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Department of Kinesiology, University of Waterloo, Waterloo, Ontario, Canada N2L 3G1
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ABSTRACT |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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We tested the hypothesis that the slower
increase in alveolar oxygen uptake
(
O2) at the onset of
supine, compared with upright, exercise would be accompanied by a
slower rate of increase in leg blood flow (LBF). Seven healthy subjects
performed transitions from rest to 40-W knee extension exercise in the
upright and supine positions. LBF was measured continuously with pulsed
and echo Doppler methods, and
O2 was measured breath by
breath at the mouth. At rest, a smaller diameter of the
femoral artery in the supine position
(P < 0.05) was compensated by a
greater mean blood flow velocity (MBV) (P < 0.05) so that LBF was not different in the two positions. At the end of
6 min of exercise, femoral artery diameter was larger in the upright
position and there were no differences in
O2, MBV, or LBF between
upright and supine positions. The rates of increase of
O2 and LBF in the
transition between rest and 40 W exercise, as evaluated by the mean
response time (time to 63% of the increase), were slower in the supine
[O2 = 39.7 ± 3.8 (SE) s, LBF = 27.6 ± 3.9 s] than in the upright
positions (O2 = 29.3 ± 3.0 s, LBF = 17.3 ± 4.0 s;
P < 0.05). These data support our
hypothesis that slower increases in alveolar
O2 at the onset of exercise
in the supine position are accompanied by a slower increase in LBF.
kicking exercise; Doppler velocimetry; echo Doppler; leg blood flow
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INTRODUCTION |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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AT THE ONSET OF SUBMAXIMAL EXERCISE in the supine
position, the rate of increase in alveolar oxygen uptake
(O2) is slower than when the
same exercise work rate is completed in the upright position (1, 2, 7,
11). It has been speculated that this slower rate of increase in
O2 might be due to a slower rate of increase in the supply of
O2 to the working muscles (3, 7).
Blood flow is one component of oxygen delivery that is altered at the
onset of exercise and may be an important modulator for oxidative
phosphorylation in this situation (6). Information on the dynamics of
the muscle blood flow response at the onset of large-muscle-mass
exercise is lacking.
Recently, it has become possible to monitor the changes in skeletal
muscle blood flow in the transition from rest to exercise and to
determine the relationship between
O2 delivery and
O2 utilization (23, 24). Grassi et
al. (5) used thermodilution techniques to monitor blood flow in
combination with direct femoral vein samples to determine
O2 extraction and found that the
time courses of increases in muscle blood flow and muscle
O2 were similar during
upright cycle ergometry. Hughson et al. (9), who used Doppler
ultrasound technology, observed a close correlation between the rate of
increase in blood flow to the forearm muscles and the muscle
O2. They further noted that
both flow and muscle O2
adapted slower when the exercising forearm was above, rather than
below, the heart.
The rationale for this study was to incorporate manipulations in
perfusion pressure in a leg exercise model to examine the effect of
blood flow delivery at the onset of large-muscle-mass exercise. To
study this, we have used combined pulsed and echo Doppler methods to
continuously quantify the femoral artery blood flow in the transition
from rest to submaximal knee extension and flexion exercise in both the
supine and the upright positions. We tested the hypothesis
that the slower rate of increase in alveolar O2 at the onset of supine
exercise would be accompanied by slower increases in leg blood flow
(LBF) in the same posture.
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METHODS |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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The experiments were carried out on seven healthy young volunteers (5 men and 2 women, age 27 ± 5, height 180 ± 5 cm, and weight 75 ± 9 kg). After reading a description of the methods and possible risks, each signed a consent form approved by the Office of Human Research at the University of Waterloo. Each subject practiced the exercise to become familiar with the activity so that high-quality cardiorespiratory and Doppler signals could be obtained in both positions at rest and during exercise. This was important because complete relaxation of knee extensors during knee flexion was necessary to achieve optimal blood flow between extension periods and to reduce motion artifact in the Doppler signals. On the data-collection day, subjects reported to the laboratory at least 2 h after their last meal. They were asked to avoid caffeine and alcohol ingestion and strenuous exercise for 24 h before the test.
Experimental design.
Testing was performed on an electrically braked knee extension and
flexion ergometer. In this study, the ergometer was configured so that
subjects worked against a resistance on both extension and flexion and
maintained a knee extension and flexion cadence of ~44 cycles per leg
per minute at a work rate of 40 W. The ergometer had an adjustable
backrest that allowed the subjects to sit with a hip angle of 120°
during the upright tests, whereas the hips were completely extended
(180°) during the supine tests. Aside from the hip angle, the
exercise task was identical in both positions. The exercise intensity
of 40 W was selected because it provided a signal
(O2 and LBF) of sufficient
amplitude that curve fitting to the time course could be accomplished
with some confidence.
Data acquisition.
Breath-by-breath ventilation and gas exchange were measured with a
computerized system (First Breath, St. Agatha, ON, Canada). Fractional
concentrations of O2,
CO2, and
N2 were measured with a mass
spectrometer (model MGA-1100, Marquette Electronics, Milwaukee, WI),
and inspired and expired volumes were measured with a volume turbine
(VMM-110, Alpha Technologies, Laguna Beach, CA). Calibration of the
mass spectrometer was performed before each test by using two gas tanks
of known concentration. Volume was calibrated by manually pumping a
3-liter syringe at a flow rate similar to that of respiration during
the exercise test. O2 was
corrected on a breath-by-breath basis for changes in lung gas stores
due to altered lung volume or alveolar composition, as described
previously (8). Matching of fractional gas concentrations with the
appropriate volume was done by accounting for the sum of the transport
lag plus the instrument response time.
Kinetic analysis.
Breath-by-breath values for
O2 were linearly
interpolated between breaths to give values at 1-s intervals. The time
course data for O2 and LBF
collected from both trials in each condition were ensemble averaged to
produce a single data set for each variable, for each subject, in each
test condition. The time course of changes in
O2 and LBF were analyzed by
fitting an exponential curve to the average results of the trials. A
two-component exponential model was fit to the data by using a least
squares procedure. As previously described (7), the model
had a baseline component (G0),
two amplitude terms (G1 and
G2), two time constants
(
1 and
2), and two time delays
(TD1 and
TD2)
![Y(<IT>t</IT>) = G<SUB>0</SUB> + G<SUB>1</SUB>[1 − <IT>e</IT><SUP>−(<IT>t</IT> − TD<SUB>1</SUB>)/&tgr;<SUB>1</SUB></SUP>] ⋅ &mgr;<SUB>1</SUB> + G<SUB>2</SUB>[1 − <IT>e</IT><SUP>−(<IT>t</IT> − TD<SUB>2</SUB>)/&tgr;<SUB>2</SUB></SUP>] ⋅ &mgr;<SUB>2</SUB>](/content/vol85/issue5/fulltext/1622/img001.gif)
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O2 or LBF.
An indicator of the rate of change of each of these variables for each
subject and condition was obtained by calculation of the mean response
time (MRT). The MRT is the time required to achieve ~63% of the
difference between baseline and the exercise plateau. The MRT
determined from the weighted mean of the time constant and time delay
for each exponential term is mathematically equivalent to what we
previously called total lag time (7). The MRT terminology is consistent
with that in other literature (e.g., Ref. 14).
![MRT = [G<SUB>1</SUB>/(G<SUB>1</SUB> + G<SUB>2</SUB>)] ⋅ (TD<SUB>1</SUB> + &tgr;<SUB>1</SUB>) + [G<SUB>2</SUB>/(G<SUB>1</SUB> + G<SUB>2</SUB>)] ⋅ (TD<SUB>2</SUB> + &tgr;<SUB>2</SUB>)](/content/vol85/issue5/fulltext/1622/img004.gif)
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Statistical analysis.
The effects of body position (upright vs. supine) on the steady-state
values of MBV, LBF, mean arterial pressure,
O2, and heart rate and on
the kinetic-fitting parameters for LBF and
O2 were analyzed by a
repeated-measures one-way ANOVA. The combined effects of body position
(upright vs. supine) and intensity (rest vs. exercise) were determined
for steady-state diameter measures by a repeated-measures two-way
ANOVA. A two-way ANOVA was performed on the MRTs for LBF and
O2 with position (upright
vs. supine) and variable (LBF vs.
O2) forming the dependent
variables. The level of significance for main effects and interactions
was set at P < 0.05, and significant
differences were analyzed with Student-Newman-Keuls post hoc test. All
data are reported as means ± SE.
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RESULTS |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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As anticipated, the mean arterial pressure measured at the level of the legs was less during exercise in the supine position than during exercise in the position at rest and during 40-W exercise (Fig. 1, Table 1). Resting heart rate was lower in the supine vs. upright position, and there was no difference in heart rate during exercise between positions (Table 1, Fig. 1). At rest, the MBV was lower in the upright vs. supine position (Table 1, Fig. 2), but, by the end of 6 min of exercise, the MBV was not different between upright and supine positions (Table 1, Fig. 2). Resting and exercise femoral artery diameter was smaller in the supine position compared with that in the upright position (Table 1, Fig. 2).
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Baseline and the end-exercise values for LBF and
O2 did not differ
between positions (Table 1, Fig. 2). When the subjects immediately
started exercise, there was a rapid increase in both LBF and
O2 in the upright and
supine positions (Table 2, Fig. 3). The rate of increase in
O2 was faster in the upright
than the in supine position, as indicated by both
2 and MRT (Table 2, Fig. 3).
There were no differences in the gain terms
(G1 and G2) for
O2. The rate of increase in
LBF was also faster in the upright than in the supine position, as
indicated by the MRT. For LBF, there was a greater contribution of the
first-phase response (G1) and a
smaller contribution of the second-phase response
(G2) in the upright compared
with the supine position (Table 2).
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The MRT of the LBF response was faster than that of the
O2 in both upright and supine
positions (Table 2). The similar temporal responses of the slower LBF
and the slower O2 were evident in the supine position (Fig. 3).
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DISCUSSION |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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The primary finding of this study was that both LBF and alveolar
O2 increased more slowly at
the onset of exercise in the supine compared with the upright
posture. The time course of change, given by the MRT, was
35% slower for O2 and 60%
slower for LBF in supine exercise compared with that for the same
exercise performed in the upright position. These data suggest that
O2 supply at the onset of exercise
might alter metabolic control and limit the rate of increase in muscle
O2. Thus these data support
our hypothesis that, in the supine position, the slower rate of
increase in alveolar O2
observed frequently at the onset of exercise (1, 2, 7, 11, 12) was a
consequence of a delayed adaptation in LBF.
The exercise model.
Exercise required contractions of both the knee extensor and flexor
muscles of both legs. This is different from the knee-extension-only exercise employed by other researchers (18, 19, 21). We use this mode
of exercise to involve a relatively large muscle mass while focusing
the activity within muscles served by the femoral artery. There is very
little, or no, involvement of muscles of the hips or above in both the
upright and supine positions, and there was no difference in the work
done against gravity. Although it is possible that slightly different
recruitment of muscles in the two postures might have accounted for the
differences in LBF and O2
kinetics, we do not believe this to be the case, because no difference
was observed in the steady-state metabolic cost. Rather, the legs were
exercised in exactly the same manner in both postures, and the
discussion is based on a constant metabolic demand in both the
transition and steady state in the two different body positions.
O2 and LBF had MRT values of
<40 s, even in supine exercise, indicating that the steady state was
achieved in <4 min, in all tests. Richardson et al. (19, 21) have
shown that the peak work rate for single-leg, knee-extension-only
exercise was in excess of 100 W in trained cyclists. Our subjects were not trained, but they used flexor and extensor muscles of both legs
during exercise at 40 W. Further studies in our laboratory have
confirmed that 40 W represents only about one-third of the peak work
rate reached in incremental exercise on this ergometer (150 W) in
typical female and male subjects (unpublished observations).
Doppler blood flow measurements have only recently been applied to the
study of blood flow during quadriceps muscle exercise (18, 23, 28). In
a recent comparison between Doppler and the thermodilution techniques
during one-leg knee-extension exercise, similar blood flow values were
observed with the two methods across a wide range of work rates (18).
Steady-state exercise.
There were no differences in the steady-state values of
O2 or LBF at rest, or at 40 W, between the upright and supine postures in this study.
Similar levels of O2 are
expected during exercise at the same absolute power output if, as in
our study, modifying body position does not alter the work done against
gravity (12). It is well established that cardiac output is greater in
the supine compared with the upright position at rest and during
lighter intensities of exercise (12), but the increase in stroke volume at the onset of exercise in the upright position reduces the difference (15). There have been few studies of leg muscle blood flow in the
different body positions. We found that the LBF at rest was not
different between body positions as a consequence of a significantly smaller femoral artery diameter and a greater MBV in the supine compared with the upright position (Table 1). Leyk et al. (13) also
found a significantly smaller diameter and a greater peak systolic
blood velocity in the supine position. However, their calculated
resting LBF was significantly greater in the supine than the upright
posture. Leyk et al. kept their subjects in a seated posture so that
the legs were above heart level, whereas our subjects were supine with
the thigh muscles at heart level and the calf muscles below the heart.
Consistent with our observations of no differences in blood flow to the
exercising muscle with body position, both Van Leeuwen et al. (27) and
Leyk et al. (13) observed no difference in LBF in upright compared with supine seated positions during calf muscle exercise. The similar levels
of LBF were achieved in the face of significantly lower mean arterial
pressure at the level of the exercising muscle in the supine exercise.
This must mean that greater local vasodilation occurred in the
exercising muscles in the supine position.
O2 was not constrained by
bulk delivery of O2. In the
absence of information about the potential transient mismatching of
blood O2 supply to
O2 demand or of the effect of
blood pooled in the leg veins while at rest, this interpretation needs
to be viewed with caution, especially because muscle
O2 continues to increase over
the first 1-2 min of exercise (Fig. 3). It is unlikely that the
complex pattern of flow distribution will be resolved in studies of
human muscle with currently available techniques.
The central cardiovascular responses at the onset of exercise appeared
to be similar in each of the upright and supine positions. Heart rate
increased very rapidly, with an overshoot in some tests. This overshoot
is a consequence of very rapid vagal withdrawal in excess of
that required to achieve the steady-state heart rate (25). In Fig.
1, it is apparent that mean arterial pressure decreased by ~10 mmHg
at the onset of exercise, presumably because of a rapid reduction in
peripheral resistance (25). Mean arterial pressure recovered rapidly as
a consequence of the increase in cardiac output and modifications in
total peripheral resistance.
LBF and metabolism.
The slower alveolar
O2 response observed when
femoral artery blood flow also adapted more slowly at the onset of
supine exercise suggests a link between
O2 transport and utilization. There is, however, no evidence in the upright position that
O2 is rate limited by the
increase in LBF at the onset of exercise. At least for the supine
position, the rate of increase in
O2 supply (LBF) appeared to limit
the rate at which O2
increased. The consequence of this was that energy not supplied by
oxidative metabolism must be supplied by anaerobic glycolysis, with net accumulation of lactate and utilization of stored high-energy phosphates. However, in both body positions, the MRT for LBF was faster
by ~10-12 s than that for
O2 (Table 2). There
are two possible explanations for these findings. First, it might be
that the change in body position induced a change in the dynamics of both O2 and LBF. As
we discussed previously, this is unlikely, because the position of the
legs remained constant while the body rotated at the hips in the two
different postures. A second explanation could be related
to the issue of within-muscle blood flow distribution as considered
above. That is, the muscle pump increases flow within a
muscle without regard for metabolic requirements. It is only with
continued exercise and the effects of negative feedback on local
vascular responses that this flow is redistributed to achieve optimal
matching of O2 supply to metabolic demand.
O2 has not been
viewed as a limiting factor in the process of oxidative phosphorylation
because one-half maximal rate occurs at an intracellular
PO2 of 0.03 Torr in studies of
isolated mitochondria (4). However, the affinity of cytochrome c for
O2 varies with the energy
state of the cell, and an intracellular PO2 value below ~25 Torr (<40
µM) could have an impact on the intracellular concentrations of
metabolic substrates required to drive the oxidative mechanisms at a
given rate of ATP production (4, 29). Given this argument, it is
understandable that the intracellular
PO2 does not have to reach zero to
contribute to the metabolic balance that establishes the rate of
oxidative phosphorylation (6, 10). That is, a relative hypoxia in the rest-to-exercise transition might cause a temporary slowing of muscle
O2 while the intracellular
environment adapts to this PO2.
Indeed, Richardson et al. (20) presented evidence from proton magnetic
resonance spectroscopy that intracellular PO2 decreases to 3.1 Torr during calf
muscle exercise at 50% maximum work rate.
The consequences of a slow adaptation of the oxidative metabolic
processes at the onset of exercise are now more apparent. When LBF (24)
and alveolar O2
(17) increased more rapidly at the onset of submaximal exercise after a
short-term period of exercise training, there were less marked
reductions in intracellular phosphocreatine and smaller increases in
blood and muscle lactate (17).
Conclusions.
These are the first estimations of LBF dynamics that have been measured
simultaneously with alveolar
O2 during transients in work
rate in upright and supine leg exercise. A reduction in perfusion
pressure in the supine position appears to have been responsible for
the slower increase in LBF and, therefore, the O2-delivery response at the onset
of exercise. These findings are in support of the hypothesis that
O2 availability can, under certain
conditions, play a limiting role in the adaptation of muscle
O2. The results further
suggest that local vascular regulatory factors might be important in
determining the time-dependent distribution of blood flow within
exercising muscles.
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ACKNOWLEDGEMENTS |
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This research was supported by the Natural Sciences and Engineering Research Council (NSERC) of Canada. M. J. MacDonald and J. K. Shoemaker were supported by NSERC Graduate Scholarships.
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FOOTNOTES |
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Address for reprint requests: R. L. Hughson, Dept. of Kinesiology, Univ. of Waterloo, Waterloo, ON, Canada N2L 3G1 (E-mail: hughson{at}healthy.uwaterloo.ca).
Received 3 July 1997; accepted in final form 9 July 1998.
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REFERENCES |
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Top
Abstract
Introduction
Methods
Results
Discussion
References
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L. F. Ferreira, S. Koga, and T. J. Barstow Dynamics of noninvasively estimated microvascular O2 extraction during ramp exercise J Appl Physiol, December 1, 2007; 103(6): 1999 - 2004. [Abstract] [Full Text] [PDF]
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S. Koga, D. C. Poole, L. F. Ferreira, B. J. Whipp, N. Kondo, T. Saitoh, E. Ohmae, and T. J. Barstow Spatial heterogeneity of quadriceps muscle deoxygenation kinetics during cycle exercise J Appl Physiol, December 1, 2007; 103(6): 2049 - 2056. [Abstract] [Full Text] [PDF]
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B. A. Parker, S. L. Smithmyer, J. A. Pelberg, A. D. Mishkin, M. D. Herr, and D. N. Proctor Sex differences in leg vasodilation during graded knee extensor exercise in young adults J Appl Physiol, November 1, 2007; 103(5): 1583 - 1591. [Abstract] [Full Text] [PDF]
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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]
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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]
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 A. J. Harper, L. F. Ferreira, B. J. Lutjemeier, D. K. Townsend, and T. J. Barstow Human femoral artery and estimated muscle capillary blood flow kinetics following the onset of exercise Exp Physiol, July 1, 2006; 91(4): 661 - 671. [Abstract] [Full Text] [PDF]
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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]
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L. F. Ferreira, A. J. Harper, and T. J. Barstow Frequency-domain characteristics and filtering of blood flow following the onset of exercise: implications for kinetics analysis J Appl Physiol, March 1, 2006; 100(3): 817 - 825. [Abstract] [Full Text] [PDF]
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S. L. MacPhee, J. K. Shoemaker, D. H. Paterson, and J. M. Kowalchuk Kinetics of O2 uptake, leg blood flow, and muscle deoxygenation are slowed in the upper compared with lower region of the moderate-intensity exercise domain J Appl Physiol, November 1, 2005; 99(5): 1822 - 1834. [Abstract] [Full Text] [PDF]
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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]
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N. D. Paterson, J. M. Kowalchuk, and D. H. Paterson Effects of prior heavy-intensity exercise during single-leg knee extension on vO2 kinetics and limb blood flow J Appl Physiol, October 1, 2005; 99(4): 1462 - 1470. [Abstract] [Full Text] [PDF]
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L. F Ferreira, A. J Harper, D. K Townsend, B. J Lutjemeier, and T. J Barstow Kinetics of estimated human muscle capillary blood flow during recovery from exercise Exp Physiol, September 1, 2005; 90(5): 715 - 726. [Abstract] [Full Text] [PDF]
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N. D. Paterson, J. M. Kowalchuk, and D. H. Paterson Kinetics of V.02 and femoral artery blood flow during heavy-intensity, knee-extension exercise J Appl Physiol, August 1, 2005; 99(2): 683 - 690. [Abstract] [Full Text] [PDF]
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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]
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L. F. Ferreira, D. K. Townsend, B. J. Lutjemeier, and T. J. Barstow Muscle capillary blood flow kinetics estimated from pulmonary O2 uptake and near-infrared spectroscopy J Appl Physiol, May 1, 2005; 98(5): 1820 - 1828. [Abstract] [Full Text] [PDF]
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N. R. Saunders, K. E. Pyke, and M. E. Tschakovsky Dynamic response characteristics of local muscle blood flow regulatory mechanisms in human forearm exercise J Appl Physiol, April 1, 2005; 98(4): 1286 - 1296. [Abstract] [Full Text] [PDF]
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B. J. Lutjemeier, A. Miura, B. W. Scheuermann, S. Koga, D. K. Townsend, and T. J. Barstow Muscle contraction-blood flow interactions during upright knee extension exercise in humans J Appl Physiol, April 1, 2005; 98(4): 1575 - 1583. [Abstract] [Full Text] [PDF]
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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]
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N. R. Saunders and M. E. Tschakovsky Evidence for a rapid vasodilatory contribution to immediate hyperemia in rest-to-mild and mild-to-moderate forearm exercise transitions in humans J Appl Physiol, September 1, 2004; 97(3): 1143 - 1151. [Abstract] [Full Text] [PDF]
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M. E. Tschakovsky and D. D. Sheriff Immediate exercise hyperemia: contributions of the muscle pump vs. rapid vasodilation J Appl Physiol, August 1, 2004; 97(2): 739 - 747. [Abstract] [Full Text] [PDF]
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Y. Fukuba, Y. Ohe, A. Miura, A. Kitano, M. Endo, H. Sato, M. Miyachi, S. Koga, and O. Fukuda Dissociation between the time courses of femoral artery blood flow and pulmonary VO2 during repeated bouts of heavy knee extension exercise in humans Exp Physiol, May 1, 2004; 89(3): 243 - 253. [Abstract] [Full Text] [PDF]
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P. Haouzi, B. Chenuel, and A. Huszczuk Sensing vascular distension in skeletal muscle by slow conducting afferent fibers: neurophysiological basis and implication for respiratory control J Appl Physiol, February 1, 2004; 96(2): 407 - 418. [Abstract] [Full Text] [PDF]
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M. E. Tschakovsky, A. M. Rogers, K. E. Pyke, N. R. Saunders, N. Glenn, S. J. Lee, T. Weissgerber, and E. M. Dwyer Immediate exercise hyperemia in humans is contraction intensity dependent: evidence for rapid vasodilation J Appl Physiol, February 1, 2004; 96(2): 639 - 644. [Abstract] [Full Text] [PDF]
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B. W. Scheuermann and T. J. Barstow O2 uptake kinetics during exercise at peak O2 uptake J Appl Physiol, November 1, 2003; 95(5): 2014 - 2022. [Abstract] [Full Text] [PDF]
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M. Endo, S. Tauchi, N. Hayashi, S. Koga, H. B. Rossiter, and Y. Fukuba Facial cooling-induced bradycardia does not slow pulmonary V.O2 kinetics at the onset of high-intensity exercise J Appl Physiol, October 1, 2003; 95(4): 1623 - 1631. [Abstract] [Full Text] [PDF]
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A. M Jones, D. P Wilkerson, K. Koppo, S. Wilmshurst, and I. T Campbell Inhibition of Nitric Oxide Synthase by L-NAME Speeds Phase II Pulmonary VO2 Kinetics in the Transition to Moderate-Intensity Exercise in Man J. Physiol., October 1, 2003; 552(1): 265 - 272. [Abstract] [Full Text] [PDF]
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D. S. DeLorey, J. M. Kowalchuk, and D. H. Paterson Relationship between pulmonary O2 uptake kinetics and muscle deoxygenation during moderate-intensity exercise J Appl Physiol, July 1, 2003; 95(1): 113 - 120. [Abstract] [Full Text] [PDF]
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T. Osada and G. Radegran Femoral artery inflow in relation to external and total work rate at different knee extensor contraction rates J Appl Physiol, March 1, 2002; 92(3): 1325 - 1330. [Abstract] [Full Text] [PDF]
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A W. Sheel, P A. Derchak, B. J Morgan, D. F Pegelow, A. J Jacques, and J. A Dempsey Fatiguing inspiratory muscle work causes reflex reduction in resting leg blood flow in humans J. Physiol., November 15, 2001; 537(1): 277 - 289. [Abstract] [Full Text] [PDF]
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B. D. Hoelting, B. W. Scheuermann, and T. J. Barstow Effect of contraction frequency on leg blood flow during knee extension exercise in humans J Appl Physiol, August 1, 2001; 91(2): 671 - 679. [Abstract] [Full Text] [PDF]
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M. J. MacDonald, H. L. Naylor, M. E. Tschakovsky, and R. L. Hughson Peripheral circulatory factors limit rate of increase in muscle O2 uptake at onset of heavy exercise J Appl Physiol, January 1, 2001; 90(1): 83 - 89. [Abstract] [Full Text] [PDF]
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J. Bangsbo, P. Krustrup, J. Gonzalez-Alonso, R. Boushel, and B. Saltin Muscle oxygen kinetics at onset of intense dynamic exercise in humans Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2000; 279(3): R899 - R906. [Abstract] [Full Text] [PDF]
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S. Koga, T. Shiojiri, M. Shibasaki, N. Kondo, Y. Fukuba, and T. J. Barstow Kinetics of oxygen uptake during supine and upright heavy exercise J Appl Physiol, July 1, 1999; 87(1): 253 - 260. [Abstract] [Full Text] [PDF]
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M. E. Tschakovsky and R. L. Hughson Interaction of factors determining oxygen uptake at the onset of exercise J Appl Physiol, April 1, 1999; 86(4): 1101 - 1113. [Abstract] [Full Text] [PDF]
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