise (F = 6.54; p = 0.015), but no interaction was detected
(F = 0.14; p = 0.873). The analysis of the time to peak power
output
values
revealed
no
significant
interaction
(F = 0.52;
p = 0.598), and no significant main effect of prior exercise
(F = 0.59; p = 0.447) and pacing strategy (F = 2.38; p = 0.106).
Figure 1. Study design for the six separate exercises conditions for a representative individual. Panels A, B and C - Paced exercises in the
control condition, using slow start, even start and fast start, respectively. Panels D, E and F - Paced exercise preceded by previous heavy exercise
(PHE), using slow start, even start and fast start, respectively.
doi:10.1371/journal.pone.0095202.g001
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Figure 3 shows the power output during the paced exercise trials
(FS, ES and SS) with and without prior exercise in a representative
subject.
The measurements of the [La] values before the paced exercises
revealed a main effect of prior exercise (F = 58.77; p,0.001), but
no interaction was detected (F = 0.01; p = 0.992). The mean [La]
values after prior exercise for the FS, ES and SS conditions were
1.8760.50, 1.7860.61 and 1.7360.74 mM, respectively. The
mean control [La] values for the FS, ES and SS conditions were
1.1460.41, 1.0160.18 and 0.9860.24 mM, respectively. The
analysis of the [La] values after the sprint revealed no significant
interaction (F = 2.00; p = 0.149), with no significant main effect of
prior exercise (F = 0.79; p = 0.381) and pacing strategy (F = 1.15;
p = 0.329). The mean [La] values after prior exercise for the FS,
ES
and
SS
conditions
were
11.061.98,
11.162.39
and
10.162.32 mM, respectively. The mean control [La] values for
the FS, ES and SS conditions were 11.363.11, 9.4662.15 and
10.262.28 mM, respectively.
Discussion
The purpose of this study was to determine the independent and
additive effects of prior heavy-intensity exercise and pacing
strategies on VO2 kinetics and performance during high-intensity
exercise. Similar to previous studies, we have demonstrated that
both priming exercise [6] and pacing strategies (i.e., FS) [5,7]
accelerated the overall VO2 kinetics (i.e., mean response time).
However, our study reveals, for the first time, that an FS pacing
strategy does not magnify the positive effects of prior heavy-
intensity exercise on the overall VO2 kinetics. Moreover, the
performance during high-intensity exercise (i.e., peak power
output and mean power output) was enhanced only by prior
heavy-intensity exercise. These data confirm and extend the
proposal that the changes (i.e., speeding/slowing) in the VO2
kinetics during the initial phase of different pacing strategies (FS,
ES and SS) are not necessarily associated with the changes in
performance during short-term high-intensity exercise [5].
Some studies have found that the overall VO2 kinetics is
accelerated by an FS pacing strategy when compared with ES and
SS strategies [5,7]. Factors such as exercise modality [5,11] and
aerobic performance level [6] do not appear to influence the
effects of the FS pacing strategy on the overall VO2 kinetics. Thus,
our data confirm that an FS pacing strategy can improve the
overall VO2 kinetics during high-intensity exercise in trained
endurance cyclists. Studies have shown a direct proportionality
between the products of PCr splitting and muscle or pulmonary
VO2 [19]. An FS pacing strategy requires a greater initial rate of
muscle ATP hydrolysis, resulting in a greater initial D [PCr]/D
time. Thus, a more rapid accumulation of the metabolites (ADP,
Pi and Ca2+) that stimulate oxidative phosphorylation would be
Figure 2. Oxygen uptake (VO2) responses during the pacing
exercise conditions in a representative subject. The horizontal
line superimposed on each panel indicates the subject’s VO2max. Panels
A, B and C - slow start, even start and fast start pacing conditions,
respectively. Grey circles and black circles - paced exercise trials, with
and without prior exercise, respectively. Notice that the VO2 response is
speeded using the fast start pacing strategy only in the control
condition. Thus, the fast start pacing strategy does not magnify the
positive effects of prior heavy-intensity exercise on overall VO2
response.
doi:10.1371/journal.pone.0095202.g002
Table 1. Parameters of the oxygen uptake (VO2) kinetics
during paced exercise trials (FS, ES and SS), with and without
prior exercise.
Control
After heavy
exercise
Significance
FS
ES
SS
FS
ES
SS
VO2b (L.min21)
1.27
1.26
1.20
1.13
1.26
1.13
NS
0.20
0.21
0.22
0.22
0.25
0.23
A (L.min21)
2.67
2.73
2.63
2.89
2.86
2.91
*F = 37.95
0.31
0.40
0.36
0.42
0.42
0.40
p,0.001
Absolute VO2 (L.min21)
3.94
3.99
3.82
4.03
4.12
4.04
*F = 12.86
0.31
0.36
0.33
0.39
0.31
0.34
p = 0.001
MRT (s)
27
32
32
24
25
26
{F = 3.59
4
5N
6N
5
5`
5`
P = 0.037
CI 95 (s)
2.2
2.2
2.5
1.5
1.9
2.1
-
0.7
0.5
0.8
0.6
0.7
0.7
O2 deficit (L)
1.22
1.48
1.45
1.16
1.15
1.22
{F = 3.95
0.25
0.27N 0.38N 0.40
0.25`
0.30`
P = 0.028
Data are the mean +SD. N = 14.
VO2b, baseline oxygen uptake; A, amplitude; Absolute VO2, VO2b+A; MRT, mean
response time; CI 95, 95% confidence interval for MRT estimation. FS, fast start;
ES, even start; SS, slow start.
*Main effect of previous exercise;
{Prior vs. pacing interaction;
`p,0.05 relative to the control condition;
Np,0.05 relative to the FS condition.
doi:10.1371/journal.pone.0095202.t001
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observed during an FS pacing strategy. Accordingly, Bailey et al.
[5] used near-infrared spectroscopy (NIRS) to verify that FS
strategies might be linked to increased muscle O2 extraction.
The classic experiments of Gerbino et al. [16] demonstrated
that prior heavy exercise accelerated the monoexponential kinetics
(i.e., mean response time) during a second bout of heavy exercise
performed 6 min after the first. Later, studies using different
experimental designs (e.g., intensities, durations of recovery time
and age group) [6,25] confirmed the seminal results obtained by
Gerbino et al. [16]. Our experimental results revealed that both
the mean response time and VO2 amplitude (the overall increase
in VO2 above the baseline) were modified by previous heavy
exercise. The increased VO2 amplitude during a second bout of
severe exercise has been considered important for exercise
tolerance/performance, because the slow component of the VO2
kinetics, the change in blood lactate concentration and the aerobic
contribution are positively modified during the second bout of
exercise. Central (increases in bulk O2 delivery) and peripheral
(convective O2 delivery and increased activity of mitochondrial
enzymes) factors are possible explanations for this altered VO2
response profile during the second bout of exercise [15].
To the best of our knowledge, this study is the first to determine
the possible additive effects of priming exercise and pacing strategy
on VO2 kinetics during severe-intensity exercise. We have
demonstrated that previous heavy-intensity exercise accelerated
the overall VO2 kinetics only during SS and ES pacing strategies.
Moreover, there was no significant difference among the FS, ES
and SS preceded by previous heavy-intensity exercise. Thus, the
effects of priming exercise on VO2 kinetics during severe-intensity
exercise are dependent on pacing strategy. Moreover, these effects
do not appear to be magnified by an FS pacing strategy. Together,
these results suggest that previous exercise has great potential to
enhance the overall VO2 kinetics and that an FS pacing strategy
does not amplify its effects.
In the present study, we did not use a biexponential model to
characterize the VO2 kinetics because we were unable to repeat
each trial to enhance the signal-to-noise ratio of the VO2 responses
(see below). Thus, the parameters of the VO2 kinetics were not
characterized. However, the exercise intensity used during the
different pacing strategies was similar to PVO2max; therefore, the
VO2 slow component, that elevates the VO2 above the steady-
state value predicted from the sub-lactate threshold VO2-work rate
relationship [26], cannot be detected under these circumstances.
Thus, in line with other studies, the previous exercise may have
only enhanced the VO2 amplitude [15], while the pacing strategy
enhanced the time constant of the primary component of the VO2
response [5,7]. Nevertheless, previous heavy-intensity exercise
blunted the effects of the FS pacing strategy on the overall VO2
kinetics. Therefore, the alterations caused by previous exercise
(available O2, convective O2 delivery, activity of mitochondrial
enzymes and motor unit recruitment) appear to prevent the effects
of an FS pacing strategy on the VO2 response. In line with this
statement, Rossiter et al. [27] have found that prior high-intensity
exercise reduced the amplitude of the [PCr] response, with the
initial rate of [PCr] change (d[PCr]/dt) remaining unaffected
during a second bout of heavy exercise. These alterations are
suggestive of a reduced t[PCr] during primed exercise [27],
although the difference between conditions (i.e., control, 34 s vs.
primed exercise, 32 s) did not reach statistical significance.
Moreover, it has been demonstrated that the intramuscular
enzyme activity status (i.e., pyruvate dehydrogenase complex -
PDC), can allow a greater flux of acetyl groups into the
mitochondria for oxidation [28]. An increased activation of
pyruvate dehydrogenase complex might reduce both substrate-
level phosphorylation (i.e., glycolysis and the creatine kinase and
adenylate kinase reactions) [28] and the primary component time
Figure 3. Power output during the pacing exercise conditions
in a representative subject. Panels A, B and C - slow start, even start
and fast start pacing conditions, respectively. Grey lozenges and black
squares - paced exercise trials, with and without prior exercise,
respectively. Notice the effect of prior exercise on performance,
irrespectively of the pacing strategy used.
doi:10.1371/journal.pone.0095202.g003
Table 2. Parameters of exercise performance during paced
exercise trials (FS, ES and SS), with and without prior exercise.
Control
After heavy exercise
Significance
FS
ES
SS
FS
ES
SS
PP (W)
606
558
553
674
617
586
*F = 61.72
101
93
94
110
110
106
p,0.001
TPP (s)
6
6
7
6
6
7
NS
2
2
3
1
1
1
MPO (W)
400
396
386
415
408
396
*F = 6.54
44
43
69
60
47
68
p = 0.015
Data are the mean +SD. N = 14.
PP, peak power output; TPP, time to peak power output; MPO, mean power
output. FS, fast start; ES, even start; SS, slow start;
*Main effect of previous exercise.
doi:10.1371/journal.pone.0095202.t002
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constant [29]. Thus, these mechanisms (altered [PCr] kinetics
and/or increased PDC activity) might have blunted the effects of
an FS pacing strategy on the VO2 response (i.e., VO2 ‘‘error
signal’’). However, future studies, with appropriated experimental
design, should be conducted to confirm (or not) these hypotheses.
Previous heavy- or severe-intensity exercises have been shown to
improve exercise tolerance during both submaximal [6] and
perimaximal exercise [14]. This positive effect seems to be
influenced by an optimal interaction between prior exercise
intensity and recovery duration [6]. We have provided the first
demonstration that prior heavy-intensity exercise enhances per-
formance (peak power output and mean power output), and this
increase occurs independently of the chosen pacing strategy.
Improved exercise tolerance during submaximal intensity has been
observed when the amplitude of the slow component of the VO2
kinetics decreased and the overall VO2 kinetics were faster [6].
Indeed, we have observed that the overall VO2 kinetics was faster
and the VO2 amplitude increased (and thus the magnitude of the
O2 deficit was reduced) after heavy-intensity exercise. Thus,
previous heavy-intensity exercise can reduce the W9 utilization
during the initial phase of exercise, improving performance during
short-term high-intensity exercise.
It has been proposed that the mild lactic acidosis caused by
prior heavy exercise might increase oxygen delivery by stimulating
vasodilatation and a rightward shift in the oxyhaemoglobin
dissociation curve (i.e. the Bohr effect) [16]. Based on data
obtained in active subjects (VO2max,50 mL.kg21.min21), some
studies have suggested that a baseline blood lactate concentration
of ,3 mM results in an increased time to exhaustion during
subsequent high-intensity exercise [6,14]. Moderate-intensity prior
exercise, which did not alter the baseline blood lactate concen-
tration, does not enhance VO2 kinetics or exercise tolerance
during subsequent high-intensity exercise performed by active
subjects [16]. Similarly, Bailey et al. [6] have shown that the effect
of prior heavy exercise on VO2 kinetics is prevented when baseline
blood [lactate] recovers to ,2 mM. However, we have verified
that a baseline blood lactate concentration of ,1.8 mM has
enhanced both overall VO2 kinetics and short-term high-intensity
performance in trained endurance cyclists. The low blood lactate
concentration found 9 min after heavy intensity exercise can be
explained, at least in part, by increased rate of blood lactate
removal found in aerobic trained athletes [30]. Interestingly,
Burnley et al. [31] have found that moderate-intensity prior
exercise enhanced both primary VO2 amplitude and exercise
performance
in
well-trained
cyclists
(VO2max
,58 mL.kg21.min21). Thus, in aerobic trained cyclists, it seems
that the presence of an elevated blood lactate concentration is not
a sine qua non condition for improving VO2 kinetics and short-term
high-intensity performance after prior exercise.
Some studies found that an FS pacing strategy can improve
exercise tolerance [7] and performance [5] during short-term
high-intensity exercise. In the present study, the pacing strategy
did not significantly influence the exercise performance, although
the overall VO2 kinetics was improved by the FS pacing strategy.
Some interventions (priming exercise and pacing) have shown
similar results [5,6], indicating that changes in the overall VO2
kinetics will not necessarily enhance exercise tolerance/perfor-
mance during subsequent high-intensity exercise. Interestingly,
Bailey et al. [5] reported that utilizing an FS pacing strategy with
active individuals (VO2max ,52 mL.kg21.min21) improved both
the overall VO2 kinetics and exercise performance during
subsequent high-intensity exercise. In the present study, we
analyzed trained endurance cyclists (VO2max = 62 mL.kg21.-
min21). Thus, differences in aerobic fitness might explain, at least
in part, these different results. Bailey et al. [5] proposed that the
attainment of VO2max during high-intensity exercise bouts, when
this is ordinarily not possible, is essential for improving exercise
performance. Given the finite speed of the VO2 response, the
exercise durations at the extreme domain [32] would be too short
to permit attainment of VO2max [21]. Thus, the attainment of
VO2max would allow a more complete depletion of W9 and
consequently allow better exercise performance [5]. Indeed, we
have verified that VO2max was not attained during the FS pacing
strategy. However, future studies using different experimental
designs should be conducted to test this relationship.
Because of the nature of the present experiments, certain
limitations of the study should be considered when interpreting its
findings. The determination of the VO2 response parameters in
the heavy- and severe-intensity domain using only one transition
can have potential limitations (i.e., low confidence in the response
parameters). Repeated bouts have traditionally been averaged to
improve the signal-to-noise ratio of data [33]. However, due to the
extremely demanding nature of the exercise testing and the
frequent laboratory visits (11), only one trial was conducted for
each experimental condition. Although we only measured one
transition, the signal-to-noise ratio of the data can be improved by
using higher VO2 amplitudes [33]. Therefore, higher VO2
amplitudes, as utilized in the present study, correspond to smaller
confidence intervals. Indeed, the 95% confidence interval for the
estimation of mean response time was ,3 s for all conditions
(Table 1).
In summary, we have demonstrated in trained endurance
cyclists that priming heavy-intensity exercise has a positive effect
on both overall VO2 kinetics and short-term high-intensity
performance. However, the FS pacing strategy only modified the
overall VO2 kinetics. This finding suggests that faster overall VO2
kinetics does not, per se, determine the performance (i.e., peak
power output and mean power output) during high-intensity
exercise. The FS pacing strategy does not magnify the positive
effects of prior heavy-intensity exercise on the overall VO2
kinetics. Thus, the modifications caused by priming exercise
preclude the effects of the FS pacing strategy on the overall VO2
kinetics. Finally, priming exercise seems to have greater potential
than FS pacing strategies to enhance both overall VO2 kinetics
and short-term high-intensity performance in trained endurance
cyclists.
Author Contributions
Conceived and designed the experiments: CCG BSD. Performed the
experiments: RACC CCG. Analyzed the data: RACC CCG BSD.
Contributed reagents/materials/analysis tools: RACC CCG BSD. Wrote
the paper: RACC CCG BSD.
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The positive effects of priming exercise on oxygen uptake kinetics and high-intensity exercise performance are not magnified by a fast-start pacing strategy in trained cyclists.
Caritá, Renato Aparecido Corrêa,Greco, Camila Coelho,Denadai, Benedito Sérgio