| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
1 Applied Physiology
Laboratory, It is presently unclear how the fast and slow
components of pulmonary oxygen uptake
(
posture; gas exchange kinetics; oxygen transport; slow component of
oxygen uptake
PULMONARY OXYGEN UPTAKE
( None of the previous studies (8, 9, 23), however, partitioned
Subjects
ABSTRACT
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
O2) kinetics would be
altered by body posture during heavy exercise [i.e., above the
lactate threshold (LT)]. Nine subjects performed transitions from
unloaded cycling to work rates representing moderate (below the
estimated LT) and heavy exercise
(O2 equal to 50% of the
difference between LT and peak
O2) under conditions of
upright and supine positions. During moderate exercise, the
steady-state increase in O2
was similar in the two positions, but
O2 kinetics were slower in the supine position. During heavy exercise, the rate of adjustment of
O2 to the 6-min value was
also slower in the supine position but was characterized by a
significant reduction in the amplitude of the fast component of
O2, without a significant
slowing of the phase 2 time
constant. However, the amplitude of the slow component was
significantly increased, such that the end-exercise O2 was the same in the two
positions. The changes in
O2 kinetics for the supine
vs. upright position were paralleled by a blunted response of heart
rate at 2 min into exercise during supine compared with upright heavy
exercise. Thus the supine position was associated with not only a
greater amplitude of the slow component for
O2 but also, concomitantly,
with a reduced amplitude of the fast component; this latter effect may
be due, at least in part, to an attenuated early rise in heart rate in
the supine position.
INTRODUCTION
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
O2) has been reported to
adjust more slowly at the onset of exercise in the supine position for both moderate- (8, 15, 18, 19, 22, 25, 34) and heavy-intensity exercise
(8, 9, 23). Despite greater cardiac output (15, 18, 23), it appears
that effective blood flow to the working leg muscles is less in the
supine posture (11, 13, 25, 33), presumably as a consequence of lower
arterial pressure in the legs when the effect of gravity (hydrostatic
gradient effect) is removed. These results imply that the slowing of
O2 kinetics in the supine
position may be the result of a blunted cardiovascular response to exercise.
O2 kinetics during supine
heavy-intensity exercise [i.e., above the lactate threshold
(LT)] into discrete components, so as to elucidate the mechanism
by which the kinetics appeared slowed in the supine position.
Furthermore, the previous studies (8, 23) did not repeat each exercise
test to improve the dynamic resolution of
O2 kinetics during supine
heavy exercise. It has been proposed that the slower
O2 kinetics and the presence of a slow component during heavy exercise in the upright position reflect inadequate perfusion and
O2 delivery to the working muscles (14, 24), which results in lactic acidosis (7, 30, 32). Therefore, if
supine exercise is associated with a relative perfusion inadequacy to
the working muscles, this should be exacerbated during heavy exercise.
On the basis of the above findings, we hypothesized that heavy exercise
in the supine position would be associated with a slower adjustment for
the predominant component of
O2 and a larger slow
component compared with the upright position. In addition, we
characterized the off-kinetics for
O2 in the two positions to
investigate whether any alterations in kinetics seen during exercise
would also be translated into parallel differences in recovery.
METHODS
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
Protocol
Incremental-exercise tests.
A ramp exercise protocol (25 W/min), preceded by 4-min unloaded cycling
on a cycle ergometer, was utilized to estimate each individual's LT
and peak O2 (the highest
O2 achieved during exercise). Responses to upright and supine posture conditions were
tested on separate days. In the supine position, the crank shaft was
positioned 30 cm above the level of the back. Handgrips were available
for support. The O2 at the
LT was estimated as the break point in the plot of
CO2 output
(CO2) against a function of
O2 (V-slope method) (6).
The break point was determined by a computer program that defined the
O2 above which
CO2 increased
faster than O2, without hyperventilation.
Constant work rate tests.
Exercise transition tests were conducted under the two posture
conditions on separate days. Each constant work rate exercise test was
performed for 6 min. The steady-state work rate that corresponded to
the LT was defined as the work rate that occurred 45 s before the LT
was actually exceeded during the ramp test. The 45-s offset represents
an average correction for the delay in the
O2 response relative to the
ramp forcing function. The moderate work rate used for both posture
conditions corresponded to a
O2 of ~80% of
the LT determined for the upright position, whereas the heavy exercise
work rate was estimated to require a
O2 equal to ~50% of the
difference (
) between the subject's LT and peak
O2, i.e., a value of (LT + 0.50), on the basis of the initial
O2-to-work rate ratio
observed during the ramp exercise in the upright position (Table
1). The exercise was preceded by 3 min, and
was followed by 6 min, of unloaded cycling at a pedal frequency of 60 rpm. To minimize random noise and enhance the underlying response
patterns for the moderate work rate tests, subjects performed a total
of four to six repetitions of the exercise transition under each
posture condition. Subjects performed two to three exercise transitions
under each posture condition for the heavy work rate.
|
Measurements
Subjects breathed through a low-resistance valve (Hans-Rudolph) connected to two pneumotachographs for measurement of inspiratory and expiratory flows, as previously described (20). Each system was calibrated repeatedly by inputting known volumes of room air at various mean flows and flow profiles. Respired gases were analyzed by mass spectrometry (model MGA-1100, Perkin-Elmer) from a sample drawn continuously from the mouthpiece. Precision-analyzed gas mixtures were used for calibration. Alveolar gas exchange variables were calculated breath by breath according to the algorithms of Beaver et al. (5). Heart rate (HR) was continuously monitored via a three-lead electrocardiogram.Analysis
Individual responses during the baseline-to-exercise transitions were time interpolated to 1-s intervals. Responses to exercise were further averaged across all transitions for each subject and condition. To further reduce the breath-to-breath noise to enhance the underlying characteristics, each average response was smoothed with a five-point moving average filter. For both the on- and off-transients, the response curve ofO2 was
fit by a three-term exponential function that included amplitudes, time
constants, and time delays, by using nonlinear least squares regression
techniques (Fig. 1) (3, 12). The
computation of best-fit parameters was chosen by the program to
minimize the sum of the squared differences between the fitted function
and the observed response. The first exponential term started with the
onset of exercise, and the second and third terms began after independent time delays
|
![+ <IT>A</IT><SUB>1</SUB>⋅[1 − <IT>e</IT><SUP>−(<IT>t</IT>−TD<SUB>1</SUB>)/&tgr;<SUB>1</SUB></SUP>] <IT>Phase 2</IT> (fast primary component)](/content/vol87/issue1/fulltext/253/img002.gif)
|
(1) |
![+ <IT>A</IT><SUB>2</SUB>⋅[1 − <IT>e</IT><SUP>−(<IT>t</IT>−TD<SUB>2</SUB>)/&tgr;<SUB>2</SUB></SUP>] <IT>Phase 3</IT> (slow component)](/content/vol87/issue1/fulltext/253/img003.gif)
|
O2(b) is the unloaded
cycling baseline value;
A0,
A1, and
A2 are the
asymptotic values for the exponential terms; 
0,
1, and
2 are the time constants; and
TD1 and
TD2 are the time delays. The
phase 1 term was terminated at the
start of phase 2 (i.e., at
TD1) and assigned the value for
that time (A'0)
|
O2 response during moderate-intensity exercise (<LT) reaches a new steady state within 3 min after the onset of exercise in normal subjects, the slow exponential term invariably dropped out during the iterative-fitting procedure. In addition, to facilitate comparison across the subjects and different absolute work rates, the gain of the fast primary response (G1 = A'1/work rate) and
relative contribution of slow component to the overall increase in
O2 at end exercise [A'2/ (A'1+
A'2)] were
calculated.
|
Recovery kinetics for O2
were initially analyzed with Eq. 1. However,
preliminary findings (see RESULTS)
demonstrated that, for both the supine and upright heavy-exercise
conditions, TD2 in recovery
converged back to a value that was not significantly different from
that found for TD1. Thus we
subsequently fit each of the recovery
O2 curves with a model
similar to Eq. 1, except that after
phase 1 both the primary and slow
exponential terms shared the same time delay
(TD1), equivalent to the
duration of phase 1 in recovery (3,
12).
The overall kinetics of the response was determined from mean response
time (MRT). It was calculated by fitting the response data of
O2 to a monoexponential
function that included a single amplitude and time constant, starting
from the onset of the transition.
For the comparison with the associated
O2 responses, the baseline,
2-min, and end-exercise values of HR and oxygen pulse [O2-to-HR ratio
(O2/HR)] during
exercise were calculated. Furthermore, the kinetics of HR (half time)
were determined in terms of the response time to achieve 50% of change
in HR from baseline to end-exercise. The values of minute ventilation
(E) and respiratory exchange ratio (R)
during exercise were also calculated.
Statistics
Data are presented as means ± SD. The data were analyzed by using a repeated-measures analysis of variance design. Significant results were further analyzed by Scheffé's post hoc test. Significance was declared at P < 0.05.| |
RESULTS |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
Incremental Exercise
Supine posture led to significant reductions in peak work rate, peakO2, estimated LT, and peak HR
compared with upright posture (Table 1).
Moderate Constant Work Rate Exercise
The response forO2 from
baseline to moderate exercise is shown in a representative subject for
the two conditions in Fig. 2A. During
moderate exercise, the steady-state increase in
O2 (as
A'1) and the
kinetics in phase 2 (as
1) were similar for the two
positions, but the overall O2
kinetics (as MRT) were slower in supine compared with the upright
position (Table 2).
|
|
The O2 deficit was calculated for
the two positions, on the assumption that the end-exercise
O2 (at 6 min) represented the O2 requirement for the exercise.
The O2 deficit was similar between the supine (0.54 ± 0.20 liter) and the upright position (0.42 ± 0.27 liter).
Heavy Constant Work Rate Exercise
Associated with the decrease in peakO2 and the LT, supine posture
resulted in an increase for the relative intensity of the heavy work
rate, as denoted by %, compared with that seen in the upright
position (Table 1). The response for
O2 during heavy exercise in a
representative subject is shown for the two conditions in Fig.
2B. The primary time constant
(1) was not significantly
longer, but instead the amplitude
(A'1) and the gain
(G1) of the fast component of
O2 during heavy exercise were
significantly reduced in supine compared with upright position (Table
3). This was compensated for by an increase
in both the absolute
(A'2) and the
relative magnitude of the slow component of
O2
[A'2/ (A'1+ A'2)], such
that the end-exercise O2 was
the same for the two positions. The overall
O2 kinetics (MRT) were slower
in supine compared with the upright position.
|
When Eq. 1 was used to model the
recovery kinetics of O2 after
heavy exercise in both the supine and upright positions, TD2 converged back to a value
that, on average, was not significantly different from
TD1 (upright:
TD2 = 25.7 ± 16.3, TD1 = 15.4 ± 2.9 s,
P > 0.05; supine: TD2 = 29.5 ± 19.4, TD1 = 17.4 ± 3.4 s, P > 0.05). Given these results, we fit the recovery
O2 response for each
condition and subject with a modified version of Eq. 1, where TD2 was
set equal to TD1 (i.e., a common
time delay for the fast and slow exponential terms). The results are
given in Table 4. There was no significant
effect of posture on either the fast or slow component of the
off-transient response of O2. Thus the relative contribution of the slow component to the overall O2 response was retained
during recovery from heavy-intensity exercise, irrespective of
positions. Therefore, the amplitudes for both the fast
(A'1) and slow
components (A'2), and the time constant for the fast component
(1), were similar between
exercise and recovery responses for each position. These results
suggest a symmetry between the exercise and recovery responses of
O2 for this relative
intensity (56-80%) of heavy exercise, especially with regard
to the amplitude and time constant of the fast exponential component.
|
The O2 deficit was significantly greater in the supine (2.32 ± 0.42 liters) compared with upright position (1.86 ± 0.52 liters, P < 0.05).
HR, O2/HR,
E, and R Responses
|
|
The response for HR from baseline to heavy exercise is shown in a
representative subject for the two conditions in Fig.
3B. The 2-min value was significantly
lower in the supine compared with the upright position (Table 5). The
reduced early response of HR during supine heavy exercise likely
contributed to the lower O2 rise, because
the oxygen pulse was similar for supine and upright heavy exercise.
There were no significant differences in the baseline and end-exercise
values of E and R for moderate exercise
between the two conditions. The baseline and end-exercise values of
E were similar for supine and upright
heavy exercise. The end-exercise values of R for heavy exercise in the
supine condition (1.07 ± 0.03) were significantly greater than for
the upright position (1.03 ± 0.05, P < 0.01).
| |
DISCUSSION |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
In the present study, supine exercise at a moderate intensity resulted
in a significant slowing of the overall
O2 response (longer MRT)
compared with the upright condition, but the exercise steady-state
amplitude (A'1) and
the kinetics in phase 2 (1) were unaltered. During
heavy-intensity exercise in the supine position, the primary time
constant (1) was not
significantly longer, but instead there was a significant reduction in
the initial O2 amplitude as
A'1. This was
compensated for by an increase in the magnitude of the slow component
of O2 such that, by the end
of exercise (6 min), there was no significant net effect of body
position on O2. The MRT was
slower in the supine compared with the upright position. These results
represent the first quantitative comparison of
O2 kinetics during heavy exercise between the supine and upright positions.
These results are consistent with previous observations of overall
slower O2 kinetics during
moderate supine exercise with both lower (15, 18, 25) and upper body
(16) exercise. O2 responses
during presumably >LT exercise have been reported only qualitatively
(23) or semiquantitatively (half time only) (8, 9) as being slower in
the supine position. In these studies, end-exercise
O2 (at 5-10 min) was not
affected by posture, similar to the results in the present study. In
neither of these previous studies, however, was the potential effect of
a longer time constant distinguished from that of a transiently lower
amplitude of the primary O2
component (A'1) as
the mechanism by which the responses appeared slowed in the supine
position. In a somewhat similar study in which the hydrostatic
contribution to perfusion pressure was manipulated, Hughson et al. (17)
found that forearm exercise with the arm above the heart led to an
estimated arm O2 response
that was attenuated early and augmented later into exercise, compared
with identical exercise with the arm below the heart. These results are
similar to the present findings.
In the present study, the finding of a reduced
A'1, but not a
statistically significant slowing of the time constant
1, during heavy supine exercise
was contrary to our hypothesis. It has been proposed that slower
kinetics during upright heavy exercise reflect a relative inadequate
perfusion and O2 delivery to the
working muscles (14, 24). The data from this study suggest that, during
heavy exercise in the supine position, O2 delivery to and utilization by
the working muscles are further compromised, resulting in a
consistently reduced amplitude of the fast component of
O2 and a slowing of the
overall kinetics response, compared with the upright position. Under
these circumstances, then, the amplitude of the fast component was more
sensitive to a limitation in O2
delivery than was the associated time constant 1. This illustrates that both
the time constant and the amplitude of the primary
O2 response need to be
considered when the effects of an intervention on
O2 kinetics during heavy
exercise are being evaluated.
The amplitude of the O2 slow
component was significantly increased in supine compared with upright
heavy exercise. Although the mechanisms underlying the slow component
remain speculative, the primary origin appears to be the working
muscles (1, 3, 29, 32, 35). It has been suggested that the
O2 slow component may be
attributable primarily to motor unit recruitment of lower efficiency,
fast-twitch fibers that have a higher
O2 cost per tension development
and a longer time constant (1-4, 10, 28). Consistent with this,
Barstow et al. (3) found that the amplitude of the slow component
during upright heavy exercise, comparable to that performed here, was
directly related to the percentage of fast-twitch (type II) fibers of
the vastus lateralis. It has been suggested that availability of
O2 plays an important role in
regulating the recruitment of high-threshold motor units, because there
is a close link between state of energy supply and types of muscle
fibers being recruited (26). Thus one interpretation of the present
data would suggest greater recruitment of type II fibers in the supine
position during heavy exercise compared with in the upright position.
An alternative interpretation may arise from comparison with the
previous work of Barstow et al. (3). In that study, the amplitude of
the primary, fast component of
O2
(A'1) was
significantly, but inversely, related to the percentage of type II
fibers, whereas the end-exercise increase in
O2 was not different as a
function of fiber type. Thus, compared with an individual with mostly
type I fibers, one with mostly type II fibers had a reduced primary
component (A'1) and
a greater slow component
(A'2). This pattern is similar to the supine response compared with upright in the present
study. However, a significant difference between the two studies is
that the results of Barstow et al. are based on intersubject comparisons across fiber type and level of fitness, whereas the present
results come from intrasubject responses to a perturbation (change
in body position). There may be a common mechanism that might explain
the similar results in both studies. It could be argued that, in the
present study, the primary mechanism producing the attenuated and
slowed O2 response in the
supine position was a blunted rise in
O2 delivery due to reduced
perfusion pressure (and HR, see below). In the study by Barstow et al.,
there were similar relationships between parameters of the fast and
slow O2 components and
fitness (as maximal O2,
ml · kg
1 · min1)
that paralleled those observed with type I fiber composition. Given the
known better perfusion in both the trained state and to fibers with
greater oxidative capacity (for review, see Ref. 21), it may be
concluded that a reduced
A'1 during the
adjustment to heavy exercise is predictive of (consistent with) an
attenuated rise in O2 delivery
early into exercise. The fact that by 6-8 min the responses were
not affected by body position (present study) or fiber type (Barstow et
al.) suggests that eventually the contracting muscle-circulatory
complex is able to achieve a similar
O2 delivery and utilization
pattern. The present results, along with the previous findings
regarding muscle fiber type and fitness, suggest that any
interpretation of the physiological mechanisms underlying the slow
component must also consider the underlying physiological processes
reflected by the primary exponential rise in
O2.
In a closed circulatory system at rest, one would predict that any
reduction in arterial pressure to a tissue bed in the supine compared
with the upright position would be countered somewhat by improved
venous return, such that perfusion pressure (arteriovenous) might be
similar. However, in the lower limbs, the combination of muscle
contractions during exercise (pump) providing energy for venous return
and the presence of venous valves to break the venous hydrostatic
column keeps leg venous pressure low irrespective of body position.
Thus, in the supine posture, the reduction in arterial pressure in the
legs is not matched by a similar improvement in venous return, which is
already facilitated. The resultant fall in perfusion
pressure leads to reduced exercise tolerance and slower
O2 kinetics (11, 15, 18, 23).
Consistent with this view, lower body negative pressure, which
increases the pressure gradient from the heart to the working muscles
of the lower limbs, partially or fully reverses the detrimental effects of supine position on exercise responses (11, 15).
The observation of a reduction in both the HR and
O2 responses to a
similar degree at 2 min during heavy exercise in the supine position
suggests that the O2 response
was matched to the HR response and that this matching became evident by
2 min into exercise. This is reinforced by the observation that
O2/HR reached a constant
value by 2 min. Because O2/HR
is equal to the product of stroke volume and the arteriovenous
O2 content difference, the
simplest interpretation is that both of these responses reached their
exercise levels by 2 min and that any further increase in
O2 was accomplished by an
increase in HR. These data thus suggest that a primary mechanism for
the slowed O2 kinetics during
heavy exercise in the supine position was an attenuated HR, and
presumably cardiac output, response. This conclusion is also supported
by the recent work of MacDonald et al. (25), who found slower response
kinetics for femoral artery blood flow after the onset of knee
extension and flexion exercise in the supine compared with the upright position.
The responses to supine exercise found herein, with the presumably
compromised adjustment of leg blood flow, can be contrasted with those
reported for heavy exercise in hypoxic conditions (inspired O2 fraction = 0.12), in which
arterial O2 content was reduced (12). Under those hypoxic conditions, peak
O2 was reduced ~25%, twice
the reduction seen with supine exercise in the present study. However,
in the hypoxic condition, the integrated cardiopulmonary system was
able to compensate for the reduced arterial
O2 content by increasing HR, and
possibly leg blood flow (but, see Ref. 36). The net effect was a
relatively small increase in the time constant for the primary rise in
O2
(1), with no effect either on
the amplitude of the fast component or on any aspect of the slow
component. It is interesting to note that, for both hypoxia (12) and
supine exercise (present study), end-exercise
O2 at 6-8 min was not different from the control, upright condition, suggesting that the
integrated muscle-circulatory system was ultimately able to adjust to
the metabolic demand for O2
delivery and utilization under both conditions.
Recovery kinetics for O2
after the heavy-exercise bouts were initially described with the same
model as was used for the exercise responses (Eq. 1), which contained separate time delays for the fast
and slow exponential terms. However, the second time delay
(TD2) converged to a value
similar to that for the fast component
(TD1), implying that both the
fast and slow exponential processes decayed together during
phase 2 of recovery. This finding of a
common time delay in recovery for the fast and slow exponential processes has also been recently reported by Scheuermann et al. (31),
using a similar approach. Furthermore, in the present study, symmetry
was found between the exercise and recovery kinetics for
O2 for the heavy-exercise
intensities for both supine and upright body positions, i.e., similar
relative contributions (amplitudes) of the fast and slow components and
similar fast time constant (1) for exercise and recovery
responses. In contrast, Paterson and Whipp (27) found asymmetry of
O2 kinetics, with a greater amplitude and a faster time constant for the fast component, and less
contribution of the slow component, during recovery compared with
exercise. Their results could be interpreted to suggest that the slow
component of O2 during heavy
exercise includes metabolism from motor units with essentially fast
O2 kinetic characteristics (e.g., type I motor units) but which are recruited progressively over
time during the exercise. In this case, these units would be predicted
to exhibit fast kinetics during recovery and thus contribute to a
faster time constant and a greater amplitude for the fast exponential
response and less contribution of a slow exponential term. The present
findings are not consistent with this interpretation, however. Symmetry
between exercise and recovery responses for similar intensities of
heavy exercise has also been reported for hypoxic exercise (12) and for
different pedal rates (3). The observation of symmetry between the
exercise and recovery kinetics for
O2 suggests that,
irrespective of the metabolic process(es) responsible for the slow
component during exercise, in recovery these metabolic processes remain
kinetically distinguishable from those associated with the fast
O2 component. It is presently unclear what the explanation(s) might be for the differences in findings between the present study and those of Paterson and Whipp (27).
In conclusion, during moderate (<LT) exercise, the
O2 kinetics are
slowed, but the steady-state increase is unchanged for supine compared
with upright cycle ergometer exercise. During heavy (>LT) exercise,
the supine position is associated with a reduction in the amplitude of
the primary O2 exponential
component without slowing of the fast component time constant, and a
concomitant increase in the slow component, such that the 6-min value
is no different from that seen during upright exercise at the same work rate. The reduced early response of
O2 in the supine position is
associated with a proportionately lower HR rise. These data suggest
that, during heavy exercise in the supine position,
O2 delivery to and utilization by
the working muscles are further compromised, compared with in the
upright position.
| |
FOOTNOTES |
|---|
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. §1734 solely to indicate this fact.
Address for reprint requests and other correspondence: S. Koga, Applied Physiology Laboratory, Kobe Design Univ., 8-1-1 Gakuennishi-machi, Nishi-ku, Kobe, 651-2196, Japan (E-mail: s-koga{at}kobe-du.ac.jp).
Received 9 February 1998; accepted in final form 30 March 1999.
| |
REFERENCES |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
1.
Barstow, T. J.
Characterization of O2 kinetics during heavy exercise.
Med. Sci. Sports Exerc.
26:
1327-1334,
1994[Medline].
2.
Barstow, T. J.,
R. Casaburi,
and
K. Wasserman.
O2 uptake kinetics and the O2 deficit as related to exercise intensity and blood lactate.
J. Appl. Physiol.
75:
755-762,
1993
3.
Barstow, T. J.,
A. M. Jones,
P. H. Nguyen,
and
R. Casaburi.
Influence of muscle fiber type and pedal frequency on oxygen uptake kinetics of heavy exercise.
J. Appl. Physiol.
81:
1642-1650,
1996
4.
Barstow, T. J.,
and
P. A. Molé.
Linear and nonlinear characteristics of oxygen uptake kinetics during heavy exercise.
J. Appl. Physiol.
71:
2099-2106,
1991
5.
Beaver, W. L.,
N. Lamarra,
and
K. Wasserman.
Breath-by-breath measurement of true alveolar gas exercise.
J. Appl. Physiol.
51:
1662-1675,
1981
6.
Beaver, W. L.,
K. Wasserman,
and
B. J. Whipp.
A new method for detecting anaerobic threshold by gas exercise.
J. Appl. Physiol.
60:
2020-2027,
1986
7.
Casaburi, R.,
T. W. Storer,
I. Ben-Dov,
and
K. Wasserman.
Effect of endurance training on possible determinants of O2 during heavy exercise.
J. Appl. Physiol.
62:
199-207,
1987
8.
Cerretelli, P.,
D. Shindell,
D. P. Pendergast,
P. E. di Prampero,
and
D. W. Rennie.
Oxygen uptake transients at the onset and offset of arm and leg work.
Respir. Physiol.
30:
81-97,
1977[Medline].
9.
Convertino, V. A.,
D. J. Goldwater,
and
H. Sandler.
Oxygen uptake kinetics of constant-load work: upright vs. supine exercise.
Aviat. Space Environ. Med.
55:
501-506,
1984[Medline].
10.
Crow, M. T.,
and
M. J. Kushmerick.
Chemical energetics of slow- and fast-twitch muscles of the mouse.
J. Gen. Physiol.
79:
147-166,
1982
11.
Eiken, O.
Effects of increased muscle perfusion pressure on responses to dynamic leg exercise in man.
Eur. J. Appl. Physiol.
57:
772-776,
1988.
12.
Engelen, M.,
J. Porszasz,
M. Riley,
K. Wasserman,
K. Maehara,
and
T. J. Barstow.
Effects of hypoxic hypoxia on O2 uptake and heart rate kinetics during heavy exercise.
J. Appl. Physiol.
81:
2500-2508,
1996
13.
Folkow, B.,
U. Haglund,
M. Jodal,
and
O. Lundgren.
Blood flow in the calf muscle of man during heavy rhythmic exercise.
Acta Physiol. Scand.
81:
157-163,
1971[Medline].
14.
Gerbino, A.,
S. A. Ward,
and
B. J. Whipp.
Effects of prior exercise on pulmonary gas-exchange kinetics during high-intensity exercise in humans.
J. Appl. Physiol.
80:
99-107,
1996
15.
Hughson, R. L.,
J. E. Cochrane,
and
G. C. Butler.
Faster O2 uptake kinetics at onset of supine exercise with than without lower body negative pressure
J. Appl. Physiol.
75:
1962-1967,
1993
16.
Hughson, R. L.,
and
M. D. Inman.
Faster kinetics of O2 during arm exercise with circulatory occlusion of the legs.
Int. J. Sports Med.
7:
22-25,
1986[Medline].
17.
Hughson, R. L.,
J. K. Shoemaker,
M. E. Tschakovsky,
and
J. M. Kowalchuk.
Dependence of muscle O2 on blood flow dynamics at onset of forearm exercise.
J. Appl. Physiol.
81:
1619-1626,
1996
18.
Hughson, R. L.,
H. C. Xing,
C. Borkhoff,
and
G. C. Butler.
Kinetics of ventilation and gas exchange during supine and upright cycle exercise.
Eur. J. Appl. Physiol.
63:
300-307,
1991.
19.
Karlsson, H.,
B. Lindborg,
and
D. Linnarsson.
Time courses of pulmonary gas exchange and heart rate changes in supine exercise.
Acta Physiol. Scand.
95:
329-340,
1975[Medline].
20.
Koga, S.,
T. Shiojiri,
N. Kondo,
and
T. J. Barstow.
Effect of increased muscle temperature on oxygen uptake kinetics during exercise.
J. Appl. Physiol.
83:
1333-1338,
1997
21.
Laughlin, M. H.,
R. J. Korthuis,
D. J. Duncker,
and
R. J. Bache.
Control of blood flow to cardiac and skeletal muscle during exercise.
In: Handbook of Physiology. Exercise: Regulation and Integration of Multiple Systems. Bethesda, MD: Am. Physiol. Soc., 1996, sect. 12, chapt. 16, p. 705-769.
22.
Leyk, D.,
D. Essfeld,
U. Hoffmann,
K. Baum,
and
J. Stegemann.
Influence of body position and pre-exercise activity on cardiac output and oxygen uptake following step changes in exercise intensity.
Eur. J. Appl. Physiol.
65:
499-506,
1992.
23.
Leyk, D.,
D. Essfeld,
U. Hoffmann,
H. G. Wunderlich,
K. Baum,
and
J. Stegemann.
Postural effect on cardiac output, oxygen uptake and lactate during cycle exercise of varying intensity.
Eur. J. Appl. Physiol.
68:
30-35,
1994.
24.
MacDonald, M.,
P. K. Pedersen,
and
R. L. Hughson.
Acceleration of O2 kinetics in heavy submaximal exercise by hyperoxia and prior high-intensity exercise.
J. Appl. Physiol.
83:
1318-1325,
1997
25.
MacDonald, M. J.,
J. K. Shoemaker,
M. E. Tschakovsky,
and
R. L. Hughson.
Alveolar oxygen uptake and femoral artery blood flow dynamics in upright and supine leg exercise in humans.
J. Appl. Physiol.
85:
1622-1628,
1998
26.
Moritani, T.,
T. Takaishi,
and
T. Matsumoto.
Determination of maximal power output at neuromuscular fatigue threshold.
J. Appl. Physiol.
74:
1729-1734,
1993
27.
Paterson, D. H.,
and
B. J. Whipp.
Asymmetries of oxygen uptake transients at the on- and offset of heavy exercise in humans.
J. Physiol. (Lond.)
443:
575-586,
1991
28.
Poole, D. C.,
T. J. Barstow,
G. A. Gaesser,
W. T. Willis,
and
B. J. Whipp.
O2 slow component: physiological and functional significance.
Med. Sci. Sports Exerc.
26:
1354-1358,
1994[Medline].
29.
Poole, D. C.,
W. Schaffartzik,
D. R. Knight,
T. Derion,
B. Kennedy,
H. J. Guy,
R. Prediletto,
and
P. D. Wagner.
Contribution of exercising legs to the slow component of oxygen uptake kinetics in humans.
J. Appl. Physiol.
71:
1245-1253,
1991
30.
Roston, W. L.,
B. J. Whipp,
J. A. Davis,
D. A. Cunningham,
R. M. Effros,
and
K. Wasserman.
Oxygen uptake kinetics and lactate concentration during exercise in humans.
Am. Rev. Respir. Dis.
135:
1080-1084,
1987[Medline].
31.
Scheuermann, B. W.,
J. M. Kowalchuk,
D. H. Paterson,
and
D. A. Cunningham.
O2 uptake kinetics after acetazolamide administration during moderate- and heavy-intensity exercise.
J. Appl. Physiol.
85:
1384-1393,
1998
32.
Stringer, W.,
K. Wasserman,
R. Casaburi,
J. Porszasz,
K. Maehara,
and
W. French.
Lactic acidosis as a facilitator of oxyhemoglobin dissociation during exercise.
J. Appl. Physiol.
76:
1462-1467,
1994
33.
Van Leeuwen, B. E.,
G. J. Barendsen,
J. Lubbers,
and
L. De Pater.
Calf blood flow and posture: Doppler ultrasound measurements during and after exercise.
J. Appl. Physiol.
72:
1675-1680,
1992
34.
Weiler-Ravell, D.,
D. M. Cooper,
B. J. Whipp,
and
K. Wasserman.
Control of breathing at the start of exercise as influenced by posture.
J. Appl. Physiol.
55:
1460-1466,
1983
35.
Whipp, B. J.
The slow component of O2 uptake kinetics during heavy exercise.
Med. Sci. Sports Exerc.
26:
1319-1326,
1994[Medline].
36.
Wolfel, E. E.,
B. M. Groves,
G. A. Brooks,
G. E. Butterfield,
R. S. Mazzeo,
L. G. Moore,
J. R. Sutton,
P. R. Bender,
T. E. Dahms,
R. E. McCullough,
R. G. McCullough,
S.-Y. Huang,
S.-F. Sun,
R. F. Grover,
H. N. Hultgren,
and
J. T. Reeves.
Oxygen transport during steady-state submaximal exercise in chronic hypoxia.
J. Appl. Physiol.
70:
1129-1136,
1991
This article has been cited by other articles:
|
|
 |
|
  M. Burnley, J. H. Doust, and A. M. Jones Time required for the restoration of normal heavy exercise VO2 kinetics following prior heavy exercise J Appl Physiol, November 1, 2006; 101(5): 1320 - 1327. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. M. Jones, N. J. A. Berger, D. P. Wilkerson, and C. L. Roberts Effects of "priming" exercise on pulmonary O2 uptake and muscle deoxygenation kinetics during heavy-intensity cycle exercise in the supine and upright positions J Appl Physiol, November 1, 2006; 101(5): 1432 - 1441. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. J. A. Berger, I. T. Campbell, D. P. Wilkerson, and A. M. Jones Influence of acute plasma volume expansion on VO2 kinetics, VO2peak, and performance during high-intensity cycle exercise J Appl Physiol, September 1, 2006; 101(3): 707 - 714. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Burnley, C. L. Roberts, R. Thatcher, J. H. Doust, and A. M. Jones Influence of blood donation on O2 uptake on-kinetics, peak O2 uptake and time to exhaustion during severe-intensity cycle exercise in humans Exp Physiol, May 1, 2006; 91(3): 499 - 509. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. P Wilkerson, J. Rittweger, N. J. A Berger, P. F Naish, and A. M Jones Influence of recombinant human erythropoietin treatment on pulmonary O2 uptake kinetics during exercise in humans J. Physiol., October 15, 2005; 568(2): 639 - 652. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Egana and S. Green Effect of body tilt on calf muscle performance and blood flow in humans J Appl Physiol, June 1, 2005; 98(6): 2249 - 2258. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. A. Kindig, R. A. Howlett, and M. C. Hogan Effect of contractile duration on intracellular PO2 kinetics in Xenopus single skeletal myocytes J Appl Physiol, May 1, 2005; 98(5): 1639 - 1645. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Koga, D. C. Poole, T. Shiojiri, N. Kondo, Y. Fukuba, A. Miura, and T. J. Barstow Comparison of oxygen uptake kinetics during knee extension and cycle exercise Am J Physiol Regulatory Integrative Comp Physiol, January 1, 2005; 288(1): R212 - R220. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. P Wilkerson, I. T Campbell, and A. M Jones Influence of nitric oxide synthase inhibition on pulmonary O2 uptake kinetics during supra-maximal exercise in humans J. Physiol., December 1, 2004; 561(2): 623 - 635. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. P. Wilkerson, K. Koppo, T. J. Barstow, and A. M. Jones Effect of prior multiple-sprint exercise on pulmonary O2 uptake kinetics following the onset of perimaximal exercise J Appl Physiol, October 1, 2004; 97(4): 1227 - 1236. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. M Jones, D. P Wilkerson, and I. T Campbell Nitric oxide synthase inhibition with L-NAME reduces maximal oxygen uptake but not gas exchange threshold during incremental cycle exercise in man J. Physiol., October 1, 2004; 560(1): 329 - 338. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. G. Fawkner and N. Armstrong Longitudinal changes in the kinetic response to heavy-intensity exercise in children J Appl Physiol, August 1, 2004; 97(2): 460 - 466. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. M. Jones, D. P. Wilkerson, S. Wilmshurst, and I. T. Campbell |
