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1 Athlete and Coach Support Services, Queensland Academy of Sport, Brisbane, Queensland 4109, Australia 2 School of Physiotherapy and Exercise Science, Griffith University, Gold Coast campus, Queensland 9726, Australia
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Abstract |
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) kinetics or the 
slow component. Eight recreational cyclists (
, 55.6 ± 1.3 ml kg –1 min–1) were studied during 8 min of heavy constant-load cycling performed under control conditions (CON) and under conditions of reduced type I muscle glycogen content (GR). 
was measured breath-by-breath for the determination of 
kinetics using a double-exponential model with independent time delays. 
was higher in the GR trial compared to the CON trial as a result of augmented phase I and II amplitudes, with no difference between trials in the phase II time constant or the magnitude of the slow component. The mean power frequency (MPF) of electromyography activity for the vastus medialis increased over time during both trials, with a greater rate of increase observed in the GR trial compared to the CON trial. The results suggest that the recruitment of additional type II motor units contributed to the slow component in both trials. An increase in fat metabolism and augmented type II motor unit recruitment contributed to the higher 
in the GR trial. However, the greater rate of increase in the recruitment of type II motor units in the GR trial may not have been of sufficient magnitude to further elevate the slow component when 
was already high and approaching 
.
(Received 24 June 2005;
accepted after revision 7 October 2005; first published online 4 November 2005)
Corresponding author M. A. Osborne: Queensland Academy of Sport, PO Box 956, Sunnybank, QLD 4109, Australia. Email: mark.osborne{at}srq.qld.gov.au
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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) can be characterized by three transient phases. Phase I is the rise in 
at the onset of exercise, lasting between 15 and 20 s. This is attributed to a rapid increase in cardiac output and pulmonary blood flow. At the beginning of moderate-intensity exercise, i.e. below the blood lactate threshold (BLT), phase II 
increases monoexponentially and reaches a new steady-state (phase III) value in about 2–3 min (Whipp, 1987). The rate of change in phase II 
kinetics is determined by an interaction between adjustments in O2 delivery to the active muscle (Barstow & Molé, 1987; Whipp, 1987) and the regulation of O2 utilization by the muscle (as reviewed by Tschakovsky & Hughson, 1999). During heavy exercise above the BLT, the attainment of a steady-state 
is delayed or may not occur, and a slow component of increasing 
(
slow component) is observed (Whipp & Wasserman, 1972), which has the potential to rise to maximal values despite the work rate being regarded as submaximal. The increasing O2 cost over time represents an increasing energy cost of performing heavy exercise. Slower phase II kinetics or a larger 
slow component are predicted to have a detrimental effect on performance during heavy exercise (Poole et al. 1994a).
The possible mechanisms responsible for the development of the 
slow component during heavy-intensity exercise include increased muscle and blood lactate concentration ([La–]), elevated plasma adrenaline concentrations, increased ventilatory and cardiac work, a rise in core or muscle temperature and the progressive recruitment of less efficient fast-twitch (type II) muscle fibres (Gaesser & Poole, 1996). Many studies have demonstrated that the progressive recruitment of less efficient type II muscle fibres may play an important role in the development of the 
slow component (Coyle et al. 1992; Shinohara & Moritani, 1992; Poole et al. 1994a; Pringle et al. 2003; Krustrup et al. 2004a,b; Sabapathy et al. 2004). The participation of type II fibres could also explain the temporal association between blood [La–] and the 
slow component, since these fibres are significant lactate producers. Several features of type II fibres suggest that they are a source of the additional O2 cost during heavy exercise. Coyle et al. (1992) observed that individuals with a high proportion of type II fibres in the vastus lateralis are less efficient during cycle exercise than individuals with a higher proportion of type I fibres. In addition, type II fibres have been shown to be less efficient than type I fibres in mouse skeletal muscle (Crow & Kushmerick, 1982; Barclay, 1996). In contrast, Barclay & Weber (2004) found no difference in net efficiency between type I and II muscles. Barclay (1996) also demonstrated that the efficiency of a muscle fibre is reduced following a moderate level of fatigue. It is likely that both type I and II fibres are recruited at the onset of exercise, and that as heavy exercise progresses a greater proportion of type II fibres are recruited as type I fibres become fatigued (Krustrup et al. 2004b). As the progressive recruitment of type II fibres continues, there may be an increase in 
beyond that seen at lower intensities when primarily type I fibres are recruited (Poole et al. 1994a; Krustrup et al. 2004b).
Few studies have experimentally altered muscle fibre recruitment pattern to see if there is a corresponding change in either on-transient 
kinetics or the 
slow component (Poole et al. 1994a; Bouckaert et al. 2004; Krustrup et al. 2004a). One way to alter muscle fibre recruitment pattern during heavy exercise is to reduce the glycogen content in a specific muscle fibre type prior to exercise (Bouckaert et al. 2004; Krustrup et al. 2004a). Cycling to exhaustion at a work rate slightly above the BLT has been shown to reduce the glycogen content of mainly type I fibres (Essén, 1978; Thomson et al. 1979). Selective glycogen reduction in type I fibres should result in a greater recruitment of type II fibres during a subsequent bout of heavy exercise (Krustrup et al. 2004a). Krustrup et al. (2004a) used single-fibre creatine phosphate and glycogen content to identify the muscle fibre recruitment pattern during moderate-intensity exercise performed after muscle glycogen reduction. These researchers demonstrated the presence of a slow component and an increase in the phase II amplitude during moderate-intensity work rates (below BLT) following type I muscle fibre depletion. In contrast, both Carter et al. (2004) and Bouckaert et al. (2004) demonstrated that reducing type I muscle fibre glycogen content did not effect the phase I, phase II or slow component amplitudes or the phase II time constant during heavy exercise. However, no measure of muscle fibre recruitment pattern was made during heavy exercise performed with reduced muscle glycogen stores in either study. Therefore, it is unclear whether prior glycogen reduction in mainly type I fibres will increase type II fibre recruitment and cause a corresponding rise in the 
slow component during heavy exercise. No previous study has examined the relationship between the slow component and muscle fibre recruitment pattern (as indicated by electromyography (EMG) activity) during heavy exercise following glycogen reduction. Therefore, the purpose of the present study was to determine whether reduced muscle glycogen content in type I fibres would alter surface EMG activity and change on-transient 
kinetics or the slow component. An increase in the integrated EMG (iEMG) indicates an increase in total neural activity (Viitasalo & Komi, 1977), while an increase in the mean power frequency (MPF) of the EMG represents an increase in average motor unit action potential conduction velocity and thus greater type II fibre recruitment (Komi et al. 2000; Scheuermann et al. 2001). Plasma catecholamine and thyroxine concentrations were measured to determine whether changes in these hormones during exercise affect the 
slow component. We hypothesized that prior muscle glycogen reduction in primarily type I fibres would result in a greater recruitment of type II fibres during a subsequent bout of heavy exercise and that this in turn would augment the amplitude of the phase II response and the 
slow component.
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Methods |
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Eight male recreational cyclists volunteered to participate in this study after giving written informed consent. The mean (± S.E.M.) values for age, height and body mass were 23.3 ± 0.9 years, 181 ± 3 cm and 72.5 ± 2.8 kg, respectively. All subjects were screened for indications of pulmonary insufficiencies, and completed a Physical Activity Readiness Questionnaire and a medical history questionnaire. The procedures and consent forms were approved by the Griffith University Human Research Ethics Committee and all procedures complied with the Declaration of Helsinki.
Experimental protocol
Each subject reported to the laboratory for three testing sessions conducted on separate days within a 2-week period. Subjects were instructed not to engage in heavy physical activity for 48 h prior to each testing session and to fast for 12 h prior to each exercise trial. The first session was used to familiarize subjects with the testing equipment and procedures, and to obtain written informed consent. In the same session, each subject performed an incremental cycling test to determine peak oxygen uptake (
) and the ventilatory threshold (Tvent). Subjects then performed two constant-load exercise tests on separate days to determine 
kinetics and to quantify the slow component. Each subject performed constant-load tests at a power output equal to 50% of the difference between the power output achieved at Tvent and 
(
50%). One test was performed under control (CON) conditions, while the other trial was performed the morning after a session designed to reduce muscle glycogen content (GR). The CON and GR trials were performed in random order. Exercise was performed on an electronically braked cycle ergometer (Excalibur Sport, Lode Groningen, The Netherlands) at a pedal cadence of 75 r.p.m. Subjects used toe clips to improve pedalling efficiency and comfort. Seat and handlebar heights were recorded and maintained during all testing sessions for each subject.
Determination of 
and Tvent
During preliminary testing, subjects completed an incremental cycling test to exhaustion (
75 r.p.m.). Subjects cycled for 3 min at 50 W before the power output was increased by 10 W 20 s–1 until volitional fatigue. Standard open-circuit spirometry techniques were used to determine gas exchange measures (MedGraphics CPX/D, MedGraphics Cardiopulmonary Diagnostic Systems, St Paul, MN, USA). The O2 and CO2 analysers and the pneumotachograph were calibrated before and after each test using precision reference gases and a syringe of known volume (3 l), respectively. 
was calculated by averaging the breath-by-breath 
over 20-s intervals, with the average of the highest three consecutive values used as the peak value. Heart rate and rhythm were monitored continuously throughout the test using an electrocardiograph (Lohmeier M607, Munich, Germany), with the ECG signal transferred into the gas analysis system for storage. The Tvent was determined as the power output corresponding to the point where a systematic increase in the ventilatory equivalent for O2 (minute ventilation/oxygen uptake, 
) occurred without an increase in the ventilatory equivalent for CO2 (minute ventilation/CO2 production, 
). The Tvent calculated by this method was verified using the modified V-slope method described by Schneider et al. (1993). If threshold placement was not agreed upon, the Tvent was determined as the average of both methods.
Constant-load cycling trials (CON and GR)
On entry into the laboratory, subjects had a catheter inserted into a prominent forearm vein for subsequent blood sampling. The catheter was regularly flushed with 0.9% saline. Subjects were then required to rest quietly for 25–30 min before starting exercise. Subjects then began cycling for 3 min at 25 W before completing an 8-min square-wave exercise test at the 50% power output. 
, 
, 
and respiratory exchange ratio (RER) were measured on a breath-by-breath basis (MedGraphics CPX/D, MedGraphics Cardiopulmonary Diagnostic Systems) throughout the constant-load exercise bout. Gas-exchange data containing occasional aberrant breaths that were clearly artefactual (e.g. coughing, swallowing) were eliminated from the data set. Heart rate was monitored continually throughout the test. Venous blood samples (2 ml) were collected in lithium heparin tubes prior to the onset of exercise, at the end of the 3-min period of cycling at 25 W, and at 1.5, 3, 4.5, 6 and 8 min throughout the exercise test for analysis of blood [La–], pH and bicarbonate concentration ([HCO3–]). Blood [HCO3–] and pH were measured within 30 s of sampling using a blood gas analyser (Ciba Corning Diagnostics Corp., Medfield, MA, USA) at 37°C. Fifty µl of blood were mixed with 100 µl of buffer solution (YSI 2357 Buffer Concentrate Kit) and a cell-lysing agent (YSI 1515 Cell Lysing Agent Kit) before blood [La–] was determined using an automated blood lactate analyser (Model 2700 Select, Yellow Springs Instruments, Yellow Springs, OH, USA). The lactate and blood gas analysers were calibrated before and after every 10 samples. Plasma [HCO3–] was calculated from the measured pH and arterial partial pressure of CO2 values using the Henderson–Hasselbalch equation (Wasserman et al. 1991). Additional blood samples (4 ml) were drawn at the end of the 3 min period of cycling at 25 W, and at 3, 6 and 8 min for analysis of plasma catecholamine and thyroxine concentrations. Samples were stored at –70°C until later analysis for adrenaline, noradrenaline (Schneider et al. 2000) and thyroxine concentrations using high-performance liquid chromatography with electrochemical detection.
The glycogen-reduction procedure
Subjects reported to the laboratory 3 h after their last mid-afternoon meal on the evening before the scheduled constant-load GR trial. Subjects cycled until volitional fatigue at 75 r.p.m. at a power output 5% above their Tvent. Exhaustion was defined as the point at which subjects could no longer maintain the pedal frequency above 50 r.p.m. Average time to exhaustion was 143 ± 8 min. Following the glycogen reduction protocol, subjects were required to fast until the following morning when they completed the GR test. Water was allowed ad libitum during and after the reduction protocol. The glycogen reduction protocol was adapted from the method of Thomson et al. (1979), who biopsied muscle to validate the procedure. Cycling at this intensity and duration resulted in a severe depletion of glycogen from type I fibres, an intermediate loss of glycogen from type IIa and minimal loss of glycogen from type IIb fibres (Thomson et al. 1979).
Determination of 
response kinetics
kinetics were determined using a double-exponential model with independent time delays. Phase I was determined as the time from the onset of heavy exercise to the sharp downward break in RER, which coincided with the initial inflection point or the end of the early plateau in 
(Barstow & Molé, 1991). The following equation was used to model 
response kinetics:
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(t) is the whole-body 
at time t; 
is the baseline 
during cycling at 25 W; and phase I is the abrupt increase in 
amplitude after the step increase to the 50% power output. Phase II and 
slow component represent the respective amplitudes, while TD1, TD2, 
1 and 2 are the respective time delays and time constants.
The relative contribution of the slow component to the overall 
response was determined as:
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response per unit time (percentage change per minute, % min–1).
The slow component was also measured as the increase in 
between the third minute of exercise and the end of constant-load exercise (8 min). The 
values at 3 min were calculated as the average 
for the preceding and subsequent 15 s of exercise, while the final 30 s was averaged for end-exercise 
(3 min 
is the 
between 2 min 45 s and 3 min 15 s; and 8 min 
is the 
between 7 min 30 s and 8 min exactly). The end-exercise 
is also reported relative to 
.
Measurement of surface EMG activity
Prior to constant-load exercise, an area covering the vastus lateralis, vastus medialis and biceps femoris muscles of the left leg was shaved and cleaned with alcohol to minimize skin impedance. Silver–silver chloride surface electrodes (5 mm diameter; interelectrode distance, 20 mm) were attached in a bipolar configuration along the mid-line of the muscle belly using standard electrode placement and positioning (Ericson et al. 1985), with a reference electrode placed over the anterior iliac crest. Electrode position was temporarily tattooed with silver nitrate to ensure consistent placement between trials. All EMG wires were taped to the skin to reduce movement artefact. The raw EMG data were sampled at 1000 Hz during the final 10 s of each minute of exercise (EMG100B Electromyogram Amplifier, Biopac Systems Inc., Santa Barbara, CA, USA) and processed using custom-written software (LabVIEW version 4.0.1, National Instruments, Austin, TX, USA). All trials were inspected on a waveform graph to eliminate pedal revolutions where clipping of the data occurred, and each revolution was then isolated to determine the temporal characteristics of each muscle burst. Attempts were made to minimize the confounding effects of changes in velocity and muscle length by analysing within a 200 ms range from the top of the downward pedal stroke. This portion of the pedal stroke is the point at which the least amount of muscle shortening occurs and where the muscle contraction is slowest. The time at which both the vastus medialis and vastus lateralis first achieved a peak or plateau in EMG activity within each revolution was selected as the approximate top of the downward pedal stroke (Ryan & Gregor, 1992). This was estimated from visual inspection of the raw EMG signal. The raw EMG data were band-pass filtered (15–500 Hz) using a fourth order Butterworth filter, and rectified to yield a linear envelope. The MPF was calculated from the power spectral density function using a 1024-point fast Fourier transformation. The iEMG and MPF for 8–10 consecutive pedal revolutions were averaged to calculate the iEMG and MPF for each minute of exercise. The iEMG and MPF activity were normalized as a percentage of the baseline activity (3 min of cycling at 25 W) recorded during each experimental trial.
Statistical analysis
All results are presented as group means ±
S.E.M. Differences between CON and GR trials for the modelled data obtained from the constant-load cycling tests were examined using paired-sample t tests. A two-way repeated measures analysis of variance (ANOVA) with experimental condition and time as the main effects was used to assess condition-related differences in the change in the respiratory data, blood measures, and iEMG and MPF at discrete time intervals. Pairwise comparisons to determine where significant differences existed were performed using a Student–Newman–Keuls test. Correlation coefficients were determined between the magnitude of the slow component as measured between the third and eighth minute of exercise 
and changes in blood [La–] ([La–](8 - 3min)) over the same period of time. Accuracy of the curve fitting procedure was assessed by calculating the coefficient of determination (r2) and coefficient of correlation (r) obtained between modelled 
and actual 
(SigmaPlot v4.01, Jandel Scientific). The random distribution of model residuals according to time was checked with linear and non-linear regression. Statistical significance was accepted at P < 0.05. The data were analysed using the Statistical Package for the Social Sciences software (SPSS, v9.0) and SigmaStat Statistical Software (SigmaStat v1.0, Jandel Scientific).
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Results |
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obtained during incremental cycling was 4.02 ± 0.15 l min–1 (55.6 ± 1.3 ml kg–1 min–1), which was achieved at a mean peak power output of 393 ± 12 W and a maximum heart rate of 186 ± 4 beats min–1. Tvent occurred at a power output of 205 ± 10 W and a 
of 2.40 ± 0.11 l min–1. The average 50% power output used during constant-load cycling was 284 ± 8 W. Blood [La–] was significantly lower at 6 and 8 min of exercise during the GR trial compared to the CON trial (Fig. 1A). Blood pH and standard [HCO3–] were significantly elevated in the GR trial from the third and sixth minute of exercise, respectively, and remained higher throughout exercise (Fig. 1B and C, respectively).
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response to a single transition in both experimental trials. These indicators include the degree of significance with a large number of data points (> 200 breaths) during the slow component phase, the coefficients of determination (r2; 99.7 ± 0.2% in the CON trial and 99.7 ± 0.1% in the GR trial) between modelled 
and actual 
, and the residuals being independent of time and randomly distributed around the regression line.
Gas-exchange responses determined at specific time intervals during the constant-load exercise bouts are presented in Table 1. There was no difference between the CON and GR trials in the 
measured at rest or at 25 W of cycling (baseline 
). However, 
was significantly elevated at all time intervals throughout exercise in the GR trial. 
was significantly reduced at rest and during baseline cycling conditions, although any reduction was no longer significant once heavy exercise began. RER was also reduced at rest and throughout exercise in the GR trial. 
was elevated at 3 and 6 min of exercise following GR compared with the CON trial, but there was no difference between trials in 
. Heart rate was unaffected by the GR protocol in the present study (Table 1).
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kinetic responses for each condition are provided in Table 2. The amplitudes of the phase I and II responses were significantly greater following GR. However, there was no difference between trials in the phase II time constant. Also, the onset and the amplitude of the slow component were not significantly different between trials. When measured as the difference in 
between the eighth and third minute of exercise 
, there was no significant difference between trials (Table 1). End-exercise 
was significantly higher during the GR trial, with subjects reaching 101 ± 0.6% of 
, whereas subjects only reached 95.5 ± 1.0% of 
in the CON trial. In an effort to compare the relative changes in 
between trials, the amplitude of the slow component was expressed as a percentage of the overall 
response per unit time (% min–1). The relative slow component (% min–1) was not significantly different between GR and CON trials (Table 2).
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slow component in the vastus lateralis in the CON trial only (CON, r
= 0.76, P
= 0.029; GR, r
= 0.47, P
= 0.236). No significant correlations were obtained between the change in 
and MPF over time in the vastus medialis or biceps femoris muscles.
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50% exercise, whereas both adrenaline and noradrenaline concentrations increased significantly throughout both exercise bouts. There was no difference between experimental trials in noradrenaline concentrations (CON: rest, 3.1 ± 0.2 nmol l–1 and peak, 27.0 ± 6.0 nmol l–1; GR: rest, 2.7 ± 0.6 nmol l–1 and peak, 28.2 ± 4.0 nmol l–1), adrenaline concentrations (CON: rest, 0.3 ± 0.1 nmol l–1 and peak, 3.7 ± 1.2 nmol l–1; GR: rest, 0.4 ± 0.1 nmol l–1 and peak, 4.5 ± 1.2 nmol l–1) or thyroxine levels (CON: rest, 14.9 ± 1.0 pmol l–1 and peak, 14.8 ± 1.0 pmol l–1; GR: rest, 14.2 ± 1.0 pmol l–1 and peak, 14.2 ± 0.9 pmol l–1). |
Discussion |
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kinetics would be altered during a subsequent bout of heavy exercise. 
was significantly higher in the GR trial compared to the CON trial as a result of augmented phase I and II amplitudes, with no difference between trials in the phase II time constant or the magnitude of the slow component. The MPF of the EMG for the vastus medialis increased significantly over time during both trials, with a greater rate of increase being observed in the GR trial compared to the CON trial. The results of the present study suggest that the higher 
in the GR trial was primarily due to augmented type II fibre recruitment. However, the greater rate of increase in the recruitment of type II fibres in the GR trial may not have been large enough to further elevate the slow component when 
was already high and approaching 
.
The phase I 
amplitude was significantly elevated in the GR trial compared to the CON trial in the present study. The rise in 
during phase I is caused by an increase in cardiac output (
) and pulmonary blood flow. Although stroke volume and heart rate kinetics were not determined in the present study, there was no difference between trials in the heart rate response measured at 1-min intervals during constant-load exercise. It is possible that an increase in 
was not detected by the measurement of heart rate alone. However, the mechanism responsible for the higher 
or pulmonary blood flow in the GR trial is unknown.
There are several possible mechanisms contributing to the larger phase II amplitude obtained in the GR trial. It is likely that the reduced carbohydrate availability in the GR state may have increased fat metabolism mainly in type I muscle fibres (Bouckaert et al. 2004), which leads to a higher 
for a given power output than carbohydrate metabolism (Vollestad et al. 1984). At the end of 3 min of cycling at 25 W, the mean RER value was significantly lower in the GR trial compared to the CON trial. Therefore, at the onset of heavy constant-load exercise (and during phase II), the contribution of fat to the total energy cost of exercise was higher in the GR trial. This suggests that increased fat oxidation may have contributed to the greater phase II amplitude observed in the GR trial. However, the difference between trials in RER and substrate utilization was relatively small, and any increase in fat oxidation in the GR trial would have resulted in only a minor contribution to the higher phase II 
amplitude.
Minute ventilation was significantly elevated by 7.1 l min–1 above the CON trial by the third minute of exercise in the GR trial and remained elevated for the duration of the exercise bout. The difference in 
between trials is unlikely to enhance pulmonary 
and would not be expected to significantly effect the phase II or slow component amplitudes (Engelen et al. 1996; Scheuermann et al. 1998).
Krustrup et al. (2004b) demonstrated a significant reduction in the glycogen content of type II muscle fibres after 3 min of heavy exercise, suggesting an early recruitment of type II motor units. While the difference between treatment conditions in the MPF was not statistically significant until the fifth minute of exercise in the present study, the data suggest an early elevation in the MPF over the period of the phase II response in the GR trial. The MPF is determined by motor unit action potential conduction velocity, which is primarily influenced by muscle fibre type and cross-sectional area (De Luca, 1997). This suggests that changes in MPF may be better than iEMG for differentiating muscle fibre recruitment patterns during exercise. Using a muscle biopsy technique, Gerdle et al. (1991) demonstrated that an increase in the MPF was associated with the use of a greater proportion of type II muscle fibres. Several features of type II fibre energetics suggest that they are a logical source of the additional 
needed to perform heavy exercise. In mouse skeletal muscle, type II fibres produce greater heat in vitro and consume more O2 for the same tension development or ATP resynthesis rate than type I fibres (Crow & Kushmerick, 1982; Willis & Jackman, 1994). Calcium pump activity, which is ATP dependant, is 5- to 10-fold greater in type II fibres, as is actomyosin turnover (Crow & Kushmerick, 1982). In contrast, Barclay & Weber (2004) found no difference in net efficiency between type I and II muscles. In another study, Barclay (1996) demonstrated that the efficiency of a muscle fibre is reduced following a moderate level of fatigue. In the present study, the recruitment of additional motor units or type II fibres at the onset of exercise could have contributed to the higher phase II 
amplitude observed in the GR trial.
Although the phase II 
amplitude increased significantly in the GR trial in the present study, there was no effect of GR on the phase II time constant. Both Carter et al. (2004) and Bouckaert et al. (2004) observed no change in phase II amplitude or the time constant following a similar GR protocol. Crow & Kushmerick (1982) demonstrated a slower (longer) time constant in type II muscle fibres than in type I fibres. Furthermore, Krustrup et al. (2004b) found a slower phase II time constant when a greater number of type II fibres were recruited during heavy exercise. In the present study, the significantly higher MPF observed in the GR trial is consistent with a greater recruitment of type II motor units. A greater number of type II motor units recruited in the GR trial would be expected to slow the phase II time constant during heavy exercise. However, Molé & Hoffmann (1999) demonstrated that 
kinetics were accelerated during moderate-intensity exercise performed with a lower RER. They attributed this to the faster dynamics of muscle fat oxidation, which represent increased oxidation of intramuscular triglycerides. During the 3-min period of cycling at 25 W (when RER was at a steady state) in the present study, the RER values were 0.87 for the CON trial (42% fat oxidation) and 0.74 in the GR trial (88% fat oxidation). Therefore, at the onset of heavy constant-load cycling, the contribution of fat to the total energy cost of exercise was higher in the GR trial. This suggests that increased fat oxidation at the onset of exercise could accelerate the phase II 
response, whereas the greater recruitment of type II fibres would act to slow phase II kinetics. Under these two opposing conditions, the phase II time constant would be unchanged during the GR trial in the present study.
In the present study, blood [La–] was significantly reduced at 6 and 8 min of exercise during the GR trial compared to the CON trial. In contrast, blood pH was significantly higher at 3 min of exercise and remained higher throughout the GR trial (Fig. 1). Following the GR protocol used in the present study, there would have been a significant loss of glycogen from type I fibres and a moderate loss of glycogen from type II fibres (Thomson et al. 1979; Krustrup et al. 2004a). A significant number of the partly and fully glycogen-depleted fibres would have been recruited during the subsequent heavy exercise bout. As a result of the reduced glycogen content, the rate of the enzymatic breakdown of glycogen would have decreased in both fibre types compared to the CON trial, resulting in a reduced rate of La– production and a lower blood [La–] during the GR trial (Klausen et al. 1973). The higher pH and the lower blood [La–] in the GR trial are consistent with the findings of other GR studies (Segal & Brooks, 1979; Heigenhauser et al. 1983; Busse et al. 1991). Gerbino et al. (1996) proposed that blood flow and O2 delivery increased more rapidly in the second of two bouts of heavy exercise, owing to the residual acidosis that permitted more rapid vasodilation and a greater O2 off-loading from the red blood cells as a result of the Bohr effect. Moreover, Gerbino et al. (1996) concluded that if muscle pH was reduced and the rate of oxidative phosphorylation in the muscle increased at the onset of exercise, a faster phase II time constant is likely to be observed. Since there was no difference between treatment conditions in the present study in either blood [La–] or pH at rest or at the end of baseline cycling (25 W), it is unlikely that metabolic acidosis influenced the phase II time constant.
Both the absolute and the relative slow component were unchanged even though blood [La–] was reduced after 4.5 min of exercise and pH was elevated after 1.5 min of exercise in the GR trial. Moreover, the rise in blood [La–] over the period of the slow component between 3 and 8 min of exercise was significantly less in the GR trial (2.9 ± 0.7 mmol l–1) than in the CON trial (4.8 ± 0.4 mmol l–1). These findings provide evidence that lactate per se and/or the accompanying metabolic acidosis does not cause the slow component. Krustrup et al. (2004a) did not observe a slow component with normal glycogen content at a work rate of 50% of 
(below the BLT), whereas a slow component was observed following GR at this work intensity while blood [La–] during exercise was significantly reduced. This demonstrates that the slow component can occur without metabolic acidosis or blood La– accumulation. The results of the present study and those of Krustrup et al. (2004a) suggest that mechanisms other than an increase in blood lactate and associated metabolic acidosis cause the 
slow component during heavy exercise.
There was no difference between experimental conditions in noradrenaline, adrenaline or thyroxine concentrations. While noradrenaline and adrenaline concentrations increased significantly over time during exercise, thyroxine concentration did not change during either trial, even though 
was elevated in the GR trial compared to the CON trial and a slow component was evident in both conditions. Thyroxine is known to increase metabolic rate and cardiac output and also to increase the rate of secretion of most endocrine glands (Guyton, 1986). The results of the present study suggest that neither plasma catecholamine nor thyroxine were responsible for the higher 
found in the GR trial compared to the CON trial. The noradrenaline and adrenaline findings are in agreement with those of Krustrup et al. (2004a) and Poole et al. (1994b), whereas no previous study has reported the thyroxine response to heavy constant-load exercise performed under these treatment conditions.
Integrated EMG increased significantly from baseline (25 W) cycling to the 50% work rate; however, iEMG did not change over time during the heavy constant-load exercise bout. In contrast, MPF increased significantly from the onset of exercise to the end of the 8 min exercise bout in both experimental trials in the vastus medialis muscle and in the GR trial in the vastus lateralis muscle. The results of the present study are supported by the observations of Borrani et al. (2001) and Saunders et al. (2000), who found a significant increase in MPF over the duration of the slow component. In contrast to these findings, Perrey et al. (2001) reported an increase in iEMG over time, with no change in MPF. Bouckaert et al. (2004) concluded that reduced muscle glycogen content resulted in a shift towards greater fat metabolism in the type I fibres, with no appreciable change in fibre recruitment pattern. This conclusion was made despite no measurement of motor unit recruitment pattern. Scheuermann et al. (2001) demonstrated that both the iEMG and MPF remained relatively constant throughout heavy exercise and concluded that changes in EMG activity were not associated with the 
slow component. These investigators (Scheuermann et al. 2001) concluded that the increased O2 cost of heavy exercise (i.e. 
slow component) is coupled with a progressive increase in ATP requirements of the already recruited motor units rather than to increases in the recruitment of additional type II motor units. These studies together indicate that enhanced fat metabolism, the recruitment additional motor units, or increased ATP requirements of already recruited motors units could all contribute to the increased O2 cost of heavy-intensity exercise. The significant rise in MPF observed over the duration of exercise in the vastus medialis in both trials and in the vastus lateralis in the GR trial in the present study is consistent with the progressive recruitment of additional motor units or less efficient type II fibres, which in turn contributes to the development of the 
slow component.
It is difficult to explain why glycogen reduction was not successful in augmenting the slow component despite the greater rate of increase in MPF over the duration of exercise and possibly a larger contribution of type II fibres in the GR trial compared to the CON trial. The force generated by type II motor units is greater than that by type I motor units (Close, 1967). If more type II fibres were used in the GR trial, then fewer motor units may need to be recruited to maintain a constant force against the pedals. Therefore, the total number of motor units recruited may have decreased or remained unchanged during exercise performed with reduced muscle glycogen content, and the O2 cost of heavy exercise may not be different. However, the constant iEMG activity observed over time under both treatment conditions is not consistent with a reduction in the total number of motor units recruited in the GR trial. It is possible that the higher MPF, and consequently the greater recruitment of type II fibres, in the GR trial may not have been large enough to be physiologically important. Using the equation of Wretling et al. (1987) as an index of muscle fibre recruitment pattern, there was only a 4% greater recruitment of type II fibres in the GR trial than in the CON trial. This treatment difference in motor unit recruitment pattern may not be large enough to increase the 
slow component when the 
response to heavy exercise was already relatively high (about 4.0 l min–1).
In conclusion, the higher MPF and the greater rate of increase in MPF over the duration of exercise in the GR trial suggest that the glycogen reduction protocol was effective in increasing motor unit or type II fibre recruitment during subsequent heavy exercise. 
was higher in the GR trial compared to the CON trial as a result of augmented phase I and II amplitudes, with no difference between trials in the phase II time constant or the magnitude of the slow component. An increased recruitment of additional type II motor units may have been responsible for the higher 
observed throughout the GR trial in the vastus medialis muscle and in the GR trial in the vastus lateralis muscle. Since MPF increased significantly over time for both CON and GR trials, it is suggested that the recruitment of additional motor units or enhanced recruitment of type II fibres contributed to the development of the slow component in both trials. However, the greater increase over time in type II fibre recruitment in the GR trial may not have been of sufficient magnitude to further elevate the slow component when the 
response to heavy exercise was already high and approaching 
.
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) and following glycogen reduction (GR; •) 
), carbon dioxide production ( 
), minute ventilation ( 
), respiratory exchange ratio (RER), heart rate (HR) and blood lactate concentration ([La–]) at specified time intervals during 8 min of constant-load cycling performed under control conditions (CON) and following glycogen reduction (GR)
) kinetics determined during constant-load cycling performed under control (CON) conditions and following muscle glycogen reduction (GR)
significant difference between 3 and 8 min of exercise (P < 0.05).