Muscle glycogen depletion alters oxygen uptake kinetics during heavy exercise.

Abstract

To test the hypothesis that muscle fiber recruitment patterns influence the oxygen uptake (VO2) kinetic response, constant-load exercise was performed after glycogen depletion of specific fiber pools.
After validation of protocols for the selective depletion of Type I and II muscle fibers, 19 subjects performed square-wave exercise at 80% VT (moderate) and at 50% of the difference between VT and VO2max (heavy) without any prior depleting exercise (CON), after HIGH (10 x 1-min exercise bouts at 120% VO2max), and after LOW (3 h of exercise at 30% VO2max) exercise.
Differences in VO2 kinetic parameters were only observed in heavy exercise AFTER HIGH: the VO2 primary component was higher (1.75 +/- 0.12 L x min) compared with CON (1.65 +/- 0.11 L x min, P < 0.05), and the VO2 slow component was lower (0.18 +/- 0.03 L x min) compared with CON (0.24 +/- 0.04 L x min, P < 0.05).
The results indicate that the VO2 response to heavy constant-load exercise can be altered by depletion of glycogen in the Type II muscle fibers, lending support to the theory that muscle fiber recruitment influences both the VO2 primary and slow component amplitudes during heavy intensity exercise.

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Muscle Glycogen Depletion Alters Oxygen
Uptake Kinetics during Heavy Exercise
HELEN CARTER1, JAMIE S. M. PRINGLE1, LES BOOBIS2, ANDREW M. JONES3, and JONATHAN H. DOUST4
1Chelsea School Research Centre, University of Brighton, Eastbourne, UNITED KINGDOM;2Sunderland Royal Hospital,
Sunderland, UNITED KINGDOM;3Manchester Metropolitan University, Alsager, UNITED KINGDOM; and4Department
of Sport and Exercise Science, University of Wales Aberystwyth, Ceredigion, UNITED KINGDOM
ABSTRACT
CARTER, H., J. S. M. PRINGLE, L. BOOBIS, A. M. JONES, and J. H. DOUST. Muscle Glycogen Depletion Alters Oxygen Uptake
Kinetics during Heavy Exercise. Med. Sci. Sports Exerc., Vol. 36, No. 6, pp. 965–972, 2004. Purpose: To test the hypothesis that
muscle fiber recruitment patterns influence the oxygen uptake (V˙O2) kinetic response, constant-load exercise was performed after
glycogen depletion of specific fiber pools. Methods: After validation of protocols for the selective depletion of Type I and II muscle
fibers, 19 subjects performed square-wave exercise at 80% VT (moderate) and at 50% of the difference between VT and V˙O2max
(heavy) without any prior depleting exercise (CON), after HIGH (10 ? 1-min exercise bouts at 120% V˙O2max), and after LOW (3 h
of exercise at 30% V˙O2max) exercise. Results: Differences in V˙O2kinetic parameters were only observed in heavy exercise AFTER
HIGH: the V˙O2primary component was higher (1.75 ? 0.12 L·min?1) compared with CON (1.65 ? 0.11 L·min?1, P ? 0.05), and
the V˙O2slow component was lower (0.18 ? 0.03 L·min?1) compared with CON (0.24 ? 0.04 L·min?1, P ? 0.05). Conclusions: The
results indicate that the V˙O2response to heavy constant-load exercise can be altered by depletion of glycogen in the Type II muscle
fibers, lending support to the theory that muscle fiber recruitment influences both the V˙O2primary and slow component amplitudes
during heavy intensity exercise. Key Words: V˙O2PRIMARY COMPONENT, V˙O2SLOW COMPONENT, MUSCLE BIOPSY,
MUSCLE FIBER RECRUITMENT, CONSTANT-LOAD EXERCISE
I
phases. After the cardiodynamic phase (phase I), V˙O2rises
in an approximately monoexponential fashion (phase II or
primary component) to attain a new steady state (phase III)
within 2–3 min (1). However, during exercise above the LT,
the attainment of a steady state is delayed or absent due to
the development of an additional V˙O2slow component,
which is superimposed on the primary component (1).
The mechanism responsible for the development of the
V˙O2slow component remains elusive. Attention has been
given to the influences of lactate, adrenaline, the cost of
ventilatory work and rises in core or muscle temperature
(10). Poole et al. (21) demonstrated that approximately 86%
of the V˙O2slow component originates in the exercising
limb, and therefore the recruitment of Type II muscle fibers
has been considered to be a possible mediator of the phe-
nomenon. Indeed, it has been shown that the proportion of
Type II fibers in the vastus lateralis is significantly corre-
n the transition from rest to constant-load exercise below
the lactate threshold (LT), the pulmonary oxygen uptake
(V˙O2) response can be partitioned into three distinct
lated with the relative magnitude of the V˙O2slow compo-
nent (1,22). Furthermore, several studies (but not all, e.g.,
25) have reported changes in neuromuscular activity in line
with development of the V˙O2slow component (4,20). This
may represent the recruitment, in some manner, of the Type
II muscle fibers which are thought to be of lower mechanical
efficiency (19). The percent Type I muscle fibers also ap-
pears to be associated with a greater increase of the V˙O2
primary component relative to power output (referred to as
the “gain” of the primary component) during constant-load
exercise (1,22) and with a greater ?V˙O2/? work rate slope
during incremental (2) exercise. Seemingly in direct contrast
to these studies, Coyle et al. (8) found a lower exercise V˙O2
for individuals with a high proportion of Type I fibers.
However, because V˙O2was measured some 5 min into
exercise, individuals with a high proportion of Type II fibers
will be seen to be less efficient due to inclusion of the
developing V˙O2slow component. Direct comparison between
this work and that of Barstow and colleagues (1,2) is difficult
because the primary component gain is not reported.
The studies to date have not established the causality of
the relationship between muscle fiber type and the V˙O2
response. It would be preferable to manipulate the indepen-
dent variable, i.e., fiber type recruitment, and observe the
effects on the V˙O2response. Therefore, the purpose of the
present study was to induce glycogen depletion in discrete
fiber pools in an attempt to alter the motor unit recruitment
patterns during constant-load exercise. The assumption is
that metabolism in these glycogen depleted fibers will be
disturbed and recruitment during subsequent exercise there-
fore impaired (27). It has been shown that prolonged low
Address for correspondence: Helen Carter, Ph.D., Chelsea School Research
Centre, University of Brighton, Gaudick Road, Eastbourne, BN20 7SP,
United Kingdom; E-mail: H.Carter@bton.ac.uk.
Submitted for publication August 2003.
Accepted for publication February 2004.
0195-9131/04/3606-0965
MEDICINE & SCIENCE IN SPORTS & EXERCISE®
Copyright © 2004 by the American College of Sports Medicine
DOI: 10.1249/01.MSS.0000128202.73676.11
965

Page 2

intensity exercise (?30% V˙O2max) depletes glycogen con-
centration exclusively in the Type I muscle fibers (11). We
hypothesized that this condition would necessitate a greater
reliance of the Type II fibers during subsequent square-
wave exercise, resulting in a reduction in the gain of the
V˙O2primary component and a greater amplitude of the V˙O2
slow component. In contrast, after high-intensity exercise
that would deplete the glycogen content of the Type IIa and
IIx fibers (28), we hypothesized there would be an increased
reliance on Type I fibers resulting in an increased gain of the
V˙O2primary component and a decreased amplitude of the
V˙O2slow component.
METHODS
Experimental design and participants. There were
two stages to this experiment, which was approved by the
University’s Ethics Committee. The participants gave writ-
ten informed consent after the experimental procedures, and
the associated risks and the benefits of participation were
explained. Fourteen recreationally active participants (age
25.5 ? 4.5 yr; mass 76.0 ? 10.1 kg; V˙O2max2.95 ? 0.5
L·min?1) volunteered to take part in stage 1. The aim of this
stage was to validate the glycogen depletion protocols to be
used in stage 2. This stage involved a muscle biopsy before
and after exercise. Nineteen participants (age 24.8 ? 4.0 yr;
mass 74.9 ? 9.2 kg; V˙O2max3.07 ? 0.71 L·min?1) partic-
ipated in stage 2 of the study which investigated the effect
of glycogen depletion on the V˙O2kinetic response. Twelve
participants completed both stages of the study. The partic-
ipants were all fully familiar with laboratory exercise testing
procedures. The participants were instructed to arrive at the
laboratory after an overnight fast, to be rested and in a fully
hydrated state having abstained from the consumption of
caffeine for the previous 4 h. The participants were also
asked to avoid strenuous exercise in the 48 h preceding a test
session and to record food intake for this period. Subjects
kept a food diary before the first lab visit and then the same
diet was replicated before each session.
Procedures. All tests were conducted on an electrically
braked cycle ergometer (Jaeger ER800, Germany), with seat
and handlebar height kept constant over the sessions for
each participant. Pedal frequency was maintained at 60 ? 5
rev·min?1for all tests. Pulmonary gas exchange was deter-
mined breath-by-breath using standard algorithms, allowing
for the time delay between gas concentration and volume
signals. Individuals breathed through a low dead space (90
mL), low resistance (0.65 mm H2O·L?1·s?1at 8 L·s?1)
mouthpiece and turbine assembly. Gases were continuously
drawn from the mouthpiece through a 2-m capillary line of
small bore (0.5 mm) at a rate of 60 mL·min?1and analyzed
for O2, CO2, and N2concentrations by a quadrupole mass
spectrometer (CaSE EX670, Gillingham, Kent, UK), which
was calibrated before each test using gases of known con-
centration. Expiratory volumes were determined using a
turbine volume transducer (Interface Associates, CA). The
volume and concentration signals were integrated by com-
puter after analog-to-digital conversion. Respiratory gas ex-
change variables (V˙O2, V˙CO2, V˙E) were calculated and
displayed for every breath. Heart rate was recorded telem-
etrically throughout the exercise tests (Polar Electro Oy,
Kempele, Finland).
At the beginning of the study, all participants performed
a ramp exercise test to volitional exhaustion in order to
determine the ventilatory threshold (VT) and the V˙O2max.
This test was performed at the same time of day in all
individuals (?1000 h). The initial power output was 20 W,
which was then increased by 5 W every 10 s (equating to 30
W·min?1).
The highest 30-s average of the breath-by-breath V˙O2
data was taken to be the V˙O2max. Attainment of V˙O2maxwas
confirmed by the incidence of a plateau phenomenon in
V˙O2, RER values above 1.10, and heart rates within 5
beats·min?1of age-predicted maximum. In all subjects, at
least two of the three criteria were met. The VT was deter-
mined by two investigators as the point above which there
was a nonlinear increase in minute ventilation (V˙E) plotted
against V˙O2and an increase in V˙E/V˙O2against V˙O2with
no increase in V˙E/V˙CO2against V˙O2(30).
Extrapolation of the relationship between V˙O2and power
output (correction was made for the lag in V˙O2) for exercise
?VT was used to estimate the power output at V˙O2max.
Subsequently, a series of power outputs were calculated:
power outputs requiring 30% and 120% of V˙O2maxfor the
glycogen depletion protocols; and power outputs requiring
80% of the V˙O2at VT (moderate-intensity exercise), and
50% of the difference in V˙O2between VT and V˙O2max
(heavy-intensity exercise, 50%?) for the performance of
“square-wave” exercise in stage 2 of the experimentation.
Stage 1: validation of protocols to deplete glyco-
gen stores in Type I and II muscle fibers. The group
of 14 participants were randomly assigned to one of two
groups. Seven participants undertook low intensity exercise
(30% V˙O2max) for 3 h, with the aim of depleting the Type
I muscle fibers (11). The remaining seven participants per-
formed 10, 1-min bouts of high-intensity exercise (at 120%
V˙O2max), separated by 5-min rest periods. This protocol has
been shown previously to preferentially deplete the Type II
fibers (28). A muscle biopsy was taken before and imme-
diately postexercise in both conditions (see below). During
the low-intensity depletion protocol, pulmonary gas ex-
change, heart rate, and blood lactate concentration were
recorded at 10 min, 30 min, and then every 30 min until the
end of exercise. During the high-intensity depletion proto-
col, blood [lactate] and heart rate were measured at rest, and
after the 5th and 10th sprints.
Muscle samples. Muscle biopsies were taken under
local anesthesia (2 mL, 1% lidocaine) from the lateral por-
tion of the vastus lateralis muscle. The biopsies were ob-
tained by a percutaneous needle biopsy technique (3) with
suction, thus allowing ?100–150 mg of tissue to be ex-
tracted. Muscle biopsies were taken within 15 s of exercise
cessation with a portion of the tissue being immediately
frozen in liquid nitrogen. The rest of the muscle sample was
mounted on a specimen holder in optimum cutting temper-
ature embedding medium (Ames Tissue-Tek) and frozen in
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isopentane cooled in liquid nitrogen. The muscle specimens
were then moved to storage at ?80°C until analysis. Serial
cross sections (10 ?m thick) were cut in a cryostat at ?20°C
and mounted on slides for histochemical analysis. Muscle
fiber type was determined by estimation of myofibrillar
ATPase activity at pH 9.4 (after preincubation at pH 4.7)
after the methods of Brooke and Kaiser (5), with fibers
being classified as Type I, IIa, and IIx. A qualitative assess-
ment of glycogen concentration in these fibers was made
using the periodic acid-Schiff (PAS) reaction (29). Serial
sections could then be matched to allow the glycogen con-
tent of each fiber pool to be determined pre- and postexer-
cise (see Fig. 1). To determine the quantitative reduction in
muscle glycogen with exercise, the unmounted portion of
the tissue was acid hydrolyzed allowing glucose residues to
be measured enzymatically (F200 fluorometer, Wheaton
Scientific, UK) as described by Lowry and Passonneau (18).
Glycogen concentrations are expressed “wet weight” (w.w.).
Stage 2: effect of glycogen depletion on the V˙O2
kinetic response during constant load exercise.
Nineteen participants took part in this stage of the study. A
period of at least two weeks elapsed before retesting of the
12 subjects taking part in both stages of the study to prevent
any impact on muscle glycogen storage by the muscle
biopsy procedure, as previously reported (7). On three sep-
arate occasions participants entered the laboratory and per-
formed a series of “square-wave” transitions of 6-min du-
ration (preceded by 3 min of baseline) in order to determine
V˙O2kinetics: two “moderate” (80% VT) intensity and one
“heavy” (50% ?) intensity transitions, separated by 6-min
recovery. Pulmonary gas exchange was measured breath-
by-breath throughout the square-wave tests. Fingertip cap-
illary blood samples were taken immediately before and
after exercise. The difference between the end-exercise [lac-
tate] and the resting [lactate] was expressed as a delta value
(? [lactate]). After 1 h of rest, a further blood sample was
taken to ensure that blood [lactate] had returned to resting
levels. The subjects then performed an identical set of
square wave transitions. In total, the subjects performed a
total of four moderate and two heavy transitions for each of
the three conditions.
On two of the visits, the square-wave exercise was pre-
ceded by a glycogen depleting protocol (as described in
stage 1). No biopsies were taken in this stage of the exper-
imentation, but measures of V˙O2, heart rate and blood
lactate were taken as previously described. At least an hour
of rest was given after the depletion protocols before com-
mencing the square-wave exercise bouts to allow muscle
temperature, blood metabolites, and V˙O2to return to resting
levels (12,14,15). During this time, no food was consumed,
but water was permitted ad libitum, with a minimum of
150% of the volume lost during the depletion regimen
(based on pre- and postexercise body mass) being con-
sumed. The order in which the subjects performed the con-
trol (CON), low-intensity depletion condition (LOW), and
the high-intensity depletion condition (HIGH) was ran-
domly assigned.
Data analysis. For each exercise transition, the breath-
by-breath data were interpolated to give second-by-second
values. The data from the equivalent transitions were then
time aligned to the start of exercise and averaged in order to
enhance the underlying response characteristics. Nonlinear
regression techniques were used to fit the V˙O2data after the
onset of exercise with an exponential function. The time
course of the V˙O2response after the onset of exercise was
described in terms of a two- (moderate intensity) or three-
(heavy intensity) component exponential function. Each expo-
nential curve was used to describe one phase of the response.
Thefirstphasebeganattheonsetofexercise,whereastheother
terms began after independent time delays (1):
V˙O2?t? ? V˙O2?b? ? Ac*?1 ? e?t/?c? Cardiodynamic component ?phase I?
? Ap*?1 ? e??t?TDp?/?p? Primary component ?phase II?
? As*?1 ? e??t?TDs?/?s? Slow component ?phase III?
where V˙O2(b) is the baseline V˙O2measured in the 3 min
preceding the onset of exercise; Ac, Ap, and Asare the
asymptotic amplitudes for the exponential curves; ?c, ?p, and
?sare the time constants; and TDpand TDsare the time
delays. The cardiodynamic response was terminated at the
onset of the primary component (at TDp), and given the
value for that time (defined Ac'). The amplitude of the
primary response (Ap') was defined as the increase in V˙O2
from baseline to the end of the primary component (i.e., Ac'
? Ap). The amplitude of the V˙O2slow component was
determined as the increase in V˙O2above the asymptotic
primary component at the end of exercise (defined As'),
rather than from the asymptotic value (As), which may lie
beyond physiological limits. Initial estimates for the time-
based parameters used in the modeling were: TDp20 s, TDs
120 s, ?c12 s, ?p25 s, and ?s260 s, based upon values
presented in the literature (1). An iterative process ensured
the residual sum of squares (RSS) was minimized. To en-
FIGURE 1—Serial cross-sections of vastus lateralis biopsy specimen at
rest (A and B) and after low-intensity exercise (C and D). Panels A and
C show the myosin ATPase activity, with fibers being classified as Type
I, IIa, and IIx. These fibers can then be matched with serial sections
PAS stained for glycogen concentration (B and D). Note the PAS dark
staining at rest (B) indicating muscle fibers plentiful of glycogen, in
contrast to post low-intensity exercise where there is differential stain-
ing in the type I fibers compared with the IIa and IIx.
GLYCOGEN DEPLETION AND V˙O2KINETICS
Medicine & Science in Sports & Exercise?
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sure that the minimized residuals were not due to localized
minimized least squares residuals, further iterations with
both under and overestimated parameters were performed.
Statistical analysis. Once the data were checked for
normal distribution and homogeneity of variation, one-way
repeated measures ANOVA and Bonferroni corrected
paired t-tests were used to test for differences with signifi-
cance accepted at P ? 0.05. The 95% confidence intervals
for the time-based parameters were calculated using proce-
dures outlined previously (17). Results are presented as
mean ? SEM.
RESULTS
Stage 1: validation of protocols to deplete glyco-
gen stores in Type I and II muscle fibers. Data col-
lected during the low-intensity depletion protocol indicated
that subjects were working at 31.9 ? 2.4% V˙O2max; RER
decreased during the 3 h (from 0.88 ? 0.02 at 10 min to 0.79
? 0.02 at 3 h); heart rate increased (from 86 ? 5
beats·min?1at 10 min to 93 ? 6 beats·min?1at 3 h); and
blood [lactate] decreased (from 1.2 ? 0.1 mM at 10 min to
0.8 ? 0.1 mM at 3 h). Immediately after the high-intensity
depletion protocol, heart rate was markedly elevated (167 ?
4 beats·min?1), as was blood [lactate] (an increase from 0.8
? 0.2 mM at rest to 7.7 ? 0.1 mM).
The percentage distribution of Type I, IIa, and IIx fibers
in the vastus lateralis muscle averaged 52.1 ? 11.3%, 31.7
? 5.7%, and 16.2 ? 10.6%, respectively. As can be seen in
Figure 2 (A and C), there was no differential PAS staining
pattern before exercise, with all fiber types stained dark. On
examination of panels B and D it can be seen that: a) there
was an impact on the muscle fiber glycogen content with
exercise and b) the depletion pattern was dependent on the
type of exercise performed. After the low-intensity deple-
tion exercise (see panel B) only ?6% of Type I fibers were
PAS dark, whereas the majority of Type IIa and IIx fibers
remained dark (?70 and 96%, respectively). The opposite
differentiation was seen after the high-intensity depletion
exercise (see panel D). Approximately 85% of Type I fibers
counted remained PAS dark, whereas the Type IIa and IIx
fibers were discernibly depleted, with only 1% of both fiber
types remaining PAS dark.
Muscle glycogen concentration was similar at rest in both
the low- (108.1 ? 14.2 mmol·kg?1w.w.) and high-intensity
(101.3 ? 12.9 mmol·kg?1w.w.) depletion groups. The
absolute glycogen concentration dropped significantly after
both the high- and the low-intensity depletion protocols.
However, the reduction was somewhat greater after the
high-intensity exercise protocol (by 55% to 46.1 ? 16.3
mmol·kg?1w.w.) than after the low-intensity exercise pro-
tocol (by 44% to 61.0 ? 21.3 mmol·kg?1w.w.).
Stage 2: effect of glycogen depletion on the V˙O2
kinetic response during constant-load exercise.
The data collected during the depletion protocols in stage 2
of the experiment were remarkably similar to those ob-
served in stage 1. During the low intensity depletion proto-
col (calculated as 31.4 ? 4.1% V˙O2max, RER and blood
[lactate] decreased during the 3 h (from 0.91 ? 0.01 to 0.78
? 0.04 and from 1.0 ? 0.07 to 0.7 ? 0.03 mM, respec-
tively) and heart rate increased (87 ? 3 beats·min?1to 92 ?
2 beats·min?1). After the high-intensity depletion protocol
FIGURE 2—Summary of the PAS staining in Type I, IIa, and IIx fibers before (A) and after (B) low intensity exercise; and before (C) and after
(D) high-intensity exercise.
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heart rate was 163 ? 2 beats·min?1, whereas blood [lactate]
had risen to 6.0 ? 0.3 mM (from 0.9 ? 0.1 mM at rest).
Table 1 shows the impact of the depletion protocols on
the V˙O2kinetic parameters and other measures during mod-
erate exercise, as compared with the control condition. The
95% confidence intervals for the time based parameters
were: TDp, 0.9, 0.8, and 0.8 s; ?p, 3.9, 2.8, and 4.2 s (for
CON, LOW, and HIGH, respectively). Although there were
no significant differences in the kinetic parameters across
the three conditions, differences were seen in end exercise
heart rate and end exercise RER. Heart rate was signifi-
cantly higher in HIGH (t18? ?3.8, P ? 0.001) and in LOW
(t18? 4.4, P ? 0.01) when compared with CON. The RER
was significantly lower in both HIGH (t18? 4.7, P ? 0.01)
and in LOW (t18? 4.6, P ? 0.01) conditions when com-
pared with CON.
Table 2 outlines the parameters of the V˙O2kinetics and
other measures taken during heavy exercise under the three
experimental conditions. The 95% confidence intervals for
the time based parameters were: TDp, 1.6, 2.9, and 2.9 s;
TDs, 14.4, 11.3, and 16.5 s; ?p, 2.9, 3.8, and 3.4 s; and ?s,
21.1, 26.1, and 26.2 s (for CON, LOW, and HIGH, respec-
tively). There were differences again in end exercise heart
rate (LOW vs CON, t18? 4.0, P ? 0.001), end exercise
RER (HIGH vs CON, t18? 3.1, P ? 0.02, LOW vs CON,
t18? 4.4, P ? 0.001) and the blood [lactate] (HIGH vs
CON, t18? 3.8, P ? 0.001) across the experimental con-
ditions. There were no differences in the V˙O2kinetic re-
sponses after LOW. However, there were differences after
HIGH, most notably in the amplitudes of the V˙O2primary
and V˙O2slow components. The gain of the V˙O2primary
component (Gp) was significantly higher after HIGH (9.4 ?
0.2 mL·min?1·W?1) compared with CON (8.8 ? 0.2
mL·min?1·W?1, t18? ?4.3, P ? 0.001). The increase in
the V˙O2primary component was accompanied by a de-
crease in the amplitude of the V˙O2slow component (As')
after HIGH both in absolute terms (0.18 ? 0.03 L·min?1
compared with 0.24 ? 0.04 L·min?1in CON, t18? 3.5,
P ? 0.003) and when expressed relative to the net increase
in V˙O2at end exercise (8.9 ? 1.3% vs 12.5 ? 1.7 in CON).
The onset of the V˙O2slow component (TDs) was also later
in exercise after HIGH (127.4 ? 7.9 s compared with 110.9
? 6.9 s in CON, t18? ?2.8, P ? 0.0015). Though there
were differences in the V˙O2primary and V˙O2slow com-
ponents across conditions, EE V˙O2was unchanged (?1.9
L·min?1).
DISCUSSION
The results of this study indicate that altering the muscle
glycogen stores of the exercising muscles leads to changes
in the V˙O2kinetic response during heavy (but not moderate)
exercise. Specifically, glycogen depletion of the Type II
muscle fibers resulted in an increase in the amplitude of the
TABLE 2. The parameters of V˙O2kinetics and other measures taken during heavy exercise (50% ?) under the conditions of normal muscle glycogen (CON), and after low-
intensity (LOW) and high-intensity (HIGH) depletion protocols.
Control
BL V˙O2(L?min?1)
0.71 (? 0.02)
TDp(s)
21.3 (? 0.8)
A?p(L?min?1)
1.65 (? 0.11)
Gp(mL?min?1?W?1)
8.8 (? 0.2)
?p(s)
23.6 (? 1.4)
TDs(s)
110.9 (? 6.9)
A?s(L?min?1)
0.24 (? 0.04)
Rel. A?s(% EE V˙O2)
12.5 (? 1.7)
?s(s)
267.4 (? 10.1)
EE V˙O2(L?min?1)
1.89 (? 0.13)
? [lactate] (mM) 3.0 (? 0.3)
EE HR (beats?min?1)
151 (? 4)
EE RER 1.02 (? 0.02)
Values are means (? SEM). BL, baseline; TDp, the onset of the primary component; ?p, the time constant of the primary component; ?s, the time constant of the slow component;
A?p, sum of Apand A?c(equal to amplitude of fast primary component); A?s, value of slow component at end of exercise; Rel. A?s(A?s/A?p? A?s), relative contribution of slow component
to net increase in V˙O2at end exercise; EE V˙O2, increase in V˙O2above baseline at end of exercise; Gp, gain of the primary component (A?pdivided by power output); EE HR, end exercise
heart rate; EE RER, end exercise RER.
* Significantly different from control, P ?0.05.
#Significantly different from LOW condition, P ? 0.05.
LowHigh
0.78 (? 0.02)
23.9 (? 1.4)
1.65 (? 0.11)
8.9 (? 0.2)
21.6 (? 2.3)
104.8 (? 5.4)
0.27 (? 0.05)
12.9 (? 2.2)
239.1 (? 14.4)
1.92 (? 0.14)
2.7 (? 0.4)
156 (? 4)*
0.97 (? 0.02)*
0.78 (? 0.02)
21.1 (? 1.4)
1.75 (? 0.12)*
9.4 (? 0.2)*
24.0 (? 1.5)
127.4 (? 7.9)*#
0.18 (? 0.03)*#
8.9 (? 1.3)*
241.7 (? 14.5)
1.92 (? 0.13)
2.2 (? 0.4)*
154 (? 3)
0.95 (? 0.01)*
TABLE 1. The parameters of V˙O2kinetics and other measures taken during moderate exercise (80% LT) under the conditions of normal muscle glycogen (CON), and after low-
intensity (LOW) and high-intensity (HIGH) depletion protocols.
Control
BL V˙O2(L?min?1)
0.70 (? 0.02)
TDp(s)
26.9 (? 0.4)
A?p(L?min?1)
0.69 (? 0.05)
Gp(mL?min?1?W?1)
9.1 (? 0.2)
?p(s)
21.0 (? 2.8)
? [lactate] (mM)0.0 (? 0.1)
EE HR (beats?min?1)
110 (? 3)
EE RER0.90 (? 0.01)
Values are means (? SEM). BL, baseline; TDp, the onset of the primary component; ?p, the time constant of the primary component; A?p, sum of Apand A?c(equal to amplitude of
fast primary component); Gp, gain of the primary component (A?pdivided by power output); EE HR, end exercise heart rate; EE RER, end exercise RER.
* Significantly different from control, P ?0.05.
LowHigh
0.78 (? 0.02)
26.8 (? 0.4)
0.70 (? 0.05)
9.2 (? 0.2)
19.3 (? 2.3)
?0.1 (? 0.1)
116 (? 3)*
0.84 (? 0.01)*
0.75 (? 0.02)
26.5 (? 0.4)
0.71 (? 0.06)
9.4 (? 0.2)
19.2 (? 2.0)
0.0 (? 0.1)
119 (? 3)*
0.85 (? 0.01)*
GLYCOGEN DEPLETION AND V˙O2KINETICS
Medicine & Science in Sports & Exercise?
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