Articles in PresS. J Appl Physiol (December 20, 2002). 10.1152/japplphysiol.00456.2002
Effect of pedal rate on primary and slow component oxygen uptake responses during heavy
cycle exercise
Jamie S. M. Pringle1, Jonathan H. Doust2, Helen Carter3, Keith Tolfrey1 and Andrew M.
Jones1
1
Department of Exercise and Sport Science, Manchester Metropolitan University, Hassall
Road, Alsager, ST7 2HL, United Kingdom; 2 Department of Sport Science, University of
and Leisure, University of Surrey Roehampton, London, SW15 3SN, United Kingdom.
Corresponding Author:
Dr Andrew Jones
Department of Exercise and Sport Science
Manchester Metropolitan University
Hassall Road
Alsager ST7 2HL
United Kingdom
Phone: 0161 2475656
Fax: 0161 2476375
E-mail: [email protected]
Copyright (c) 2002 by the American Physiological Society.
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Wales Aberystwyth, Ceredigion, SY23 2AX, United Kingdom; 3 School of Sport, Exercise
2
Abstract
We hypothesised that a higher pedal rate (assumed to result in a greater proportional contribution
& O slow
of type II motor units) would be associated with an increased amplitude of the V
2
component during heavy cycle exercise. Ten subjects (mean ± S.D. age 26 ± 4 years, body mass
71.5 ± 7.9 kg) completed a series of square-wave transitions to heavy exercise at pedal rates of
35, 75, and 115 rev.min-1. The exercise power output was set at 50 % of the difference between
& O peak, and the baseline power output was
the pedal rate specific ventilatory threshold and V
2
adjusted to account for differences in the O2 cost of unloaded pedalling. The gain of the
rev.min-1 (mean ± SEM 10.6 ± 0.3, 9.5 ± 0.2, and 8.9 ± 0.4 mL.min-1.W-1 respectively; P<0.05).
& O slow component was significantly greater at 115 rev.min-1 (328 ± 29
The amplitude of the V
2
mL.min-1) compared to 35 rev.min-1 (109 ± 30 mL.min-1) and 75 rev.min-1 (202 ± 38 mL.min-1),
(P<0.05). There were no significant differences in the time constants or time delays associated
with the primary and slow components across the pedal rates. The change in blood [lactate] was
significantly greater at 115 rev.min-1 (3.7 ± 0.2 mM) and 75 rev.min-1 (2.8 ± 0.3 mM) compared
to 35 rev.min-1 (1.7 ± 0.4 mM), (P<0.05). These data indicate that pedal rate influences oxygen
uptake kinetics during heavy exercise at the same relative intensity, presumably by altering
motor unit recruitment patterns.
& O kinetics and pedal rate
Running head: V
2
Key words: energetics; muscle efficiency; respiratory kinetics
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& O primary component was significantly higher at 35 rev.min-1 compared to 75 and 115
V
2
3
Introduction
& O observed beyond
The physiological mechanisms underpinning the slow rise in pulmonary V
2
2-3 minutes of constant-load exercise above the ventilatory threshold (VT) remain obscure. This
& O ‘slow component’ has important implications for exercise tolerance because it causes
V
2
& O to increase to values that are higher than would be expected for the external power output;
V
2
& O may even reach its maximum (16).
indeed, in some circumstances, V
2
& O slow component have been proposed including
A number of putative mechanisms for the V
2
output; lactate clearance or gluconeogenesis; and elevated core and/or muscle temperature (for
review, see 42). However, neither elevation of blood [lactate] by infusion of epinephrine (17),
nor elevation of muscle temperature by passive warming (22), increased the amplitude of the
& O slow component. Furthermore, Poole et al (29) demonstrated that extra-muscular sources
V
2
& O , such as the oxygen cost of additional respiratory muscle work, could
of increased V
2
& O slow component. This study indicated that the
contribute no more than ~ 15 % to the V
2
primary source of the additional O2 cost of heavy exercise was located within the exercising
muscle, with the recruitment of ‘low-efficiency’ type II muscle fibres being a strong candidate
(29). Barstow et al. (2) demonstrated that the % type II fibres in the vastus lateralis was
& O slow component during heavy
significantly correlated with the relative amplitude of the V
2
cycle exercise, and these observations have recently been confirmed (31). It is therefore possible
& O slow component is related to the recruitment of type II muscle fibres during heavy
that the V
2
exercise.
It is widely accepted that the recruitment of type II muscle fibres is enhanced with increases in
pedal rate for the same external power output (23, 35). Therefore, altering pedal rate at the same
relative power output during heavy exercise might provide a useful model for examining the
& O slow component. Barstow et al (2) have
effect of type II muscle fibre recruitment on the V
2
& O slow component, but the exercise power
previously reported no effect of pedal rate on the V
2
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the increased oxygen cost associated with: increased rates of pulmonary ventilation and cardiac
4
outputs used were estimated from the responses to a single ramp test at 60 rev.min-1, and subjects
only performed one exercise bout at each of the pedal rates which might limit confidence in the
parameters derived from the curve-fitting procedures. Furthermore, the range of pedal rates
tested was relatively narrow (45-90 rev.min-1), and it is possible that this did not significantly
affect motor unit recruitment patterns (23, 35). The effect of more extreme differences in pedal
& O slow component therefore remains to be determined.
rate on the V
2
Previous investigations into the effect of pedal rate on the physiological response to exercise
have typically studied subjects exercising at the same external power output over a number of
different pedal rates, and reported the gross efficiency (i.e. the absolute external power output
output, gross efficiency decreases with increases in pedal rate, an effect that can be attributed
largely to the ‘extra’ O2 cost of turning the legs at the faster movement frequency. Failure to
account for differences in the O2 cost of ‘unloaded’ cycling could obscure any differences in
& O above baseline per
mechanical efficiency across pedal rates (as expressed by the change in V
2
unit change in external power output; equivalent to ‘delta’ efficiency). Furthermore, to allow
meaningful physiological comparisons, the relative metabolic stress of the exercise must be
& O peak and the VT that might exist across pedal
normalised relative to any differences in the V
2
rates.
The purpose of the present study was to test the hypothesis that increased pedal rate (assumed to
& O slow
result in a greater recruitment of type II motor units) would be associated with a larger V
2
& O response across the pedal rates, the baseline
component. To facilitate comparisons of the V
2
& O , and the increase in power output
power output was adjusted in order to equate the baseline V
2
above that at baseline was designed to result in the same relative metabolic rate (i.e. 50 % of the
& O peak for each pedal rate).
difference between VT and V
2
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& O ), (7, 15, 37). These studies have shown that, for any given power
divided by the absolute V
2
5
Methods
Subjects
Ten healthy subjects (eight males; mean ± S.D. age 26 ± 4 years, body mass 71.5 ± 7.9 kg) were
briefed as to the benefits and risks of participation and gave written informed consent to
participate in the study, which was approved by the Ethics Committee of the Manchester
Metropolitan University. All subjects were involved in regular exercise training and were
familiar with laboratory exercise testing procedures. Subjects were instructed to avoid strenuous
exercise in the 48 hours preceding a test session and to arrive at the laboratory in a rested and
same time of day (± one hour).
Design of the study
Subjects first completed three separate ramp tests to exhaustion, at pedal rates of 35, 75 and 115
rev ⋅ min-1, on an electrically braked cycle ergometer (Jaeger E800, Mindjhaart, the Netherlands)
& O peak. Seat and handlebar height and angle were recorded for the
to determine the VT and V
2
first test and reproduced for all subsequent tests. The ergometer was regularly calibrated over
the range of power outputs and pedal rates employed in this study. At all three pedal rates, the
actual power output was highly correlated with the ‘display’ power output (r = 0.98-0.99, S.E.E.
= 3-6 W).
Prior to one of the ramp tests, the subjects performed a 12-min bout of cycling at 20 W (the
lowest power output available on the ergometer). This consisted of three 4-min stages at each of
& O averaged over the final 2 min of each stage was taken to
the three pedal rates. The V
2
represent the ‘unloaded’ O2 cost for that particular pedal rate.
Within two weeks of completing the ramp tests, each subject returned to the laboratory to
perform constant-load exercise bouts at the different pedal rates. To enhance the signal/noise
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fully hydrated state, at least three hours post-prandial. For each subject, tests took place at the
6
& O signal, subjects performed 3-4 square- wave transitions at each pedal rate from
ratio in the V
2
baseline (see below) to a power output calculated to require 50 % of the difference between VT
& O peak for each pedal rate (i.e. 50 % ∆; ‘heavy’ exercise). The order of these tests was
and V
2
randomised. Following one of the transitions at each of the three pedal rates, the subjects
completed a maximal 6-s sprint test to determine the extent of post-test fatigue relative to a
rested control trial. In addition, the subjects performed 4-8 transitions to 80 % of the VT at one
pedal rate (75 rev.min-1) in order to establish the primary component gain in the ‘control’
condition of moderate exercise.
The ramp tests started with the subject pedalling at the required pedal rate with an applied load
of 20 W for 3 minutes. The power output was then increased by 5 W every 12 s (25 W ⋅ min-1)
until volitional exhaustion was reached or the required pedal rate could not be maintained.
During all exercise tests, pulmonary gas exchange was measured breath-by
- breath (see below).
& O data were interpolated to give second-by
- second values. The highest
The breath-by- breath V
2
& O value in any 30 s period was taken to be the V
& O peak. The VT was determined as the
V
2
2
& O was evident
point at which a non-linear increase in carbon dioxide production relative to V
2
(4).
Square-wave transitions
Each subject completed 3-4 square-wave transitions consisting of 4-min of baseline pedalling
followed by an abrupt transition to 6-min of heavy exercise at a power output calculated to
require 50 % ∆ at each of the three pedal rates (35, 75 and 115 rev.min-1). The subjects also
performed a total of 4-8 transitions to 80 % VT at 75 rev.min-1. In each laboratory visit, subjects
completed a moderate intensity exercise transition followed 10 min later by a heavy exercise
transition; this sequence was repeated following 60 min recovery. Following one heavy
transition at each of the three pedal rates, subjects immediately dismounted the electrically-
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Determination of peak oxygen uptake and ventilatory threshold
7
braked ergometer and mounted an adjacent friction-braked ergometer (Monark 824E, Varberg,
Sweden) within 10 s. After ~ 3 s of zero-load cycling to raise the pedal rate to 60 rev.min-1, they
performed a maximal 6-s sprint with the loading of the ergometer set at 7.5 % of the subject’s
body mass. The angular velocity of the flywheel was sampled at 20 Hz by a PC and power
output was calculated and recorded. The peak power output in each sprint was compared to that
previously obtained under resting conditions (i.e. with no prior exercise).
The power outputs at 50 % ∆ were calculated by extrapolation of the linear relationship between
& O and power output in the sub-VT portion (S1) of the respective ramp tests, with correction
V
2
‘baseline’ pedalling was performed with added load in order to account for differences in the O2
cost of unloaded cycling resulting from increased internal work at higher pedal rates. The exact
& O / ∆ power output relationship established from the
load applied was calculated using the ∆ V
2
& O was therefore similar across the three
S1 region of the corresponding ramp test. Baseline V
2
pedal rates before the transitions to heavy exercise. The power output required to elicit 50 % ∆
for each of the pedal rates was then added to the respective baseline power outputs to produce
the exercise power outputs for each of the three conditions.
A fingertip capillary blood sample was taken immediately before and after two transitions at
each pedal rate to determine the change in blood [lactate] (∆ [La]). Approximately 20-25 µL of
blood was collected into capillary tubes and analysed for whole blood [La] using a YSI 1500
Sport lactate analyser (Yellow Springs Instruments, Ohio, USA.). Heart rate was recorded every
5 s during all exercise tests by telemetry (Polar Electro Oy, Kemple, Finland).
Measurement of pulmonary gas exchange and minute ventilation
For all exercise trials, pulmonary gas exchange and minute ventilation were continuously
measured breath-by
- breath. Subjects wore a nose-clip and breathed through a low dead space
(35 mL), low resistance (< 0.1kPa · L-1 · s-1 at 16 L · s-1) mouthpiece and volume sensor
assembly. Gases were continuously drawn from the mouthpiece assembly through a capillary
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& O which occurs during ramp exercise. At the two lowest pedal rates,
made for the lag time in V
2
8
line and analysed for O2 and CO2 concentrations by fast-response analysers (O2: differential
paramagnetic; CO2: infra-red absorption) (Oxycon Alpha, Jaeger, The Netherlands). The system
was calibrated prior to each test with gases of known concentration. Expiratory volumes were
determined using a Triple V turbine volume sensor (Jaeger, The Netherlands) which was
calibrated before each test with a 3 L graduated gas syringe (Hans Rudolph In., Kansas City,
MO. USA.) according to the manufacturer’s instructions. The concentration and volume signals
were integrated by personal computer and pulmonary gas exchange and ventilation variables
were calculated and displayed in real-time for each breath.
Data analysis
values and time-aligned to the start of exercise. The repeat transitions for each condition were
then averaged in order to enhance the underlying response characteristics. Non-linear regression
& O data after the onset of exercise with an
techniques were used to fit the first six minutes of V
2
exponential function. An iterative process was used in order to minimise the sum of squared
error between the fitted function and the observed values. The empirical model consisted of two
(moderate exercise) or three (heavy exercise) exponential terms, each representing one phase of
the response. The first exponential term started with the onset of exercise (time = 0), whereas
the other terms began after independent time delays:
& O (t) =
V
2
& O (BL) + Ac × (1 - e-t/τc)
V
2
phase I
+ Ap × (1 - e-(t-TDp)/τp)
phase II
+ As × (1 - e-(t-TDs)/τs)
phase III
& O (t) is the V
& O at any given time point; V
& O (BL) is the baseline oxygen uptake
where: V
2
2
2
value; Ac, Ap, As are the asymptotic amplitudes for the exponential terms; τc, τp and τs are the
time constants; and TDp and TDs are the time delays. The phase I term was terminated at the
& O at the end of
start of phase II (i.e. at TDp) and assigned the value for that time (Ac΄). The V
2
phase I (Ac΄) and the amplitude of phase II (Ap) were summed to calculate the amplitude of the
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& O data for each transition were interpolated to give second-by-second
The breath-by- breath V
2
9
& O slow component was determined as the
primary component (Ap΄). The amplitude of the V
2
& O from TDs to the end of the modelled data (defined As΄).
increase in V
2
Statistical analysis
The statistical software package SPSS (version 10.0, SPSS Inc, Chicago, IL) was used for all
statistical analysis. Comparisons between responses at the different pedal rates were compared
using a one-way, repeated measures ANOVA with post hoc Bonferroni-adjusted paired t-tests.
Statistical significance was accepted at 5%. Results are presented as mean ± SEM unless stated
Results
Ramp tests
& O peak was not significantly different across pedal rates (3.58 ± 0.18, 3.55 ± 0.24, and
The V
2
& O at VT was
3.66 ± 0.216 L.min-1 at 35, 75, and 115 rev.min-1 respectively). However, the V
2
significantly higher at 115 rev.min-1 (1.91 ± 0.10 L.min-1) compared to 35 (1.69 ± 0.07 L.min-1)
& O peak at VT was not significantly
and 75 (1.72 ± 0.11 L.min-1) rev.min-1 (P<0.05). The % of V
2
& O peak).
different between pedal rates (~ 50 % of V
2
Square-wave transitions
& O at VT.
The relative intensity achieved for moderate exercise at 75 rev ⋅ min-1 was 82 ± 3 % V
2
Table 1 shows the main results of the square-wave transitions to heavy exercise performed at the
different pedal rates. There was no significant difference in the relative intensity achieved at the
end of the primary component (BL + A1’) across the pedal rates (~ 55 ± 4 % ∆). The baseline
& O was not different across the different pedal rates, thus we were successful in accounting for
V
2
differences in the O2 cost of internal work.
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otherwise.
10
& O response to heavy exercise at each pedal rate in a typical individual
Figure 1 shows the V
2
while Figure 2 shows the mean response across all ten subjects. On average, there were no
& O kinetic response, although there was a
significant differences in the temporal aspects of the V
2
tendency for TDp and TDs to occur earlier with increases in pedal rate and for the primary
& O primary
component time constant to be longer at higher pedal rates. The amplitude of the V
2
component was not significantly different across pedal rates (1466 ± 133, 1536 ± 153, and 1593
± 157 ml.min-1, at 35, 75, and 115 rev.min-1, respectively). However, the amplitude of the
& O slow component increased with pedal rate and was significantly higher at 115 compared to
V
2
& O slow component at 115 rev.min-1 resulted in the end-exercise
greater amplitude of the V
2
& O being significantly higher at this pedal rate compared to 35 rev.min-1.
V
2
& O response to each condition when V
& O is expressed relative to the
Figure 2 shows the V
2
2
change in power output from the baseline to the exercise power output for each pedal rate i.e. as
& O /∆WR). The gain of the primary component decreased with increases in pedal
a ‘gain’ (∆ V
2
rate and was significantly lower at 75 (9.5 ± 0.2 mL.min-1.W-1) and 115 (8.9 ± 0.4 mL.min-1.W-1)
compared to 35 rev ⋅ min-1 (10.6 ± 0.3 mL.min-1.W-1) and to moderate exercise (10.8 ± 0.5
mL.min-1.W-1), (P<0.05). The gain of the slow component increased as pedal rate increased and
was significantly higher at 115 rev ⋅ min-1 (1.8 ± 0.2 mL.min-1.W-1) compared to 35 rev ⋅ min-1
(0.8 ± 0.2 mL.min-1.W-1, P < 0.05), but not 75 rev.min-1 (1.3 ± 0.2 mL.min-1.W-1). The end
exercise gain was not significantly different across the pedal rates (10.8 to 11.3 mL.min-1.W-1).
The change in blood lactate concentration (∆ blood [La]) from baseline to the end of exercise
increased with pedal rate and was significantly greater at 75 and 115 rev ⋅ min-1 compared to 35
& O slow component (As′/EE V
& O ) was significantly
rev ⋅ min-1. The relative amplitude of the V
2
2
correlated with ∆ blood [La] at 35 rev ⋅ min-1 (r = 0.65), 75 rev ⋅ min-1 (r = 0.75), and 115 rev ⋅
min-1 (r = 0.66), (all P<0.05).
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& O . The
35 rev ⋅ min-1 both in absolute terms and when expressed relative to the end exercise V
2
11
Sprint tests
Peak power output in the control condition (without prior exercise) was 1055 ± 58 W. Prior
heavy exercise led to a small but non-significant increase in peak power output at 35 rev.min-1
(1090 ± 76 W) and 75 rev.min-1 (1076 ± 88 W). However, prior heavy exercise at 115 rev.min-1
caused a 7 % reduction in peak power output (983 ± 55 W) that was significantly lower than the
value following prior exercise at 35 rev.min-1 (P<0.05).
Discussion
in a significant reduction in the gain of the primary component and a significant increase in the
& O slow component, the latter being consistent with our hypothesis.
amplitude of the V
2
Barstow et al. (2) reported that differences in pedal rate between 45 and 90 rev.min-1 had no
& O slow component. However, it is possible that this range of
effect on the amplitude of the V
2
pedal rates was too narrow to cause substantial differences in motor unit recruitment patterns
(23, 35). We used more extreme pedal rates in our study (between 35 and 115 rev.min-1) in an
attempt to evoke more substantial differences in the contribution of type II fibres to the external
power output. Our study may be considered to have other advantages over the Barstow et al (2)
study. Barstow et al (2) used a single ramp test at 60 rev.min-1 to estimate the power outputs
required to elicit 50% ∆ across the range of pedal rates they employed. In the present study,
& O peak, VT and the ∆ V
& O /∆WR
subjects performed separate ramp tests to determine the V
2
2
relationship for each of the three pedal rates used. This allowed us to calculate more precisely
& O (i.e. 50% ∆) for each pedal rate.
the exercise power output required to elicit the target V
2
& O /∆WR relationship established from the ramp tests to calculate
Furthermore, we used the ∆ V
2
& O resulting
the additional loading that was required to account for differences in baseline V
2
& O nor
from the increased internal work at higher pedal rates. As a result, neither the baseline V
2
& O achieved) was significantly different across
the relative exercise intensity (expressed as % ∆ V
2
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Increasing pedal rate during constant-load heavy exercise of the same relative intensity resulted
12
pedal rates. Finally, in our study, subjects completed 3-4 transitions at each of the pedal rates
(compared to a single transition in the Barstow et al study (2)) providing improved confidence in
the modelled parameters.
We have no direct evidence from our study that increased pedal rate resulted in increased type II
fibre recruitment. However, a number of studies have indicated that the contribution of type II
muscle fibres is greater at high movement frequencies (5, 6, 32, 34, 35). Beelen et al. (6)
& O peak,
demonstrated that after 6 minutes of pedalling at 90 % of the pedal-rate specific V
2
glycogen depletion was greater in the type II fibre population at 120 rev.min-1 compared with 60
rev.min-1. In another study, Beelen and Sargeant (5) demonstrated a greater reduction in peak
mean that prior exercise at the higher pedal rate resulted in fatigue of the type II fibre population.
Similarly, in our study, heavy exercise at 115 rev.min-1 caused a 7 % reduction in peak power
output compared to the control condition. The differences in blood [lactate] observed between
pedal rates might also be interpreted to indicate an enhanced recruitment of type II fibres at the
highest pedal rate. However, it is difficult to separate the influence of fibre recruitment, per se,
from the possible influence of absolute blood [lactate] on the slow component. Although the
& O and blood [lactate] with time during heavy exercise may
correlation between increases in V
2
be coincidental (17), it is also true that the slow component is only observed at power outputs
that elicit a metabolic acidosis, and that reductions in the slow component amplitude with
training are linked to reductions in ∆ blood [lactate] (e.g. 30). The influence of changes in pedal
& O response to heavy exercise in subjects with differences in muscle fibre type
rate on the V
2
distribution is not known, and it is possible that subjects with “extremes” of muscle fibre type
distribution respond differently to changes in pedal rate. However, Barstow et al. (2) could
determine no interaction between the muscle fibre type of their subjects and changes in pedal
rate between 45 and 90 rev.min-1.
Assuming that higher pedal rates did indeed enhance type II fibre recruitment, our results are
consistent with cross-sectional studies that have demonstrated a significant correlation between
& O slow component (2, 31). Barstow
% type II muscle fibres and the relative amplitude of the V
2
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power output following exercise at 120 rev.min-1 compared to 60 rev.min-1 and interpreted this to
13
et al. (2) reported that the % type II muscle fibres in the vastus lateralis was significantly
& O slow component during heavy cycle
positively correlated with the relative amplitude of the V
2
exercise. More recently, we have also reported significant correlations between % type II muscle
& O slow component during both heavy (r = 0.74) and
fibres and the relative amplitude of the V
2
severe (r = 0.64) exercise (31). Earlier studies (predominantly in rodent muscle) indicated that
type II muscle fibres produced more heat and consumed more oxygen for the same rate of
tension generation and ATP turnover than type I muscle fibres (12, 41). This presumed lower
efficiency of contraction of type II muscle fibres led to the hypothesis that the progressive
recruitment of type II motor units during heavy exercise was responsible for the development of
thermodynamic efficiencies of slow (~ 0.21) and fast (~ 0.27) twitch fibres from human vastus
lateralis muscle were not significantly different despite almost fourfold differences in ATP
hydrolysis rate and maximum mechanical power. Interestingly, peak efficiency in type IIA
fibres was reached at a higher shortening velocity and greater relative load compared to type I
fibres. This suggests that although the contribution of type II fibres to the exercise power output
is likely to be greater at higher pedal rates during heavy cycle exercise, the effect on exercise
efficiency might not be easily predicted.
& O primary
An interesting finding in the present study was the reduction in the gain of the V
2
component with higher pedal rates at the same relative exercise intensity, an effect that is also
evident in the data of Barstow et al. (2). It has generally been considered that the primary gain
term represents the initially anticipated O2 cost of exercise that is subsequently modified with
& O slow component emerges (3). Recent studies, however, indicate that the
time as the V
2
primary gain term (typically ~10 ml.min-1.W-1) should not be considered an immutable feature of
& O response to exercise. Several studies have demonstrated a clear trend for the primary
the V
2
gain term to fall as power output is increased (9, 10, 21, 26), and it has been suggested that this
might reflect an increased contribution of the characteristics of O2 consumption in type II fibres
& O signal (10, 21). In the present study, the primary gain was significantly
to the pulmonary V
2
lower during heavy exercise compared to moderate exercise at 75 rev.min-1 (Figure 2). The
primary gain is negatively correlated to the % type II fibres during heavy (2, 31) and severe (31)
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the slow component (2, 16, 42). However, in a recent study, He et al. (19) reported that the peak
14
exercise. Also, the optimum velocity of shortening for mechanical efficiency in type II fibres is
closer to 115 than to 35 rev.min-1 (13, 19, 23, 35), and the greater contribution of type II muscle
fibres at high power outputs and movement frequencies may serve to minimise muscle activation
and maximise muscle efficiency (35). Therefore, the fall in the primary gain term with increases
in pedal rate and exercise intensity might be explained by a greater proportional contribution of
type II fibres at higher pedal rates and greater exercise intensities.
& O slow component is often assumed to be the
Although the mechanism responsible for the V
2
progressive recruitment of type II fibres with time as heavy exercise proceeds (2, 16, 43), it is
also possible that a high proportion of (fatigue-sensitive) type II fibres are recruited at the onset
type II fibres have a larger gain and slower kinetics than type I fibres, then our results are
consistent with the view that a greater relative contribution of type II fibres to the power output
would result in a lower primary gain and a greater slow component (2, 31). The suggestion that
type II fibres may be recruited initially during heavy exercise is supported by a number of
glycogen depletion studies (1, 14, 39, 40). It has been reported that all type I and IIA fibres are
& O max (40), and that all type I, IIA and IIB fibres
recruited from the start of exercise at 75 % V
2
& O max (1, 14). Vollestad and Blom (39)
are recruited within 4-7 min of exercise at 84-100 % V
2
demonstrated that virtually all the muscle fibres in the vastus lateralis were recruited within 10
& O max, and noted that the loss of force in fatigued fibres
min of the onset of exercise at 91 % V
2
must be compensated by increased activity in other fibres in order to maintain the required
tension. Therefore, an alternative hypothesis to explain the slow component (and its greater
amplitude at higher pedal rates) is that fatigue in the type II fibre pool as exercise proceeds
necessitates an increased activity (i.e. increased firing frequency) of type I fibres. Recent
evidence indicates that type I fibres are relatively less efficient at higher force requirements and
contraction velocities than are type II fibres (19). Increased activation of type I muscle fibres
during heavy exercise (especially at higher pedal rates) might therefore reduce muscle efficiency.
Additionally, fatigued type II fibres might continue to consume oxygen as they recover (i.e. there
will be a continued phosphate and O2 cost associated with Ca2+ and Na+-K+ pumping as
homeostasis is restored), but without contributing appreciably to force production. This
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of heavy exercise. This might be particularly true at high pedal rates (34). If it is accepted that
15
suggestion is consistent with the recent data of Rossiter et al (33) which indicates that the slow
component is associated with a high phosphate cost of force production, rather than a high
oxygen cost of phosphate production. Furthermore, the scenario of early recruitment and
subsequent fatigue of the type II fibre pool followed by increased activation of the type I fibres is
consistent with reports of an increased or unchanged integrated electromyogram but no change in
the mean power frequency during heavy exercise (8, 28, 36). However, this suggestion remains
speculative at present.
While changes in motor unit recruitment patterns appear to provide the most likely explanation
for the differences in the physiological responses we observed, other factors must also be
timing or duty cycle) of muscle recruitment and/or demand the involvement of other muscle
groups. The reported effect of pedal rate on muscle activation is inconsistent, with some studies
indicating an increase in EMG at higher pedal rates (24) and others indicating that EMG is
minimised if pedal rate is increased with increases in power output (23). However, there is some
evidence that cycling at high pedal rates requires the recruitment of additional muscles to
stabilise the trunk (18) and causes a reduction in the effectiveness of the force applied at the
pedals (27). Differences in contraction frequency might also influence blood flow to the
exercising muscle. Hoelting et al. (20) recently demonstrated that increasing contraction
frequency resulted in a reduction in mean blood flow during knee extension exercise. A reduced
blood flow might result in increased type II fibre recruitment and increased lactate production.
& O at 6
The greater slow component amplitude at 115 rev.min-1 resulted in the end-exercise V
2
minutes being significantly higher at this pedal rate than at 35 and 75 rev.min-1. It is of note that
previous studies that examined the influence of pedal rate on exercise efficiency have not
& O slow component on the measurement of exercise efficiency
considered the influence of the V
2
at power outputs above the VT. Our observations, made through careful partitioning of the
& O response into its constituent primary and slow components, indicate that inconsistencies in
V
2
the reported effect of differences in pedal rate on delta efficiency (11, 15, 25, 38) might be
& O was measured.
related both to the intensity of exercise and the time during exercise when V
2
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considered. For example, it is possible that higher pedal rates affect the extent or pattern (e.g.
16
In conclusion, for exercise at the same relative intensity and after controlling for differences in
the O2 cost of unloaded pedalling, higher pedal rates were associated with a lower gain of the
& O primary component and a greater amplitude of the V
& O slow component. Assuming that
V
2
2
type II fibres possess slower kinetics and lower efficiency than type I fibres, one interpretation of
these data is that they are related to the greater contribution of type II muscle fibres (relative to
type I muscle fibres) during heavy exercise at higher pedal rates. However, this simple
interpretation is confounded by the fact that type II fibres are relatively more efficient at higher
contraction velocities. While this latter point might help to explain the lower primary component
gain, alternative explanations for the larger slow component at higher pedal rates should be
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considered.
17
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22
Table 1. Mean ± SEM oxygen uptake response for 6 min of heavy cycle exercise at 35, 75 and 115
rev.min-1.
Pedal rate (rev ⋅ min )
-1
35
75
115
Baseline power (W)
75 ± 4
70 ± 5
20 ± 0
Exercise power (W)
214 ± 9
231 ± 11
202 ± 17
a
∆ blood [lactate] (mM)
a
1.7 ± 0.4
2.8 ± 0.3
3.7 ± 0.2
1208 ± 40
1229 ± 72
1290 ± 49
1466 ± 133
1536 ± 153
1593 ± 157
As’ (mL.min )
109 ± 30
202 ± 38
328 ± 29
&O )
As’ (% EE V
2
6.8 ± 1.6
12.6 ± 2.8
17.6 ± 1.6
& O 6-3 min (mL.minV
2
59 ± 19
181 ± 47
232 ± 37
1574 ± 145
1738 ± 148
1921 ± 166
2783 ± 130
2967 ± 128
TDp (s)
25 ± 4
20 ± 2
17 ± 1
TDs (s)
143 ± 11
138 ± 13
114 ± 12
τp (s)
23.8 ± 1.8
28.2 ± 3.1
30.2 ± 3.1
Amplitude parameters
& O (mL.min-1)
V
2
BL
-1
a
a
a
1
)
EE
& O (mL.min-1)
V
2
Total
& O (mL.min-1)
V
2
a
3211 ± 179
a
a, b
Temporal parameters
BL, baseline; Ap’ and As’, amplitudes of the primary and slow components respectively; EE
in
& O increase
V
2
& O above baseline at end of exercise. TDp and TDs, time delays for the primary and slow components
V
2
respectively; τp, time constant of the primary component (phase II). a significantly different from 35 rev.min1 b
, significantly different from 75 rev.min-1.
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Ap’ (mL.min-1)
23
Figure Legends
Figure 1:
& O response to heavy exercise at 35, 75, and 115 rev.min-1 in a typical subject.
V
2
Figure 2:
& O response to heavy exercise at 35, 75 and 115 rev.min-1 when expressed as a gain
The mean V
2
& O /∆WR). The mean response to moderate exercise at 75 rev.min-1 is also shown for
(∆ V
2
comparison.
& O /∆WR) terms for heavy
Primary component, slow component and end-exercise gain (∆ V
2
exercise at 35, 75 and 115 rev.min-1. a significantly different from 35 rev.min-1.
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Figure 3:
1500
1000
500
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Time (s)
360
300
240
180
120
60
0
-60
0
-120
115
75
35
2000
V O2 (mL · min-1)
24
3500
3000
2500
25
35 rev · min
75 rev · min
-1
10
-1
75 rev · min
8
.
-1
11
9
-1
Moderate at
-1
7
115 rev · min
-1
6
5
4
3
2
1
0
-60
0
60
120
180
Time (s)
240
300
360
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V O2 gain (mL · min · W )
12
26
13.0
12.0
9.0
a
-1
-1
10.0
·
a
8.0
7.0
End exercise gain
6.0
Primary gain
5.0
Slow component gain
4.0
3.0
2.0
a
1.0
0.0
35
75
115
-1
Pedal rate (rev · min )
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V O2 gain (mL · min · W )
11.0