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O2 kinetics during heavy exercise
are related to changes in muscle activity
1 Chelsea School Research Centre, University of Brighton, Eastbourne, East Sussex BN20 7SP; 2 Department of Sport and Exercise Science, University of Wales Aberystwyth, Aberystwyth, Ceredigion SY23 3DA; and 3 Department of Exercise and Sport Science, Manchester Metropolitan University, Alsager ST7 2HL, United Kingdom
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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We hypothesized
that the elevated primary O2 uptake
(
O2) amplitude during the second of two
bouts of heavy cycle exercise would be accompanied by an increase in
the integrated electromyogram (iEMG) measured from three leg muscles
(gluteus maximus, vastus lateralis, and vastus medialis). Eight healthy
men performed two 6-min bouts of heavy leg cycling (at 70% of the
difference between the lactate threshold and peak
O2) separated by 12 min of recovery. The
iEMG was measured throughout each exercise bout. The amplitude of the
primary O2 response was increased after
prior heavy leg exercise (from mean ± SE 2.11 ± 0.12 to
2.44 ± 0.10 l/min, P < 0.05) with no change in
the time constant of the primary response (from 21.7 ± 2.3 to
25.2 ± 3.3 s), and the amplitude of the
O2 slow component was reduced (from
0.79 ± 0.08 to 0.40 ± 0.08 l/min, P < 0.05). The elevated primary O2 amplitude
after leg cycling was accompanied by a 19% increase in the averaged
iEMG of the three muscles in the first 2 min of exercise (491 ± 108 vs. 604 ± 151% increase above baseline values,
P < 0.05), whereas mean power frequency was unchanged
(80.1 ± 0.9 vs. 80.6 ± 1.0 Hz). The results of the present
study indicate that the increased primary O2 amplitude observed during the second
of two bouts of heavy exercise is related to a greater recruitment of
motor units at the onset of exercise.
O2 uptake primary component; O2 uptake slow component; electromyogram; warm-up
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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GERBINO ET AL.
(12) originally observed that prior heavy exercise (above
the lactate threshold) could significantly speed the overall
O2 uptake (O2) kinetics
during heavy exercise. These authors suggested that the residual lactic
acidosis at the onset of the second heavy exercise bout may have led to
vasodilatation and improved O2 delivery: alleviation of an
O2 delivery limitation then led to a speeding of the
O2 kinetics. These data and
interpretations were supported by MacDonald et al. (22),
who showed that both prior heavy exercise and inspiratory hyperoxia
could reduce the "mean response time" during heavy exercise.
However, a number of recent studies, which partitioned the
O2 response into its three identifiable
kinetic components, found no evidence of a speeding of the primary
O2 kinetics (7, 10, 11, 20, 34). Instead, the speeding of the overall
O2 kinetics noted by Gerbino et al. and
MacDonald et al. could be attributed to a reduction in the amplitude of
the O2 slow component (11). These recent reports suggest that O2 delivery is not
limiting at the onset of heavy exercise and that some other mechanism
is responsible for the characteristic effect of prior heavy exercise on
the O2 response profile.
Our laboratory's most recent work on this issue (10)
demonstrated that the reduction in the amplitude of the
O2 slow component during a second bout
of heavy exercise was preceded by an increase in the amplitude of the
primary O2 response without a change in
the primary O2 kinetics. We speculated
that the elevated primary O2 amplitude
observed after heavy exercise may have been the result of increased
motor unit recruitment at the onset of heavy exercise. However, to
date, this hypothesis remains untested. Recent work by Scheuermann et
al. (34) suggests that patterns of motor unit recruitment
do not play a significant role in the development of the
O2 slow component or in the effects of
prior heavy exercise. One limitation of this study, acknowledged by the
authors, was the measurement of the integrated electromyogram (iEMG) of
a single muscle group to infer the muscle activity responsible for
power production during cycling.
Therefore, the aim of this study was to test the hypothesis that the
elevated primary O2 amplitude during the
second of two bouts of heavy exercise is accompanied by an increase in
iEMG during the primary phase of the response (i.e., in the first 2 min
of exercise).
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Eight healthy male subjects (mean ± SD, age 24 ± 4 yr; height 1.79 ± 0.04 m; mass 74.0 ± 5.1 kg; peak
O2 51 ± 8 ml · kg
1 · min1) gave
written informed consent to participate in this study, which was
approved by the ethics committee of the Manchester Metropolitan University.
Experimental design.
The subjects initially performed a ramp exercise test to estimate the
ventilatory threshold (VT) and determine peak
O2
(O2 peak) (see below). Subsequently, on
two separate occasions, the subjects performed two 6-min bouts of heavy
leg cycle exercise separated by 12-min recovery. On one of the test
days, "noninvasive" data [near-infrared spectroscopy (NIRS) and
electromyography (EMG)] were acquired. On the other test day,
"invasive" data (muscle pH and arterialized venous blood) were
acquired. Pulmonary gas exchange and heart rate (HR) were measured
throughout all exercise tests, as described below.
Measurement of VT and O2 peak.
The VT and O2 peak were determined by
using a ramp exercise test (30 W/min) performed to the limit of
tolerance on an electrically braked cycle ergometer (Ergoline, Jaeger).
Subjects self-selected a cadence of 70-90 rpm and maintained this
throughout all subsequent exercise tests. The breath-by-breath data
were collected and displayed at 10-s intervals. The VT was determined visually as an increase in CO2 production relative to
O2.
O2 peak was taken as the highest 10-s
value recorded before volitional exhaustion. The intensity of the heavy
leg exercise bouts was set at a power output that would elicit a
O2 that was 70% of the difference
between VT and O2. This power output was
chosen to maximize the potential effect of prior exercise on the
response parameters measured.
Experimental protocol. The protocol was similar in design to that of Burnley et al. (10). The subjects performed two "square-wave" bouts of heavy exercise of 6-min duration, separated by 12 min of recovery. The heavy exercise bouts were each preceded by 3 min of baseline pedaling (at 20 W, the lowest power output available on the cycle ergometer), and pulmonary gas exchange was measured breath by breath throughout exercise. This protocol was performed twice.
During one test session, NIRS and EMG data were acquired. The oxygenation status of the right vastus lateralis muscle at approximately midthigh was monitored by use of a commercially available NIRS system (Omron Heo-200). The system consisted of a probe attached to a data logger that received NIRS signals at 2 Hz. The probe consisted of two light-emitting diodes and two photodetectors, which detected photons at wavelengths of 840 [oxyhemoglobin (HbO2)] and 760 nm (Hb). The penetration depth when using these probes has been estimated at 2.5-3.0 cm (manufacturer's instructions). The NIRS data were collected continuously during exercise after the probe gain was set with the subject at rest in a seated position. The data were subsequently downloaded onto a personal computer, and the resulting text files were stored on disk for later analysis. The NIRS data represented a relative gain based on the optical density measured in the first datum collected and could not, therefore, be used to estimate absolute tissue O2 saturation. Surface EMG recordings from three muscles were made by using a radio telemetry system (MIE MT8, Medical Research, Leeds, UK). The left leg was used for EMG electrode placement. The leg was first shaved around the belly of the gluteus maximus, vastus lateralis, and vastus medialis and rubbed with an abrasive gel. Bipolar silver-silver chloride electrodes were then attached to the belly of each muscle with a 2-cm center-to-center distance separating them. Earth electrodes for each muscle were placed over inert tissue (tendon, ligament, or bone). The electrodes were attached via preamplifiers to a telemetry belt that relayed the data to an analog-to-digital converter. All wiring connecting the electrodes to the belt were taped down to prevent movement artifact. EMG recordings, of 30-s duration, began 45 s before exercise onset, at exercise onset, and every 45 s thereafter during both heavy exercise bouts. The signals detected by the electrodes were preamplified with a gain of 4,000 and a frequency band of 20-500 Hz. The EMG signal was sampled at a frequency of 1,000 Hz and underwent 12-bit analog-to-digital conversion. The digital signal was first displayed raw and subsequently full-wave rectified and integrated over 10-ms intervals. The iEMG was calculated over each 30-s sampling period, and all iEMG data were normalized to the value recorded in the unloaded pedaling phase 30 s before the onset of the first bout of leg exercise. All iEMG data were, therefore, expressed as a percentage of the initial unloaded pedaling value. The normalized iEMG of the individual muscles was summed and averaged to provide an estimate of "total" muscle activity during exercise. The first three EMG data sets acquired during the heavy exercise bouts were used as an index of muscle activity in the primary phase of the response to exercise (i.e., muscle activity in the first 2 min of exercise). The mean power frequency (MPF) was calculated as the mean frequency generated by the fast Fourier transform of the sampled EMG signal. During the other test session, muscle pH was measured before each of the heavy exercise bouts by using a needle-tipped pH electrode, which was inserted 3 cm into the right vastus lateralis muscle through an incision made under local anesthetic (3-4 ml of 1% lignocaine). The pH meter (Corning 245 pH meter) was calibrated before each test and checked by using distilled water. Muscle pH was determined ~1 min before the period of unloaded cycling began for both exercise bouts. Arterialized venous blood (~2.5 ml) was sampled from the dorsum of a heated hand by using a 21-gauge butterfly cannula at rest, at time 0 (the onset of exercise) and at 2, 4, and 6 min of exercise. The cannula tubing was flushed between each sample with saline. These samples were immediately capped, stored in an ice slurry, and analyzed in duplicate for pH by use of an automated blood-gas analyzer (CIBA-Corning 278 blood gas system, Medfield, MA) within 1 h of collection. The remainder of the sample was analyzed in duplicate for blood lactate concentration ([lactate]; YSI 1500, Yellow Springs Instruments, OH).Measurement of pulmonary gas exchange and HR.
Pulmonary gas exchange was measured breath by breath during all
exercise tests. Subjects breathed through a low-resistance turbine
volume transducer (Jaeger Triple V), which had a dead space of 90 ml.
Gas was continuously drawn down a capillary line into rapid-response
gas analyzers (Jaeger Oxycon Alpha, Hoechberg, Germany).
O2, carbon dioxide production, and
minute ventilation were calculated and displayed breath by
breath once the delay between the volume and concentration signals had
been accounted for. The volume transducer was calibrated before each
test with a 3-liter calibration syringe (Hans Rudolph), and the
analyzers were calibrated with gases of known concentration. HR was
recorded every 5 s by using short-range radio telemetry (Polar
Sports Tester, Kempele, Finland). The O2 pulse was
calculated in the unloaded pedaling baseline and after 2 min and at the
end of exercise as absolute O2/HR.
Data analysis.
The breath-by-breath data were linearly interpolated to provide
second-by-second values. For each subject, the two performances of each
protocol were time aligned and averaged to provide one set of
second-by-second data for each variation of the protocol. The time
course of the O2 response after the
onset of exercise was described in terms of a three-component
exponential function, using iterative nonlinear regression techniques
in which minimizing the sum of squared error was the criterion
for convergence, using purpose-built fitting software. Each exponential
curve was used to describe one phase of the response. The first phase
began at the onset of exercise, whereas the other terms began after
independent time delays (5)
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![+ A<SUB>s</SUB> ∗ [1 − <IT>e</IT><SUP>(<IT>t−</IT>TD<SUB>2</SUB>)/&tgr;s</SUP>] phase III (slow component)](/content/vol93/issue1/fulltext/167/img003.gif)
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O2(b) is the baseline
O2 measured in the 3 min preceding the
onset of exercise; Ac,
Ap, and As are the
amplitudes of the exponential curves fitting the cardiodynamic,
primary, and slow components, respectively; 
c,
p, and s are the time constants;
t is time; and TD1 and TD2 are the
time delays. The cardiodynamic component was terminated at
TD1 and given the value for that time (defined
A'c). The amplitude of the primary response (A'p) was defined as the increase in
O2 from baseline to the asymptote of the
primary component. The absolute amplitude of the primary
O2 response was calculated as the sum of
baseline O2 and
A'p. The amplitude of the
O2 slow component was determined as the
increase in O2 from TD2 to
the end of exercise (defined A's), rather
than from the asymptotic value (As), which may
project beyond the value at 6 min (end exercise).
Statistical analysis. The responses to the square-wave bouts of heavy exercise were compared by using paired t-tests. The iEMG data series was analyzed by using a two-way (exercise bout × time) repeated-measures ANOVA. The F ratios were considered statistically significant when P < 0.05.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The heavy exercise bouts were performed at 70% of the change
between lactate threshold and peak O2,
which required a power output of 275 ± 50 W. The baseline values
for O2, blood [lactate], blood pH, and muscle pH are shown in Table
1. Baseline
O2 was restored, whereas blood
[lactate] was still elevated (P < 0.001) and blood
pH was reduced (P < 0.01) after 12 min of recovery. Baseline muscle pH was similar before both exercise bouts
(~7.10; P = 0.84). The increase in blood [lactate]
as a result of the performance of heavy exercise is also shown in Table
1. The increase in blood lactate during the second exercise bout was
significantly reduced compared with that during the initial bout of
heavy exercise (P < 0.001).
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The primary O2 time constant was
unaltered by prior heavy leg exercise (P = 0.36),
whereas the primary O2 response
amplitude A'p was significantly increased
by prior heavy exercise (by ~330 ml/min; P < 0.001;
Table 1). This increase in the net primary amplitude led to a
significant increase in the absolute primary O2 response
[O2(b) + A'p; P < 0.001]. The
amplitude of the O2 slow component was
reduced by ~390 ml/min after prior heavy exercise (P < 0.001). The effects of prior heavy leg exercise on the amplitudes of
the O2 response led to the attainment of a similar end-exercise O2 for the
initial heavy exercise bout and the second heavy leg exercise bout
(P = 0.94). The O2
responses for each subject are shown in Fig.
1.
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The temporal profiles of the normalized iEMG responses to the two bouts
of heavy leg exercise are shown in Fig.
2. In the first bout of exercise, the
averaged iEMG increased systematically throughout exercise, reaching
its peak value at the end of exercise (Fig. 2A). In
contrast, the iEMG response to the second bout of heavy exercise tended
to be higher in the first 2 min of exercise but then remained
essentially unchanged until the end of exercise. A similar pattern was
evident in all three muscles (Fig. 2, B-D). The MPF was not significantly different between the first and second
bouts of heavy exercise (80.1 ± 0.9 vs. 80.6 ± 1.0 Hz, P = 0.38; Fig. 2). To gain insight into the
relationship between the primary O2
amplitude and the iEMG at the onset of exercise, the iEMG in the first
2 min of each bout was averaged and compared. The results of this
analysis are shown in Fig. 3A.
Prior heavy exercise significantly increased the iEMG in the first 2 min of the second bout of heavy exercise (from 491 to 604% of the
unloaded pedaling value, on average; P < 0.05).
Furthermore, when the primary O2
amplitude (A'p) was divided by the
normalized iEMG (Fig. 3B), there was no difference between
the two exercise bouts (P = 0.45), indicating that the
increased primary O2 amplitude in the
second exercise bout was correlated to an increased EMG.
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The NIRS responses are shown in Fig. 4.
Figure 4A shows the superimposed relative O2
saturation profiles for the two bouts of heavy exercise. The level of
HbO2 was higher before the onset of the second bout of
heavy exercise and remained higher throughout the second bout of heavy
exercise compared with the initial heavy bout. In both heavy bouts, an
initial period of hemoglobin desaturation at the onset of exercise
reverted to a small and gradual resaturation from 1 min onward. (It
should be noted here that NIRS is unable to distinguish between changes
in HbO2 and oxymyoglobin because the absorption spectra of
Hb and myoglobin are identical, and the relative contribution to the
NIRS signal from these two sources is uncertain.) The total Hb (the
summation of the Hb and HbO2 signals) is shown in Fig.
4B. Total Hb was higher before the onset of the second heavy
exercise bout and remained higher during the first 5 min of exercise.
In both bouts, there was evidence of a transient fall in total Hb at
exercise onset, reaching a nadir at ~30 s. Subsequently, total Hb
increased systematically in both bouts until the cessation of exercise.
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The HR responses to heavy exercise are shown in Table
2. HR was higher in the baseline period
before the second bout of heavy exercise commenced (P < 0.001), whereas baseline O2 pulse
(O2/HR) was significantly lower
(P < 0.001). After 2 min of exercise, HR was
significantly higher after prior leg exercise, although O2
pulse was similar (P = 0.47). HR and O2
pulse were similar at the end of exercise.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The present study demonstrates that the increased primary
O2 amplitude observed after heavy cycle
exercise is accompanied by an increased iEMG in the first 2 min of
exercise, consistent with our hypothesis.
A common feature of previous studies, in which the recovery between
consecutive heavy exercise bouts has been extended to allow the
restoration of baseline O2, is an
elevation of the primary O2 amplitude in
the second heavy exercise bout (7, 10). This effect occurs
without a change in the primary O2 time
constant and is followed by a significant reduction of the O2 slow component amplitude as exercise
continues (10, 11, 20, 34). It has been suggested that the
elevated primary O2 amplitude may be
caused by an increase in motor unit recruitment at the onset of
exercise (10). Previous studies have suggested that
increased motor unit recruitment may (35) or may not
(34) contribute to the development of the
O2 slow component. However, these
studies measured only the EMG signal from one muscle (the vastus
lateralis). Because cycle exercise involves the activity of most of the
lower limb muscle mass for power production (16), and
because the pulmonary O2 response to
exercise primarily represents muscle oxygen consumption
(30), it is important to measure the EMG from as many
muscles as practically possible to relate muscle activity to pulmonary
O2 (31).
In the present study, methodological factors such as differences in
electrode placement were eliminated by only comparing consecutive bouts
of heavy leg exercise after a single preparation process. Three muscles
were studied in the present work, and the normalized iEMG values from
each were summed and averaged to provide an indication, only, of
overall muscle activity during consecutive bouts of cycling exercise.
It is acknowledged that this treatment is somewhat arbitrary because
the contribution of each of the three muscles to force generation and
O2 consumption is not known. The iEMG during the early part
of the second bout of heavy exercise was significantly higher compared
with the first bout in all three muscles studied. These data do not
concur with those of Scheuermann et al. (34), who did not
detect any change in the iEMG during exercise at 50% of the change
between lactate threshold and peak O2.
The reason for these divergent findings may reside in the differences
in exercise intensity (being higher in the present study) or to the
normalization methods employed (Scheuermann et al. normalized their
data to the end, rather than the beginning, of exercise). In the
present study, the increase in the primary O2 amplitude in the second heavy bout
was accompanied by a 19% increase in the iEMG during the first 2 min
of exercise and no change in the MPF, clearly indicating an increase in
motor unit recruitment after prior heavy exercise. It was also of
interest that the increase in iEMG with time was less steep in the
final 3 min of the second bout of heavy exercise (Fig. 2) commensurate with the reduction in the amplitude of the
O2 slow component. Indeed, the iEMG
profiles during the two heavy exercise bouts were remarkably similar to
the O2 profiles. However, there was no
significant relationship between the reduction in the
O2 slow component after prior heavy
exercise and changes in the EMG responses. This was due, in large part,
to substantial intersubject variability in iEMG toward the end of the
exercise bouts. The present data, therefore, provide only qualitative
support to the hypothesis that the O2
slow component can be attributed, in part, to the serial recruitment of
additional motor units (29, 31, 33).
Previous investigators have suggested that
A'p represents a "target amplitude"
dictated by external power output and work efficiency that is
subsequently modified with time during heavy exercise (5, 6,
26). This target amplitude is altered after prior heavy exercise
such that the primary response initially projects to a
O2 that is closer to the
O2 required later in exercise (as
estimated from end-exercise O2). In the
present study, it is clear from the unchanged MPF that the increase in iEMG early in the second heavy exercise bout represents additional motor unit recruitment (presumably comprising both principal fiber types) and not increased firing frequency or the preferential recruitment of higher threshold motor units. Fatigued fibers may be
activated but may fail to produce any tension, resulting in the need to
recruit more muscle fibers to maintain the power output and an increase
in the O2 cost of exercise (18). An increase in motor unit recruitment for the same power output could reduce the
apparent work efficiency because an estimated 30-50% of the energetic cost of fiber recruitment is committed to processes independent of tension development (i.e., those maintaining
intracellular homeostasis; Ref. 36). This is consistent
with the proportionality between the iEMG and the primary
O2 amplitude presented in Fig. 3B. Recruitment of a larger motor unit pool at the onset of
exercise, the fibers of which are able to generate tension, would
result in a reduction in the tension generated by each individual fiber and therefore reduce the metabolic disturbance experienced by the
muscle as a whole. The smaller increase in [lactate] and smaller O2 slow component responses in the
second heavy leg bout seem to support this interpretation. In addition,
Rossiter et al. (32) have recently demonstrated that
phosphocreatine degradation during heavy leg extension exercise in the
prone position is significantly blunted (although not speeded) by a
prior priming bout. Interestingly, these authors showed that this
attenuation of the phosphocreatine concentration decrement was
associated with speeded primary O2 kinetics and not an elevated primary amplitude. The reason for the
difference between these findings and those of other studies, including
the present study, is not clear, although the possibility that
differences in exercise mode account for these findings has been
considered previously (32).
The elevation of HR in the baseline period, coupled with the greater
HbO2 saturation and total Hb in the vastus lateralis observed before the onset of the second bout of heavy leg exercise, provides indirect evidence that O2 delivery to the
exercising muscle was increased by prior heavy exercise. These findings
are consistent with the original proposal that a prior bout of exercise that induces a residual lactic acidosis increases muscle perfusion (12), although it should be noted that differences in the
NIRS signal might also have been due to greater cutaneous blood flow in
the second bout consequent to heat storage. However, it is important to
emphasize that any increase in muscle perfusion did not alter the
primary O2 time constant because this
was unchanged in the second bout of exercise. This provides additional
evidence that the primary O2 kinetics
are not limited by O2 availability during heavy exercise
(4, 14, 15, 17). Krustrup et al. (21)
recently demonstrated that O2 delivery exceeded muscle O2 consumption, even during the first of a series of
high-intensity exercise bouts in humans. The increased EMG signal at
the onset of the second bout of heavy exercise indicates that there is
an increased demand for O2 and that the increase in
O2 delivery supports rather than causes the increased
primary O2 amplitude.
The kinetics of muscle oxygenation at the onset and offset of exercise
have recently been estimated (8, 37). Mathematical modeling of the HbO2 signal with a model similar to that
used to characterize the O2 response has
also been attempted in a preliminary report (28), and the
time constants derived correlated with the primary
O2 time constants, although the actual
values of the muscle oxygenation and O2
time constants differed considerably. Mathematical modeling of the
present data has not been attempted, because the temporal profile of
the HbO2 signal did not conform to a simple monoexponential
function with or without a delay. Indeed, as shown in Fig.
4A, there appeared to be an apparent reoxygenation beyond
the first minute of the exercise bout. As emphasized by MacDonald et
al. (23), this response is not evident in measurements of
venous O2 saturation, indicating that it is likely to be an
artifact of the manner in which NIRS data is acquired. McCully and
Hamaoka (24) suggest that, because the NIRS probe measures
the weighted average of oxygenation status in the blood contained in
the arterioles, capillaries, and venules, the weighting during exercise
might shift from the venules toward the capillaries as blood flow
increases and a greater red cell volume is located in the more
oxygenated capillaries.
It was of interest that, despite significant residual lactacidemia at the onset of the second heavy exercise bout, muscle pH (measured 8 min after the first heavy exercise bout) was not significantly different from that measured under rested conditions before the first bout. We measured muscle pH by use of a needle-tipped electrode inserted into the vastus lateralis muscle. By using this technique, a measure of pH in the muscle compartment is obtained, which will represent the average pH of the intracellular and extracellular fluid (1). Allsop et al. (1) suggested that the muscle pH values recorded by using needle-tipped electrodes are ~0.1-0.2 units higher than those measured by using the homogenate technique employed in biopsy studies, reflecting a larger contribution of the extracellular fluid to the electrode measure. However, this technique should still identify any changes in muscle pH before the onset of subsequent exercise.
The similarity of the muscle pH values at rest and 8 min after heavy exercise is at first sight counterintuitive. Both blood [lactate] and blood pH were significantly altered compared with the control condition, consistent with previous reports (9, 10, 12). However, it is known that the maintenance of muscle pH homeostasis involves several mechanisms, including Na+/H+ exchange, lactate-proton cotransport, and bicarbonate-dependent transport (19). It has been demonstrated that net muscle H+ release occurs at a significantly faster rate than lactate release (19). This net H+ release continues even when the muscle that had previously been releasing lactate has switched to net lactate uptake (3). It is, therefore, likely that the present data reflect the relatively rapid restoration of muscle pH homeostasis; as a consequence, the present data provide evidence against a role for reduced muscle pH, per se, in the effect of prior heavy exercise.
The data of the present study might provide some insight into the
spatial and temporal character of the factor or substance that causes
an increase in motor unit recruitment. Because the effect of prior
heavy exercise occurred after 12 min of recovery, the present study
provides additional evidence that the factor responsible demonstrates a
slow recovery time course (10, 27). The role of lactate as
a mediator of the effect of prior heavy exercise has yet to be refuted.
The present data confirm that an elevation in the primary
O2 amplitude is associated with a
residual elevation in blood [lactate]. Moritani et al.
(25) showed that surface EMG amplitude increased after
occlusion during repeated isometric contractions at 20% of the maximal
voluntary contraction. The fact that EMG amplitude remained elevated
for 2 min after cuff release and was accompanied by elevated blood (and
presumably muscle) [lactate] demonstrated the important role of the
metabolic state of the exercising muscle in motor unit recruitment
strategy. Thus it is possible that lactate itself may be responsible
for altered motor unit recruitment at the onset of a second bout of
heavy exercise. Simultaneous arterial and venous blood sampling has
shown that inactive muscle may undergo net lactate uptake (2,
13), and this may explain the similar (but quantitatively
smaller) effect on the O2 kinetics when the prior heavy exercise is performed by the arms (9).
In summary, the present study has shown that the elevation in the
primary O2 amplitude after a bout of
prior heavy exercise is associated with an elevation in iEMG and no
change in MPF during the first 2 min of heavy exercise. Prior heavy leg
exercise produced a residual increase in blood [lactate] and a
reduction in blood pH but did not affect baseline muscle pH. There was
evidence of an increased O2 delivery to the exercising leg
muscle in the second exercise bout, as indicated by increased baseline
HR, total Hb, and HbO2 saturation, and a reduced
O2 pulse. However, the primary O2 time constant was unaffected by prior
heavy exercise. These results suggest that the elevated primary
O2 amplitude during a second bout of
heavy exercise can be attributed to an increase in motor unit
recruitment at the onset of exercise.
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FOOTNOTES |
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Address for reprint requests and other correspondence: A. M. Jones, Dept. of Exercise and Sport Science, Manchester Metropolitan Univ., Hassall Rd., Alsager, Cheshire ST7 2HL, United Kingdom (E-mail: a.m.jones{at}mmu.ac.uk).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
10.1152/japplphysiol.01217.2001
Received 10 December 2001; accepted in final form 6 March 2002.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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1.
Allsop, P,
Jorfeldt L,
Rutberg H,
Lennmarken C,
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Hall GM.
Delayed recovery of muscle pH after short duration, high intensity exercise in malignant hyperthermia susceptible subjects.
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Bangsbo, J,
Aagaard T,
Olsen M,
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) and
second (
) bouts of heavy exercise. Note that
