308

ARTICLE
The effect of priming exercise on O2 uptake kinetics, muscle
O2 delivery and utilization, muscle activity, and exercise
tolerance in boys
Alan R. Barker, Emily Trebilcock, Brynmor Breese, Andrew M. Jones, and Neil Armstrong
Appl. Physiol. Nutr. Metab. Downloaded from www.nrcresearchpress.com by Fudan University on 05/16/15

Abstract: This study used priming exercise in young boys to investigate (i) how muscle oxygen delivery and oxygen utilization,
and muscle activity modulate oxygen uptake kinetics during exercise; and (ii) whether the accelerated oxygen uptake kinetics
following priming exercise can improve exercise tolerance. Seven boys that were aged 11.3 ± 1.6 years completed either a single
bout (bout 1) or repeated bouts with 6 min of recovery (bout 2) of very heavy-intensity cycling exercise. During the tests oxygen
uptake, muscle oxygenation, muscle electrical activity and exercise tolerance were measured. Priming exercise most likely
shortened the oxygen uptake mean response time (change, ±90% confidence limits; –8.0 s, ±3.0), possibly increased the phase II
oxygen uptake amplitude (0.11 L·min−1, ±0.09) and very likely reduced the oxygen uptake slow component amplitude
(–0.08 L·min−1, ±0.07). Priming resulted in a likely reduction in integrated electromyography (–24% baseline, ±21% and –25% baseline,
±19) and a very likely reduction in ⌬ deoxyhaemoglobin/⌬oxygen uptake (–0.16, ±0.11 and –0.09, ±0.05) over the phase II and slow
component portions of the oxygen uptake response, respectively. A correlation was present between the change in tissue oxygenation
index during bout 2 and the change in the phase II (r = –0.72, likely negative) and slow component (r = 0.72, likely positive) oxygen
uptake amplitudes following priming exercise, but not for muscle activity. Exercise tolerance was likely reduced (change –177 s, ±180)
following priming exercise. The altered phase II and slow component oxygen uptake amplitudes in boys following priming exercise
are linked to an improved localised matching of muscle oxygen delivery to oxygen uptake and not muscle electrical activity. Despite
For personal use only.

more rapid oxygen uptake kinetics following priming exercise, exercise tolerance was not enhanced.
Key words: oxidative metabolism, children, warm-up, muscle fibres.

Résumé : Cette étude utilise l’exercice physique comme amorce chez de jeunes garçons pour examiner : (i) le mécanisme de la
livraison d’oxygène, de l’utilisation de l’oxygène et de l’activité musculaire dans la modulation de la cinétique de la consomma-
tion d’oxygène au cours de l’exercice physique et pour vérifier si (ii) l’accélération de la cinétique de la consommation d’oxygène
suivant l’amorce par l’exercice améliore la tolérance à l’effort. Sept garçons âgés de 11,3 ± 1,6 ans effectuent un seul exercice
(séance 1) ou une série d’exercices incorporant 6 min de récupération (séance 2); l’exercice consiste à pédaler à une intensité très
élevée sur un vélo. Au cours de l’expérimentation, on évalue la consommation d’oxygène, l’oxygénation musculaire, l’activité
myoélectrique et la tolérance à l’effort. L’exercice d’amorce abrège vraisemblablement le temps moyen de réponse du consom-
mation d’oxygène (modification, IC 90 % : –8,0 s, ±3,0), probablement par l’accroissement de l’amplitude du consommation
d’oxygène durant la phase II (0,11 L·min–1, ±0,09) et fort probablement par la diminution de l’amplitude de la composante lente
de la consommation d’oxygène (–0,08 L·min–1, ±0,07). L’amorce a vraisemblablement pour effet de diminuer l’iEMG (–24 %, ±21 % par
rapport à la référence, et –25 %, ±19 par rapport à la référence) et de diminuer fort probablement ⌬ deoxyhaemoglobin/
⌬ consommation d’oxygène (–0,16, ±0,11 et –0,09, ±0,05) durant la phase II et la composante lente de la réponse du consommation
d’oxygène, respectivement. On observe une corrélation entre la variation de l’index d’oxygénation tissulaire au cours de la
séance 2 et la variation de l’amplitude de la consommation d’oxygène durant la phase II (r = –0,72, vraisemblablement négative)
et la phase lente (r = 0,72, vraisemblablement positive) suivant l’exercice d’amorce, mais pas en ce qui concerne l’activité
musculaire. On observe vraisemblablement une diminution de la tolérance à l’effort (variation de –177 s, ±180) à la suite de
l’exercice d’amorce. La modification chez les garçons de l’amplitude de la consommation d’oxygène durant la phase II et la
composante lente suivant l’exercice d’amorce sont liées à un meilleur appariement local entre la livraison musculaire de
l’oxygène et le consommation d’oxygène, mais pas en ce qui concerne l’activité myoélectrique. Même en présence d’une
cinétique de la consommation d’oxygène plus rapide à la suite d’un exercice d’amorce, la tolérance à l’effort n’est pas améliorée.
[Traduit par la Rédaction]
Mots-clés : métabolisme aérobie, enfants, échauffement, fibres musculaires.

Introduction
The pulmonary oxygen uptake (V̇O2) kinetic response during
exercise provides a noninvasive insight into muscle O2 uptake
dynamics (Krustrup et al. 2009). Both cross-sectional and longitu-
dinal studies have demonstrated growth and maturation to slow
V̇O2 kinetics during moderate (Fawkner et al. 2002; Breese et al.
2012), heavy (Fawkner and Armstrong 2004; Breese et al. 2010) and
very heavy- (Breese et al. 2012) intensity exercise. These observa-
tions have been linked to age-related changes in intramuscular
phosphate dynamics (Barker et al. 2008a), muscle O2 extraction

Received 26 April 2013. Accepted 6 September 2013.

A.R. Barker, E. Trebilcock, B. Breese, A.M. Jones, and N. Armstrong. Children’s Health and Exercise Research Centre, Sport and Health Sciences,
University of Exeter, Exeter EX1 2LU, UK.
Corresponding author: Alan R. Barker (e-mail: A.R.Barker@exeter.ac.uk).

Appl. Physiol. Nutr. Metab. 39: 308–317 (2014) dx.doi.org/10.1139/apnm-2013-0174 Published at www.nrcresearchpress.com/apnm on 24 September 2013.
 Barker et al.
(Leclair et al. 2012), muscle O2 delivery (Leclair et al. 2012) and (or)
muscle fibre recruitment patterns (Breese et al. 2012). However,
such mechanisms have been studied in isolation despite knowl-
edge that these factors interact to limit V̇O2 kinetics during exer-
cise (Poole et al. 2008).
Investigating the limiting factors of V̇O2 kinetics in children or
adolescents offers an alternative approach to understanding why
V̇O2 kinetics are altered during growth and maturation. In this
regard, a recent study found a bout of “priming” (or prior) very
heavy-intensity exercise in 9- to 13-year-old boys to reduce the V̇O2
mean response time (MRT), increase the phase II V̇O2 amplitude
and reduce the V̇O2 slow component amplitude during subse-
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quent very heavy cycling exercise (Barker et al. 2010). These obser-
vations were reasoned to result from an improved muscle O2
availability, as inferred from near infrared spectroscopy (NIRS)-
derived deoxyhaemoglobin (HHb) kinetics (Koga et al. 2012). How-
ever, this study did not examine the dynamic matching of muscle
HHb relative to V̇O2 during the exercise transient, which may
provide additional insights into the factors limiting oxidative me-
tabolism. A study on healthy young men found that a bout of
heavy-intensity priming exercise resulted in more rapid V̇O2 ki-
netics during subsequent moderate-intensity exercise and this
was related to an improved muscle O2 delivery as evidenced by an
abolished HHb/V̇O2 “overshoot” shortly after the onset of exercise
(Murias et al. 2011a). An overshoot in the HHb/V̇O2 dynamics
shortly after the onset of exercise is present in young adults with
a phase II V̇O2 time constant (␶) >21 s, but not in those with more
rapid phase II kinetics (Murias et al. 2011b), suggesting the hypoth-
esised “tipping point” (Poole et al. 2008) for an O2 delivery depen-
For personal use only.
dency on V̇O2 kinetics may reside in this region. Interestingly, the
group mean phase II V̇O2 ␶ in the priming study by Barker et al.
(2010) was 22 ± 7 s for 9- to 13-year-old boys, which sits strikingly
close to the proposed tipping point for an O2 delivery dependency
on V̇O2 kinetics. It is, however, currently unknown whether chil-
dren display a HHb/V̇O2 overshoot at the onset of exercise and if
so, whether this can be abolished with priming exercise.
In addition to altered muscle O2 delivery, muscle fibre type and
motor unit recruitment strategies are known to impact V̇O2 kinet-
ics during exercise (Barstow et al. 1996; Jones et al. 2011), and have
been linked to the priming effect on V̇O2 kinetics in adults
(Burnley et al. 2002; Layec et al. 2009). Changes in muscle activa-
tion have been used to explain, in part, the slowing of V̇O2 kinetics
in youth following experimental manipulation of pedal rate
(Breese et al. 2011) and baseline metabolic rate (Breese et al. 2012).
It may be predicted, therefore, that the altered V̇O2 phase II and
slow component amplitudes previously reported by Barker et al.
(2010) following priming exercise in youth may be related, in part,
to altered muscle activation strategies. This hypothesis, however,
remains to be tested.
As the faster V̇O2 kinetics following priming exercise is consis-
tent with an improved oxidative contribution to energy turnover
and a smaller O2 deficit, an enhanced exercise tolerance may be
anticipated (Burnley and Jones 2007). However, a potential en-
hancement in exercise tolerance is dependent on the recovery of
intramuscular high-energy phosphates and fatigue-inducing me-
tabolites (e.g., Pi and H+) (Chidnok et al. 2013), which will be re-
lated to both the intensity of the priming bout and the recovery
duration between bouts (Bailey et al. 2009). We are, however, not
aware of any study that has investigated the potential for priming
exercise to improve exercise tolerance in youth.
The purpose of the present study was to use priming exercise to
further our understanding of the limiting factors of V̇O2 kinetics
in boys. Specifically, we were interested in establishing (i) how
muscle O2 delivery and O2 utilization, and muscle activity may
limit V̇O2 kinetics during very heavy exercise; and (ii) whether
priming exercise can improve exercise tolerance. We hypoth-
esised that (i) the altered phase II and slow component V̇O2 ampli-
tudes following priming exercise will be related to an improved
309
matching of muscle O2 delivery relative to V̇O2 and a blunted in-
crease in muscle activity over time; and (ii) the priming-induced
accelerated V̇O2 will enhance exercise tolerance.
Materials and methods
Participants
Seven male participants volunteered to take part in the study
(age: 11.3 ± 1.6 years; stature: 1.50 ± 0.13 m and body mass: 42.0 ±
11.1 kg). All participants and their parent(s)/guardian(s) provided
informed assent and consent respectively, to partake in the proj-
ect, which was approved by the institutional ethics committee.
The participants were healthy, recreationally active, and showed
no contraindications to exercise to exhaustion.
Experimental protocol
Participants visited the laboratory on 4 separate occasions over
a 3-week period, with at least 24 h of rest provided between visits.
All participants arrived at the laboratory in a rested state and were
requested to refrain from food and caffeine for at least 2 h prior to
testing. The first laboratory session consisted of basic anthropo-
metrical measures and an exercise test to determine maximal
oxygen uptake (V̇O2max) and the gas exchange threshold (GET).
During the subsequent 3 visits, the participants completed either
a single bout or double bouts of very-heavy-intensity exercise. All
tests were performed on an electronically braked cycle ergometer
(Lode, Netherlands).
Visit 1: Incremental exercise
A combined ramp and supra-maximal exercise test to exhaus-
tion was employed to determine V̇O2max and the GET (Barker et al.
2011b). The highest 15-s averaged V̇O2 during the ramp or supra-
maximal test was taken as V̇O2max. The V̇O2 at the GET was iden-
tified as a disproportionate increase in expired carbon dioxide
(V̇CO2) relative to V̇O2 (Beaver et al. 1986) and verified using the
ventilatory equivalents for V̇O2 and V̇CO2 (Wasserman et al. 2005).
Visits 2– 4: Square-wave exercise
Each participant completed, in a randomized order, 3 exercise
protocols that consisted of a either a single or double bout of
square-wave exercise: (i) 6 min of cycling at 10 W followed by a
single 6-min exercise transition to a power output equivalent to
60% ⌬ (60% of the difference between the GET and V̇O2max); and
(ii–iii) 6 min of cycling at 10 W followed by two 6-min exercise
transitions to a power output equivalent to 60% ⌬, with 6 min of
cycling at 10 W used as the recovery between the transitions. To
provide a measure of exercise tolerance, the participants were
asked to exercise until exhaustion in protocol 1 and during bout 2
in protocol 3.
Experimental measures
Breath by breath gas exchange and ventilation were determined
using a metabolic cart (Metalyser 3B Cortex, Biophysik, Leipzig,
Germany) that was calibrated prior to each test. Heart rate was
recorded using short range radio telemetry (Polar Vantage NV,
Polar Electro, Kempele, Finland).
Changes in the concentrations of O2Hb and HHb of the left leg
were measured noninvasively using a commercially available near-
infrared spectrometer (NIRO-300, Hamamatsu Photonics KK), as pre-
viously described (Barker et al. 2010). The emitter-detector probe
was affixed over the vastus lateralis muscle, defined as the mid-
way point between the greater trochanter and lateral epicondyle
of the left leg, using double-sided adhesive tape and an elastic
bandage to prevent movement during data collection. As the rel-
ative contribution of haemoglobin and myoglobin to the NIRS
signal is currently unknown, the dynamics of O2Hb and HHb were
considered to reflect changes in both haemoglobin and myoglo-
bin concentrations. The HHb signal is considered to reflect the
dynamic (im)balance between muscle O2 supply and O2 utilization
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 310
and was used to provide a description of muscle O2 extraction
(Koga et al. 2012). In addition, the tissue oxidation index (TOI) was
used to describe the oxygenation of the muscle during exercise.
All NIRS variables were collected a 6 Hz, averaged into 1-s intervals
and expressed as a change from baseline, taken after 10 min of
seated rest on the cycle ergometer.
The neuromuscular activity of the vastus lateralis muscle of the
right leg was determined using a 4-channel surface electromyog-
raphy (EMG) system (ME3000PB Muscle Tester, Mega Electronics),
as previously described (Breese et al. 2012). Briefly, following site
preparation, graphite snap electrodes (Unilect 40713, Unomedical,
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Stonehouse, UK) were adhered to the skin surface in a bipolar
arrangement with an interelectode distance of 20 mm at the mid-
way point between the greater trochanter and lateral epicondyle
of the right leg. The ground electrode was placed on the rectus
femoris muscle of the right leg. Additional experiments demon-
strated that the use of the rectus femoris for the ground electrode
produced a similar EMG profile during square-wave exercise when
compared with the tibial head (data not presented). An elastic
bandage was wrapped around each participant’s leg to prevent
displacement of the electrodes during cycling. All EMG measure-
ments were sampled at 1000 Hz, between a bandwith of 8–500 Hz
with a common mode rejection ratio of 110 dB, gain of 305 and
maximum noise of 1.6 ␮V. The raw EMG signals were amplified
(amplifier input impedance > 1 M⍀), collected online and stored
on a personal computer using MegaWin software (Mega Electronics)
for subsequent analysis.
Data analysis
For personal use only.
Breath by breath changes in V̇O2 for each square-wave exercise
bout were analyzed using methodology previously described from
our laboratory (e.g., Fawkner and Armstrong 2004; Barker et al.
2010; Breese et al. 2012). Following the removal of data lying
greater than 3 SD from a local moving mean, the repeat square-
wave exercise transitions for bout 1 and bout 2 were interpolated
to 1 s and averaged into 5-s data bins. The averaged V̇O2 response
for bout 1 and bout 2 were baseline corrected by subtracting the
mean V̇O2 between –60 and –15 s from the exercise response.
Following removal of phase I (cardio-dynamic) by omitting the
initial 15 s of data (Hebestreit et al. 1998), the phase II portion of
the V̇O2 response was characterised using the following nonlinear
equation:
(1) V̇O2(t) ⫽ ⌬V̇O2A × [1 ⫺ e⫺(t⫺TD)/␶]
where V̇O2(t), V̇O2A, TD and ␶ represent the value of V̇O2 at a given
time (t), the amplitude of V̇O2 from baseline to its asymptote, time
delay and the time constant of the response, respectively.
Following the methods of Rossiter et al. (2002), eq. 1 was initially
fit up to the first 60 s of exercise and then increased iteratively by
5 s to end-exercise (LabView, version 6.1, National Instruments,
Newbury, UK). The best fit curve for the phase II portion of the
response was established using (i) a plot of the V̇O2 ␶ against time,
to identify the point at which the influence of the V̇O2 slow com-
ponent lengthened the estimated ␶ following an initial plateau;
and (ii) deviation from an optimal fitting of the model as judged by
a systematic departure of the model’s residuals. The phase II pa-
rameter estimates from eq. 1 were then resolved by least-squares
non-linear regression (GraphPad Prism, GraphPad Software, San
Diego, Calif., USA). The magnitude of the V̇O2 slow component
was calculated as the difference between the mean of the final 30 s
at 6 min of exercise and the phase II asymptote. The V̇O2 slow
component amplitude was also expressed in relative terms using
V̇O2 at 6 min of exercise. To provide a description of the overall
kinetic response (mean response time: MRT), eq. 1 with TD con-
strained to 0 s, was fit from exercise onset to 6 min of exercise.
Appl. Physiol. Nutr. Metab. Vol. 39, 2014
The muscle HHb profiles were averaged into 5-s data bins, time-
aligned to exercise onset, and ensemble averaged to yield a single
response for the control and primed exercise conditions. The HHb
kinetics (primary and slow component phases) were modeled in a
similar fashion to the procedures described for V̇O2 above, but
with some slight modifications. The exponential-like increase in
HHb after the onset of exercise occurred after a discernible delay.
The time at which the exponential-like increase in HHb com-
menced was identified as the point of a 1 SD increase above base-
line (DeLorey et al. 2003). Equation 1 was then applied to resolve
the HHb TD and ␶ following removal of the data preceding the
exponential-like increase. The HHb MRT was calculated by sum-
ming TD and ␶ to provide an overall description of the kinetics in
the primary phase. Changes in TOI were described at baseline and
6 min of exercise.
The ratio of HHb to V̇O2 was calculated using 2 different meth-
ods, as described by Murias et al. (2011a), to investigate the impact
of priming exercise on the matching of O2 delivery to O2 utiliza-
tion. First, the absolute ratio of HHb and V̇O2 (HHb/V̇O2) was cal-
culated at baseline, the primary amplitude and at 6 min of
exercise. Second, the ratio of the index of ⌬HHb to ⌬V̇O2 (⌬HHb/
⌬V̇O2) was determined by normalizing the respective response
profiles with 0% and 100% representing baseline and 6 min of
exercise, respectively. The ⌬HHb and ⌬V̇O2 signals were time-
aligned by deleting the initial 15 s of the V̇O2 data to account for
phase I. The mean ⌬HHb/⌬V̇O2 was calculated over the phase II
and slow component phases of the V̇O2 kinetic response for each
individual. At any given time a ⌬HHb/⌬V̇O2 ratio of 1.00 represents
an equivalent matching between muscle O2 delivery and O2 utili-
zation to that observed at 6 min of exercise. Conversely, a ⌬HHb/
⌬V̇O2 ratio >1.00 or <1.00 theoretically represents either an
increase or decrease in O2 extraction, respectively, for a given V̇O2
compared with that observed at 6 min of exercise.
The raw EMG data were analyzed within MegaWin software
(Mega Electronics). The EMG signal was initially filtered using a
high and low pass of 20 Hz and 500 Hz, respectively. A second-
order Butterworth filter was then employed to remove contami-
nation from movement artifacts, rectified and integrated over a
15-s time bin. The integrated EMG (iEMG) signal was then time-
aligned to exercise onset and ensemble averaged to yield a single
response for the control and primed exercise conditions. The
iEMG data were expressed as a percentage change from the am-
plitude recorded whilst cycling at 10 W during bout 1 prior to the
square-wave exercise transition. The iEMG response was then an-
alyzed by calculating the mean iEMG amplitude between baseline
and the onset of the V̇O2 slow component, and from the V̇O2 slow
component to 6 min of exercise. In addition, the change in iEMG
over time from the onset of the V̇O2 slow component to 6 min was
quantified using linear regression (GraphPad Prism, GraphPad
Software) as previously described (Breese et al. 2012).
Statistical analyzes
In line with recent statistical recommendations (Hopkins et al.
2009), we used 90% confidence limits (CL) to calculate probabilistic
magnitude based inferences for the observed effect of priming
exercise on V̇O2 kinetics, muscle HHb and iEMG dynamics, and
exercise tolerance. Using a published spreadsheet (Hopkins 2007),
the mean difference between the physiological variables in bout 1
and bout 2 were calculated with a 90% CL to represent the uncer-
tainty of the true effect. In the absence of data concerning the
smallest worthwhile change for the physiological outcomes re-
ported in the current study, Cohen’s (1988) standardised mean of
0.2 was employed, as recommended by Batterham and Hopkins
(2006). Based on the smallest worthwhile change, the probabil-
ity that the observed effect was beneficial, trivial or harmful
was calculated using the spreadsheet. The following probabil-
ity thresholds were used to inform these decisions: <0.5%, most
unlikely; 0.5%–5%, very unlikely; 5%–25%, unlikely; 25%–75%,
Published by NRC Research Press
 Barker et al. 311

possibly; 75%–95%, likely; 95%–99.5%, very likely; >99.5%, most Fig. 1. Mean oxygen uptake (V̇O2) profile during bout 1 (open circles)
likely (Batterham and Hopkins 2006; Hopkins et al. 2009). An and bout 2 (filled circles). The onset of exercise is illustrated by the
effect was deemed trivial when the majority (>50%) of the 90% CL vertical dotted line. Note the increased phase II V̇O2 amplitude and
lay between beneficial and harmful. Conversely, an effect was the reduced V̇O2 slow component amplitude in bout 2.
deemed unclear when the likelihood of a beneficial and harmful
effect was >5%. Pearson’s correlation coefficients and their 90% CL
were used to explore the relationship between changes in V̇O2
kinetics and mechanistically important variables (e.g., muscle
TOI) following priming exercise. Probabilistic-based inferences
for the smallest worthwhile correlation were calculated, as de-
scribed above for the changes in means. Descriptive statistics
were calculated using SPSS (version 19.0, Chicago, Ill., USA) and
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are presented as means ± SD.

Results
Ramp and supra-maximal exercise
The group mean V̇O2max, maximal heart rate and peak power
output was 2.12 ± 0.56 L·min−1, 192 ± 8 beats·min−1 and 170 ± 57 W,
respectively. The GET occurred at a V̇O2 of 1.20 ± 0.28 L·min−1,
which represented 59% ± 16% V̇O2max. The mean power output at
60% ⌬ was 124 ± 47 W.

V̇O2 kinetics
The group mean V̇O2 response during the control and primed
cycling exercise bouts is shown in Fig. 1. Table 1 provides the
inferential statistics for the V̇O2 kinetic response parameters.
Baseline V̇O2 was possibly lower in bout 2 compared with bout 1 with bout 2 (Fig. 4B). This was captured in the normalized ⌬HHb/
(effect size (ES) = –0.21). The influence of priming exercise on the
⌬V̇O2 response (Fig. 4C). The mean normalized ⌬HHb/⌬V̇O2 re-
phase II ␶ (ES = −0.35) and TD (ES = −0.17) was unclear but the
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sponse was likely higher (overshoot, ES = 0.88) than unity in bout 1

phase II amplitude (ES = 0.23) and gain (ES = 0.74) were possibly
and very likely higher, respectively, in bout 2 compared with
bout 1. A slow component was manifest in all V̇O2 responses and
was lower both in absolute (likely, ES = −0.92) and relative terms
(very likely, ES = −1.17) in bout 2 compared with bout 1. The
V̇O2 MRT was most likely reduced in bout 2 (ES = −1.07).
Muscle oxygenation kinetics
The group mean HHb and TOI response profiles during bout 1
and bout 2 are shown in Fig. 2 with the HHb kinetic parameters
presented in Table 2. Bout 2 was associated with a very likely
reduced HHb (ES = −0.62) and a very likely higher TOI (bout 1:
66.8 ± 2.9 vs. bout 2: 71.5 ± 3.7; change, ±90%CL: 4.7, ±2.4, ES = 1.23)
at baseline. The HHb TD was very likely reduced in bout 2 (ES =
−0.99), although priming exercise had an unclear effect on HHb ␶
(ES = 0.04) and MRT (ES = −0.44). The primary amplitude for HHb
was likely higher (ES = 0.31) in bout 2 but priming exercise had an
unclear effect on the HHb slow component (ES = 0.11). End-
exercise HHb was possibly lower in bout 2 but the increase in HHb
above baseline was possibly higher in bout 2 (bout 1: 8.2 ± 4.3 vs.
bout 2: 9.4 ± 3.6; change: 1.3, ±1.1, ES = 0.28). End TOI (bout 1: 52.4 ±
4.5 vs. bout 2: 54.2 ± 4.5; change: 1.8, ±1.8, ES = 0.35) was likely
higher in bout 2. Baseline TOI in bout 2 had a likely positive
relationship with the change in the phase II V̇O2 amplitude fol-
lowing priming exercise (r = 0.57, ±0.54) but an unclear relation-
ship with the change in the V̇O2 slow component amplitude
(r = −0.47, ±0.59). The delta change in TOI from baseline to 6 min
during bout 2 had a likely negative relationship with the change
in the phase II V̇O2 amplitude (r = −0.72, ±0.43) and a likely positive
relationship with the slow component (r = 0.72, ±0.43) amplitude,
following priming exercise (Fig. 3).
Matching of HHb to V̇O2
The magnitude of the absolute HHb/V̇O2 ratio was lower in
bout 2 compared with bout 1 at baseline (very likely, ES = −0.74),
the primary phase (likely, ES = −0.33) and 6 min (likely, ES = −0.29)
of exercise (Table 2). The group mean normalized dynamics of
⌬HHb/⌬V̇O2 are shown in Fig. 4 and show a profoundly altered
adjustment of ⌬HHb relative to ⌬V̇O2 in bout 1 (Fig. 4A) compared
and very likely lower than unity (“undershoot”, ES = −1.33) in bout
2 over the phase II V̇O2 region. At 6 min of exercise, the normal-
ized ⌬HHb/⌬V̇O2 ratio remained likely higher than unity for bout
1 (1.02 ± 0.02, ES = 0.81) but was unclear for bout 2 (1.00 ± 0.02, ES =
−0.18). The mean normalized ⌬HHb/⌬V̇O2 was very likely reduced
in bout 2 compared with bout 1 over both the phase II (bout 1:
1.08 ± 0.11 vs. bout 2: 0.92 ± 0.07; change: –0.16, ±0.11, ES = −1.47)
and slow component (bout 1: 1.05 ± 0.04 vs. bout 2: 0.96 ± 0.05;
change: –0.09, ±0.05, ES = −1.64) phases.
iEMG
The group mean iEMG response during bout 1 and bout 2 is
presented in Fig. 5. The mean iEMG response in bout 2 was likely
reduced at baseline (bout 1: 100% ± 0% vs. bout 2: 82% ± 24%;
change: –18, ±18, ES = –0.91), up until the onset of the V̇O2 slow
component (bout 1: 253% ± 55% vs. bout 2: 229% ± 79%; change: –24,
±21, ES = –0.30) and from the onset of the V̇O2 slow component to
6 min of exercise (bout 1: 251% ± 60% vs. bout 2: 227% ± 80%;
change: –25, ±19, ES = –0.31). The appearance of a linear slope for
iEMG over the V̇O2 slow component portion of the response was
unclear for bout 1 (0.07 ± 0.17, ES = 0.34) and bout 2 (–0.03 ± 0.08,
ES = –0.28). Likewise, the linear iEMG slope from the onset of the
V̇O2 slow component to 6 min of exercise was unclear between
bouts (bout 1: 0.07 ± 0.17 vs. bout 2: –0.03% ± 0.08%; change: –0.09,
±0.14, ES = –0.61). The relationship between the V̇O2 slow compo-
nent and the change in iEMG over the slow component region was
unclear for bout 1 (r = –0.31, ±0.64) and bout 2 (r = 0.02, ±0.68). The
change in the iEMG amplitude between bout 1 and 2 shared an
unclear relationship with the change in the phase II (r = 0.22,
±0.66) and slow component (r = –0.16, ±0.67) V̇O2 amplitudes.
Exercise tolerance
Priming exercise resulted in a likely reduction in exercise toler-
ance (bout 1: 739 ± 248 s vs. bout 2: 562 ± 181 s; change: –177, ±180,
ES = –0.71), with an impaired exercise tolerance observed in all but
1 participant.

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 312 Appl. Physiol. Nutr. Metab. Vol. 39, 2014

Table 1. Oxygen uptake kinetics during bout 1 and bout 2.

Bout 1 Bout 2 Change,
Variable (mean ± SD) (mean ± SD) ±90% CL Inference
Baseline V̇O2 (L·min ) −1 0.74±0.09 0.72±0.10
Phase II ␶ (s) 25.5±2.2 23.5±6.4 −1.9, ±3.5 Unclear
Phase II TD (s) 9.8±2.9 9.3±2.0 −0.5, ±1.7 Unclear
Phase II V̇O2 amplitude (L·min−1) 0.93±0.34 1.04±0.45 0.11, ±0.09 Possibly higher
Phase II gain (mL·min−1·W−1) 9.2±0.9 10.1±1.2 0.9, ±0.6 Very likely higher
V̇O2 slow component onset (s) 159±60 187±40 29, ±36 Likely higher
V̇O2 slow component amplitude (L·min−1) 0.12±0.10 0.05±0.02 −0.08, ±0.07 Likely lower
V̇O2 slow component relative amplitude (%) 6.3±3.4 2.8±1.3 −3.5, ±2.6 Very likely lower
End-exercise V̇O2 (L·min−1) 1.80±0.49 1.81±0.50 0.01, ±0.04 Trivial
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End-exercise V̇O2 gain (mL·min−1·W−1) 10.3±1.0 10.6±1.3 0.3, ±0.3 Possibly higher
V̇O2 mean response time (s) 45.1±7.4 37.1±5.4 −8.0, ±3.0 Most likely faster
Note: Effect represents the magnitude of the change by subtracting bout 2 from bout 1. 90% CL represents the uncertainty of the
observed effect. The 90% CL of the true effect can be established by adding and subtracting the 90% CL to the effect. Inference represents
the probabilistic inference that the magnitude of the observed effect is different from the smallest worthwhile change using Cohen’s
standardized effect of 0.2 (see methods for details). CL, confidence limit; V̇O2, oxygen uptake; TD, time delay.

Fig. 2. Mean deoxyhaemoglobin (HHb) (A) and TOI (B) dynamics
during bout 1 (open circles) and bout 2 (filled circles). The vertical
dotted line signifies the onset of exercise. Note that in bout 2 the
tissue oxidation index (TOI) is elevated at baseline and throughout
the exercise transition.
For personal use only.
component. Changes in the phase II V̇O2 ␶ were unclear. However,
the present study has revealed the following novel findings in
young boys: (i) priming exercise increased baseline muscle TOI
and caused subtle adjustments to the dynamics of HHb by reduc-
ing the HHb TD; changes in the HHb primary ␶ and MRT were
unclear; (ii) priming exercise reduced the normalized ⌬HHb/⌬V̇O2
ratio by abolishing the overshoot that was present in bout 1 and
causing an undershoot in bout 2; (iii) priming exercise reduced
muscle activity as inferred by a lower iEMG amplitude in bout 2
compared with bout 1; (iv) large relationships between indices of
enhanced muscle O2 availability (e.g., baseline TOI, ⌬ TOI) during

Discussion
In agreement with our earlier study (Barker et al. 2010), priming
exercise resulted in a speeding of the V̇O2 MRT because of an
increase in the phase II V̇O2 amplitude and a reduced V̇O2 slow
bout 2 and the change in the V̇O2 phase II and slow component
amplitudes following priming exercise were found. In contrast,
changes in iEMG following priming exercise did not correlate
with the altered V̇O2 response; and (v) exercise tolerance was re-
duced by ⬃24% on average following priming exercise. Collec-
tively, these findings suggest that localized changes in both
muscle O2 delivery and muscle O2 utilization, and not muscle
activity, play an important role in limiting V̇O2 kinetics during
very heavy exercise in youth. However, despite the more rapid
adjustment of oxidative metabolism brought about by priming
exercise, this did not improve exercise tolerance.
Poole et al. (2008) have proposed that a “tipping point” may
exist with regard to the dependence of the phase II V̇O2 ␶ on
muscle O2 delivery. In this regard, it has been suggested that when
the phase II V̇O2 ␶ is greater than 21 s, the V̇O2 kinetic response
becomes, in part, muscle O2 delivery-dependent (Murias et al.
2011a, 2011b). This is based on the finding that the normalized
⌬HHb/⌬V̇O2 ratio demonstrated an overshoot in adult partici-
pants with a phase II V̇O2 ␶ greater than 21 s, suggesting a greater
rate of change in fractional O2 extraction relative to V̇O2, possibly
because of a reduced microvascular O2 delivery (Murias et al.
2011b). It is therefore interesting that in bout 1 of the current study
the mean phase II V̇O2 ␶ was 25.5 s and an overshoot in the nor-
malized ⌬HHb/⌬V̇O2 ratio (1.08) was observed over the phase II
V̇O2 region. This overshoot is identical to (1.08) that previously
reported in young adults with similar phase II kinetics (Murias
et al. 2011a) and may suggest that the phase II V̇O2 ␶ is, in part,
limited by muscle O2 delivery in young people. In support of this
reasoning is evidence of a slowed phase II V̇O2 ␶ in children during
cycling exercise during hypoxia (15% O2) (Springer et al. 1991).
However, evidence of a speeding of the phase II V̇O2 ␶ during
conditions when muscle O2 delivery is elevated is needed to fully
support the view that muscle O2 availability limits V̇O2 kinetics in
youth.
In the current study the priming intervention elevated muscle
O2 availability during bout 2, as evidenced by the increased TOI at
baseline and throughout exercise. In addition, as recently shown
in young healthy adults (Murias et al. 2011a), priming exercise

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 Barker et al. 313

Table 2. Muscle oxygenation kinetics during bout 1 and bout 2 cycling conditions.
Bout 1 Bout 2 Change,
Variable (mean ± SD) (mean ± SD) ±90% CL Inference
HHb baseline (a.u.) −4.6±2.8 −6.9±3.5 −2.2, ±0.9 Very likely lower
HHb primary TD (s) 9.0±2.8 6.2±2.1 −2.8, ±1.6 Very likely lower
HHb primary ␶ (s) 14.7±6.1 15.0±3.1 0.2, ±3.9 Unclear
HHb primary MRT (s) 23.7±6.1 21.2±3.7 −2.6, ±3.9 Unclear
HHb primary amplitude (a.u.) 7.0±2.9 8.1±3.3 1.1, ±0.9 Likely higher
HHb slow component amplitude (a.u.) 1.2±1.6 1.3±0.5 0.1, ±1.1 Unclear
HHb slow component amplitude (%) 9.0±16.6 14.8±7.2 5.9, ±15.7 Unclear
HHb at 6 min (a.u.) 3.6±3.7 2.6±3.6 −1.0, ±0.9 Possibly lower
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HHb/V̇O2 baseline (a.u./L·min−1) −6.07±3.23 −9.23±4.11 −3.16, ±1.24 Very likely lower
HHb/V̇O2 primary (a.u./L·min−1) 1.47±1.57 0.75±2.19 −0.72, ±0.58 Likely lower
HHb/V̇O2 at 6 min (a.u./L·min−1) 2.06±1.95 1.36±2.24 −0.70, ±0.47 Likely lower
Note: Effect represents the magnitude of the change by subtracting bout 2 from bout 1. 90% CL represents the uncertainty of the
observed effect. The 90% CL of the true effect can be established by adding and subtracting the 90% CL to the effect. Inference represents
the probabilistic inference that the magnitude of the observed effect is different from the smallest worthwhile change using Cohen’s
standardized effect of 0.2 (see Materials and methods section for details). CL, confidence limit; HHb, deoxyhaemoglobin; TD, time
delay; MRT, mean response time; V̇O2, oxygen uptake.

Fig. 3. The relationship between the change in tissue oxidation
index (TOI) from baseline to 6 min of exercise in bout 2 to the
change in the phase II (A) and slow component (B) oxygen uptake
(V̇O2) amplitudes following priming exercise.
For personal use only.
V̇O2 ␶ was found, which is in agreement with an earlier study
from our laboratory using the same priming intervention in 9- to
13-year-old boys (Barker et al. 2010). This finding therefore sup-
ports the notion that the phase II V̇O2 ␶ in young boys is princi-
pally limited by intramuscular metabolic factors, likely related to
the creatine kinase mediated splitting of muscle phosphocreatine
(PCr) and (or) the activity of rate limiting oxidative enzymes
(Meyer 1988; Kindig et al. 2005; Poole et al. 2008). Such a conclu-
sion is indirectly supported by the similar kinetics for phase II V̇O2

reduced the normalized ⌬HHb/⌬V̇O2 ratio during phase II V̇O2 to
0.92 on average, suggesting a better matching of localized muscle
O2 delivery to O2 utilization during the exercise transient, imply-
ing that a reduced rate of O2 extraction was required to meet the
increased V̇O2. However, despite this elevated muscle O2 availabil-
ity in bout 2, an unclear effect for priming exercise on the phase II
and muscle PCr at the onset and offset of exercise in young people
(Barker et al. 2008b).
An interesting finding in the current study was the presence of
a reduced HHb TD following priming exercise. This is likely to
reflect an earlier mismatch between muscle O2 delivery and utili-
zation during bout 2, suggesting an enhanced O2 extraction early
(initial ⬃ 5 s) in the exercise transient. This occurred despite an
elevated muscle O2 availability during the baseline of bout 2, and
may reflect a more rapid activation of oxidative metabolism, pos-
sibly because of an increased activity of rate-limiting oxidative
enzymes, such as pyruvate dehydrogenase (Gurd et al. 2009), and
(or) activation of the mitochondrial electron transport chain
(Gandra et al. 2012). Following the HHb TD, however, HHb rose
with exponential-like kinetics but the resulting HHb ␶ and MRT
(TD + ␶) was found to have an unclear effect following priming
exercise, suggesting the overall dynamic balance between muscle
O2 delivery and O2 utilization during the primary phase was un-
altered by priming exercise. While this finding agrees with previ-
ous studies in adults (DeLorey et al. 2007; Murias et al. 2011a), it
contrasts the recent work form our laboratory showing no
changes in the HHb profile (TD, ␶ or MRT) following priming ex-
ercise in young boys (Barker et al. 2010). Such inter-study differ-
ences in HHb dynamics have also been reported across similar
adult studies (DeLorey et al. 2007; Gurd et al. 2009; Murias et al.
2011a), and may be explained by the heterogeneity in the HHb
response dynamics that is observed across the quadriceps muscle
(Koga et al. 2007).
In agreement with earlier investigations in children and adults
(Burnley et al. 2001, 2002; Bailey et al. 2009; Barker et al. 2010), the
phase II V̇O2 amplitude was elevated following priming exercise,
resulting in an increase in the V̇O2 phase II gain. As shown previ-
ously in adults (Burnley et al. 2001), this was independent of an
elevated baseline metabolic rate, as baseline V̇O2 during bout 2
had returned to, and was possibly lower than bout 1. Based on
unchanged HHb (muscle O2 extraction) dynamics and an increase
in bulk blood flow, we recently interpreted this to be caused by an
improved muscle O2 delivery (Barker et al. 2010). The current
study extends this interpretation as the change in the phase II V̇O2
amplitude following priming exercise was positively correlated

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 314 Appl. Physiol. Nutr. Metab. Vol. 39, 2014

Fig. 4. Group mean normalised deoxyhaemoglobin (HHb) (open Fig. 5. Mean integrated electromyography (iEMG) during bout 1
circles) and oxygen uptake (V̇O2) (filled circles) dynamics during (open circles) and bout 2 (filled circles). The vertical dotted line
bout 1 (A) and bout 2 (B). Panel C expresses these changes as a ratio signifies the onset of exercise.
(⌬HHb/⌬V̇O2) for bout 1 (open squares) and bout 2 (filled squares).
Note that a ⌬HHb/⌬V̇O2 “overshoot” is present in bout 1, but this is
abolished to an “undershoot” in bout 2.
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with bout 2 baseline TOI (r = 0.57) and negatively with the delta
change in TOI during bout 2 (r = –0.72). However, in addition to a
potential role for muscle O2 delivery, the elevated phase II V̇O2
amplitude following priming exercise has been linked to an in-
For personal use only.

crease in muscle activation (Burnley et al. 2002; Layec et al. 2009).

For example, Burnley et al. (2002) reported an elevated iEMG dur-
ing heavy-intensity cycling following priming exercise, which was
proportional to the rise in the phase II V̇O2 amplitude. In the
current study, however, we observed a reduced iEMG amplitude
during the phase II V̇O2 portion of the response, which according
to previous interpretations in adults (Burnley et al. 2002; Bailey
et al. 2009; Layec et al. 2009), suggests a reduction in motor unit
recruitment. Unlike indices in muscle O2 availability, however,
the reduction in iEMG did not correlate with the increase in the
phase II V̇O2 amplitude following priming exercise. This finding
does not support a mechanistic role for muscle activation in alter-
ing the phase II V̇O2 amplitude in young boys following priming
exercise, which is in agreement with the adult data of Scheuermann
et al. (2001). Rather, coupled with the elevated muscle O2 availabil-
ity at the onset of exercise, priming exercise may have increased
the distribution of O2 to the active muscle fibres, with the out-
come being an elevated phase II V̇O2 amplitude.
An alternative explanation for the increased phase II V̇O2 am-
plitude in the current study could relate to the possibility that
muscle efficiency was reduced following priming exercise. For
example, Sahlin et al. (2005) reported an elevated phase II V̇O2
amplitude following high-intensity priming exercise under con-
ditions of elevated muscle and blood lactate and reduced muscle
PCr, which remained until end exercise (10 min). These authors
and others (Jones et al. 2008) have suggested that residual muscle
fatigue from the initial priming bout may reduce muscle effi-
ciency. However, not all data support this notion (Layec et al.
2009), and it is pertinent to note that the increased O2 cost of
exercise in the present study was abolished by 6 min of exercise
(see Fig. 1), suggesting that if exercise efficiency was altered in the
present study, it was confined to the earlier portion of the bout.
Over 80% of the V̇O2 slow component during high-intensity ex-
ercise has been shown to originate from the exercising limbs
(Poole et al. 1991) with the progressive recruitment of muscle fi-
bres, specifically high-order type II fibres, considered to be the
main mechanism (Barstow et al. 1996; Krustrup et al. 2004; Endo
et al. 2007). In this context it is pertinent to note that during bout 1
or bout 2 we did not observe a meaningful linear rise in iEMG over

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 Barker et al.
time over the V̇O2 slow component region. Furthermore, while
priming exercise reduced both the relative (56%) and absolute
(58%) V̇O2 slow component amplitude in the current study, this
was not correlated with iEMG, despite the reduced iEMG ampli-
tude in bout 2. This lack of an association between changes in
iEMG and the V̇O2 slow component corroborates some (Scheuermann
et al. 2001) but not all (Burnley et al. 2002; Bailey et al. 2009)
previous adult work, and provides support for the notion that the
progressive recruitment of muscle fibres per se, is not mechanis-
tically linked to the development of the V̇O2 slow component in
young boys. Our study cannot, however, discount the possibility
that the metabolic cost associated with the recovery of previously
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active muscle fibres (e.g., Vanhatalo et al. 2011) plays an important
role in the development of the V̇O2 slow component in young
people.
An alternative explanation for the reduced V̇O2 slow compo-
nent amplitude in the current study may be related to an elevated
bulk O2 delivery and (or) the matching of muscle O2 availability to
O2 utilization (DeLorey et al. 2007; Gurd et al. 2009; Murias et al.
2011a). We recently reported in young boys that a reduced V̇O2
slow component following priming exercise was observed with an
elevated cardiac output (bulk blood flow) to V̇O2 ratio, although it
could not be concluded that the elevated bulk blood flow resulted
in an increased muscle O2 availability (Barker et al. 2010). The
present study extends this work and provides evidence that an
increase in muscle O2 availability was related to the reduction in
the V̇O2 slow component amplitude. First, we observed a correla-
tion between the change in the V̇O2 slow component following
priming exercise and TOI at baseline of bout 2 (r = –0.47) and the
For personal use only.
change in TOI from baseline to 6 min of exercise in bout 2 (r =
0.72). Second, the mean normalized ratio of ⌬HHb/⌬V̇O2 over the
slow component region was markedly reduced from 1.05 to 0.96
with priming exercise, suggesting a better matching of localized
muscle O2 delivery to V̇O2. It has been proposed that the enhanced
muscle O2 availability afforded by priming exercise reduces the
rate of fatigue development, presumably by reducing the muscle
metabolic perturbation (e.g., fall in PCr and increase in Pi and H+)
(Hogan et al. 1999), and the requirement to recruit additional
(high-order) muscle fibres during high-intensity exercise (Jones
et al. 2011). This may account for the reduced iEMG amplitude
reported following priming exercise in the present study, but as
mentioned earlier, no meaningful correlation was observed be-
tween changes in iEMG and the V̇O2 kinetic response.
Despite observing faster overall V̇O2 kinetics, and presumably a
reduction in the muscle O2 deficit following priming exercise, we
observed a 24% reduction in time to exhaustion (likely reduced),
with 6 out of the 7 participants having a reduced exercise toler-
ance. This finding agrees with some previous adult studies that
have reported an impaired exercise tolerance following very heavy
intensity priming exercise (Carter et al. 2005; Ferguson et al. 2007).
However, others have reported either an unchanged (Koppo and
Bouckaert 2002) or enhanced exercise tolerance (Bailey et al. 2009)
following priming exercise. It is well established that the tolerable
duration of high-intensity exercise is well described by a hyper-
bolic function of time, the asymptote of which is termed critical
power (CP), and the curvature constant (W=), which describes a
finite amount of work that can be completed above CP (Jones et al.
2010). In adults (Poole et al. 1988), but not children (Barker et al.
2011a), constant work-rate exercise above CP until exhaustion oc-
curs with the attainment of V̇O2max because of the presence of the
V̇O2 slow component. Consequently, the kinetics of V̇O2, V̇O2max,
CP and W= all have the potential to determine exercise tolerance
during high-intensity exercise (Burnley and Jones 2007). However,
as priming exercise does not alter CP or V̇O2max (Ferguson et al.
2007; Vanhatalo and Jones 2009), and the V̇O2 slow component
was attenuated following priming exercise in the current study,
our observed reduction in exercise tolerance is likely explained by
an altered W=. Indeed, a recent study has suggested that the res-
315
toration of muscle metabolic status (e.g., PCr, H+) towards baseline
levels is likely to be of importance in determining exercise toler-
ance above CP (Bailey et al. 2009), and has recently been confirmed
experimentally in humans (Chidnok et al. 2013). In the context of
the present study it is likely that the 6 min recovery duration
employed was insufficient for sufficient recovery of W= (related to
restoration of muscle PCr and H+) prior to the second bout of
exercise. Therefore, although children are reportedly character-
ized with a more rapid muscle metabolic recovery following high-
intensity exercise compared with adults (Ratel et al. 2006), the
6-min recovery duration used between the exercise bouts in the
current study is unlikely to have been sufficient to restore muscle
PCr and H+ back to baseline prior to the second bout of exercise. A
recovery period of ≥6 min is therefore likely to be needed to
realize an enhancement in high-intensity exercise tolerance fol-
lowing priming exercise of an intensity (60% ⌬) and duration
(6 min) used in the current study.
Considerations and limitations
The findings in the present study should be viewed in relation
to the following considerations. First, the normalized ⌬HHb/⌬V̇O2
ratio is typically expressed relative to the steady-state responses
achieved during moderate intensity exercise (Murias et al. 2011a;
2011b). As a steady-state is not observed during very heavy exercise
(i.e., >CP) in youth, the normalized ⌬HHb/⌬V̇O2 ratio was ex-
pressed relative to the amplitudes obtained at 6 min of exercise.
Despite this different approach, the magnitude of the overshoot
in normalized ⌬HHb/⌬V̇O2 over the phase II region was similar to
that previously reported in young adults (Murias et al. 2011b), and
was meaningfully blunted following priming exercise, which is
also consistent with previous adult work during moderate exer-
cise (Murias et al. 2011a; De Roia et al. 2012). Second, similar to
previous studies documenting changes in HHb relative to V̇O2
(DeLorey et al. 2007; Murias et al. 2011b; De Roia et al. 2012), we
obtained the HHb signal from a single probe positioned over the
vastus lateralis muscle. As large variations in the HHb response
dynamics, and by inference the matching of muscle O2 delivery to
utilization, exist both within and between the quadriceps muscle
(Koga et al. 2007, 2011), this may limit the fidelity in relating HHb
dynamics to whole-body V̇O2. Finally, muscle activity in the pres-
ent study was quantified using surface iEMG over the vastus late-
ralis muscle, which is in accord with previous adult research in
this area (Scheuermann et al. 2001; Bailey et al. 2009). Although
the vastus lateralis muscle is progressively recruited throughout
very heavy exercise, at least in adults (Endo et al. 2007), it cannot
be discounted that the use of a single site iEMG measure in the
current study may have resulted in an incomplete picture with
regard to changes in muscle activity following priming exercise.
For example, some adult studies have undertaken a more compre-
hensive measure of muscle activity (gluteus maximus, vastus late-
ralis, vastus medialis) following priming exercise and observed an
increase in iEMG amplitude over the phase II V̇O2 portion of the
response (Burnley et al. 2002). However, it should be noted that
the iEMG data in the current study are consistent with a recent
study documenting an increase in iEMG over the V̇O2 slow com-
ponent region in men but not boys (Breese et al. 2012).
Conclusions
The present study employed simultaneous measurements of
muscle O2 delivery, O2 utilization and muscle activity following
priming exercise to better understand the factors limiting V̇O2
kinetics and high-intensity exercise tolerance in youth. Priming
exercise resulted in more rapid overall V̇O2 kinetics with the V̇O2
response returning closer to mono-exponentiality because of an
increased phase II V̇O2 amplitude and a reduction in the V̇O2 slow
component. Mechanistically these changes were related to an im-
provement in the matching of muscle O2 delivery to V̇O2 as evi-
denced by a reduction in ⌬HHb/⌬V̇O2 and an association with an
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 316
elevated TOI before and during the second bout of exercise. While
muscle activity, as measured using iEMG, was reduced following
priming exercise, this did not correlate with the altered V̇O2 ki-
netics. Finally, despite the enhanced aerobic energy provision fol-
lowing the priming intervention, exercise tolerance was reduced
by 24% on average, possibly because of an insufficient recovery
period between exercise bouts that did not permit adequate re-
covery of the muscle metabolic status towards baseline.
Acknowledgements
We thank the participants for their time and commitment to
this project. We also acknowledge the laboratory support pro-
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vided by Mr. David Childs and Mr. Owen Tomlinson.
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