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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 used an
exercise paradigm with repeated bouts of heavy forearm exercise to test
the hypothesis that alterations in local acid-base environment that
remain after the first exercise result in greater blood flow and
O2 delivery at the onset of the second bout of exercise.
Two bouts of handgrip exercise at 75% peak workload were performed for
5 min, separated by 5 min of recovery. We continuously measured blood
flow using Doppler ultrasound and sampled venous blood for
O2 content, PCO2, pH, and lactate
and potassium concentrations, and we calculated muscle O2
uptake (
O2). Forearm blood flow was
elevated before the second exercise compared with the first and
remained higher during the first 30 s of exercise (234 ± 18 vs. 187 ± 4 ml/min, P < 0.05). Flow was not
different at 5 min. Arteriovenous O2 content difference was
lower before the second bout (4.6 ± 0.9 vs. 7.2 ± 0.7 ml
O2/dl) and higher by 30 s of exercise
(11.2 ± 0.7 vs. 10.8 ± 0.7 ml O2/dl,
P < 0.05). Muscle O2
was unchanged before the start of exercise but was elevated during the
first 30 s of the transition to the second exercise bout
(26.0 ± 2.1 vs. 20.0 ± 0.9 ml/min, P < 0.05). Changes in venous blood PCO2, pH, and
lactate concentration were consistent with reduced reliance on
anaerobic glycolysis at the onset of the second exercise bout. These
data show that limitations of muscle blood flow can restrict the
adaptation of oxidative metabolism at the onset of heavy muscular exertion.
blood flow; metabolism; blood acid-base; O2 transport; Doppler ultrasound
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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CENTRAL AND PERIPHERAL
CIRCULATORY limitations have an impact on the ability of humans
to adapt to the metabolic demands of increased exercise intensities.
Slower adaptation of O2 uptake (O2) at the onset of very heavy exercise
might reflect the interaction of central and peripheral circulatory
limitations to O2 transport and utilization (8,
15). Gerbino et al. (8) showed that O2 increased more rapidly in response to
a second bout of exercise, and MacDonald et al. (15)
demonstrated even faster adaptation when arterial O2
content was increased. These studies suggest that better adaptation is
a consequence of improved O2 transport in the second of two
high-intensity exercise bouts. Proposed mechanisms for the improved
O2 transport include elevated blood flow and greater
O2 extraction. Both could be consequences of alterations in
local acid-base status, which might promote increased vascular conductance and a right shift of the O2-hemoglobin
dissociation curve, but direct confirmation is not available.
Our laboratory developed a forearm exercise experiment model that
allows continuous monitoring of arterial blood flow in conjunction with
measurement of arteriovenous O2 content difference for
determination of muscle O2
(11). In the present study, we
investigated the mechanisms that enable skeletal muscle
O2 to adapt more rapidly to the second
of two high-intensity exercise bouts. We hypothesized that
venous blood would demonstrate an altered acid-base environment after
the first bout of exercise. This alteration would then promote greater
blood flow through more rapid vasodilation, as well as greater
O2 extraction, in the second bout of exercise, thus
allowing muscle O2 to increase more
rapidly at the onset of exercise. The metabolic consequence of this
rapid adaptation of oxidative metabolism would be reduction in venous
blood lactate and less change in blood pH.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Six healthy men (age 33 ± 5 yr, height 181 ± 2 cm, weight 74 ± 3 kg, mean ± SE) volunteered to participate in this study. They were not specifically trained, and all gave written consent on a form that was approved by the Office of Research Ethics at the University of Waterloo.
Exercise protocol. Subjects performed all exercises on a handgrip ergometer, in which the resistance was varied by adjusting the magnitude of load that was raised and lowered by repeated contractions with the right hand. The subjects were in a supine posture with the arm extended at heart level. The exercise protocol for all tests involved raising the weight for 0.5 s, lowering the weight for 0.5 s, and resting for 2 s before the next contraction, for a total cycle of 3 s. Initially, each subject performed a ramp handgrip exercise protocol, and the information from this test was used to determine the workloads to achieve 75% of peak load for the subsequent testing. In the ramp procedure, the resistance was continually increased by adding water at a flow rate of 1 l/min into a bucket that was raised and lowered. On a separate day, subjects reported to the laboratory in a rested state, at least 2 h after eating. They assumed a supine position, and a 21-gauge catheter (Angiocath, Becton-Dickinson, Sandy, UT) was inserted retrograde at the antecubital fossa in a deep forearm vein in the right arm. Another catheter was inserted in a dorsal hand vein on the left hand. This hand was warmed to obtain arterialized venous blood samples (7). The test session consisted of measurement of resting data for 5 min, which was followed, sequentially, by 5 min of exercise, 5 min of rest, 5 min of exercise, and an additional 5-min rest period.
Data collection.
Forearm blood flow (FBF) was measured by Doppler ultrasound, as
described previously (6, 11, 20). This is a highly reproducible method that has a coefficient of variation of 3-4% for estimates of diameter and 13-20% for measurements of velocity and blood flow (20). Most variations in velocity and flow
appear to arise from spontaneous fluctuations in the normal blood flow, as seen with beat-by-beat heart rate or blood pressure
(2), and are not a function of error in the method
(6, 20). Brachial artery diameter was estimated by echo
Doppler ultrasound, with a 7.5-MHz linear array probe (model SSH-140A,
Toshiba, Tochigi-Ken, Japan). Mean blood velocity (MBV) was determined
with a 4-MHz pulsed Doppler ultrasound probe (model 500V, Multigon
Industries, Mt. Vernon, NY). Brachial artery diameter was obtained
twice at rest, at minutes 1 and 5 of each
exercise bout, and during recovery. The spectrum of the pulsed Doppler
was processed on-line with a mean velocity processor (17).
Calibration signals in the Doppler shift frequency range were generated
from the Doppler signal processor. The blood flow velocity of our
system was calibrated against blood pumped through tubing
(20). MBV was obtained through integration of the area
under the curve for each heartbeat and by averaging the response over
3-s intervals, so that a contraction and relaxation phase were included
during exercise. FBF was estimated beat by beat by multiplying the
average MBV by the cross-sectional area [area = 
(D/2)2], where diameter (D) was
updated at the times indicated in Table 1. MBV and heart rate signals were
collected on a computer-based system at 100 Hz.
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Blood samples. Venous blood samples were obtained twice during rest, at 30 s, 2 min, and 5 min of exercise, and at 30 s and 2 min of recovery. Arterialized venous blood samples were obtained twice during rest and during the fifth minute of both exercise and recovery.
Approximately 1 ml of blood was collected in heparinized syringes that were immediately capped, gently agitated, and then stored in an ice bath. Within 1 h of collection, all whole blood samples were analyzed at 37°C for PO2, PCO2, hematocrit, plasma concentrations of lactate ([La
]) and potassium ([K+]), and
plasma pH by using selective electrodes in a blood-gas electrolyte
analyzer (NovaStat Profile Plus 9, Waltham, MA). The analyzer was
calibrated at regular intervals. Hemoglobin concentration was
calculated from the measured hematocrit by assuming normal mean
corpuscular hemoglobin of 33% of the total cell volume. O2 saturation and content were obtained from the output of the analysis system after application of standard equations.
Blood data analysis. Arteriovenous O2 content difference was calculated from the difference in assumed arterial O2 content and actual forearm venous O2 content. To estimate arterial O2 content, we assumed that it was constant for each subject, using 97% saturation for the calculation (arterial O2 content = 1.34[hemoglobin] × O2 saturation/100). Assumption of a constant arterial O2 content is reasonable in this study because we normally observe 97% saturation of arterial blood by noninvasive oximetry. Furthermore, forearm handgrip exercise represents a relatively small cardiovascular challenge that does not compromise arterial blood oxygenation in the lungs.
A 10-s average of FBF, centered on the time over which the blood samples were drawn, was used to match blood flow and O2 extraction for calculation of forearm muscleO2. Arterial blood [La]
was estimated from the arterialized venous samples. Arterialized hand
vein samples provided a reasonable estimation of arterial lactate
concentrations because the O2 saturation in the
arterialized samples of a previous study was calculated as 93.7 ± 0.5 (SE) % (n = 6) (7).
Data analysis.
Effects of previous arm exercise and time on the values for FBF,
arteriovenous O2 content difference, muscle
O2, pH, [La],
[K+], and PCO2 were analyzed by
using a two-way repeated-measures ANOVA. This first level of analysis
revealed significant interaction effects of exercise bout and time for
all variables. Therefore, all subsequent analyses are reported from
one-way ANOVA comparisons at each time point, thus testing for
differences between the first and second exercise bouts. The level of
significance was set at P < 0.05. Any differences were
further analyzed with Student-Newman-Keuls post hoc test. All data are
presented as means ± SE.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The peak workload achieved in the ramp exercise protocol was 17.1 ± 0.9 kg. The workload used during the step test protocol was 12.8 ± 0.7 kg, which represented ~75% of the peak workload.
At the onset of the first bout of exercise, FBF immediately began a
rapid adaptation (Fig. 1), which is
characteristic of the response for both forearm and leg exercise
(16, 21). The pattern of adaptation altered in the second
bout, resulting in a faster adjustment to steady state. This response
was mainly due to increases in MBV, with relatively small changes in
diameter over the course of exercise or recovery, in either the first
or second bout (Table 1). In the second bout of high-intensity
exercise, FBF was significantly elevated before the start of exercise
(111 ± 23 vs. 36 ± 6 ml/min, P < 0.05) and
at 30 s of exercise (234 ± 18 vs. 187 ± 4 ml/min,
P < 0.05) compared with the first bout of exercise
(Fig. 2). With cessation of muscle
contractions, there was a marked elevation in FBF after both the first
and second bouts of exercise (Fig. 1). Postexercise hyperemia was
prolonged after both exercise bouts, with FBF still markedly elevated
above the preexercise resting value at the end of the 5-min recovery period.
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Resting muscle O2 was not significantly
different before the first or second exercise bouts (Fig. 2). This was
achieved by the combination of lower FBF and greater arteriovenous
O2 content difference in the true resting state before the
start of the first exercise bout. Before the second exercise bout, FBF
was elevated, whereas the arteriovenous O2 content
difference was significantly reduced (4.6 ± 0.9 vs. 7.2 ± 0.7 ml O2/dl, P < 0.05) and higher by 30 s of exercise (11.2 ± 0.7 vs. 10.8 ± 0.7 ml
O2/dl, P < 0.05). At 30 s of
exercise, muscle O2 was significantly
greater in the second compared with the first exercise bout (Fig. 2).
The elevated muscle O2 was caused by
significantly greater FBF and arteriovenous O2 content
difference in the 30-s sample in the second exercise bout. The
arteriovenous O2 content difference was significantly lower
in the second exercise bout compared with the first at the 5-min
sampling point. This did not result in a difference in muscle
O2 at this time point, as the FBF was slightly, but not significantly, elevated in the second test.
Arterialized venous pH, [La], and [K+]
did not change significantly across the entire duration of the exercise protocol.
The elevated venous [La] and reduced venous pH in the
second exercise bout, before the start of exercise and at 30 s,
are consistent with the expected metabolic acidosis in the exercising forearm after an initial bout of high-intensity exercise (Figs. 3 and 4).
Also, after the first bout of exercise, there was an elevation in
venous blood PCO2. Before the start of the
second bout, PCO2 had declined to the point
that it was not significantly elevated over the initial resting values.
As exercise progressed, the relative acidosis was greater in the first
exercise bout compared with the second. This was observed as
significantly lower venous [La] and
PCO2, which contributed to the significantly
greater pH at the end of the second bout of exercise. The differences
in acid-base were maintained throughout recovery, showing the greater acidosis after the first exercise bout.
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Before the onset of the second exercise bout, venous plasma [K+] was reduced compared with the first bout. Although there was a marked increase in venous [K+] with exercise, there were no differences in [K+] between exercise bouts. At 30 s after the second exercise bout, venous plasma [K+] was elevated compared with after the first bout (Fig. 3).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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This study provides confirmation that circulatory factors can
limit the adaptation of muscle O2 at the
onset of high-intensity exercise. Muscle
O2 was measured during two, identical,
high-intensity forearm exercise challenges in which the second
challenge was 5 min after the first. We found that muscle
O2 was significantly elevated during the
first minute of the second exercise bout compared with the first bout.
Consistent with our hypotheses, the residual effects of the first
exercise bout on the acid-base status of the muscle were associated
with an elevation in FBF and a greater O2 extraction during
the second exercise bout. Despite the differences between the present
model and whole body exercise, these data, obtained in the exercising
forearm, suggest that adaptation of aerobic metabolism at the onset of
whole body high-intensity exercise might also be limited by the
availability of O2 in healthy subjects and in patients with
heart disease (1, 13, 22).
O2 at the onset of exercise.
The present experiments allowed us to explore the potential roles of
bulk O2 supply, as determined by FBF and O2
extraction, in limiting O2 at the onset
of heavy exercise. Both factors were proposed, in previous modeling
(3) and experimental studies (8, 11, 15), as
potential rate-limiting steps in the delivery of O2 for
aerobic metabolism. The data from this experiment provide the first
direct confirmation of the important role of both effects in modifying
O2 utilization during the rest-to-exercise transition for
small muscle mass exercise. The forearm exercise model used in this
study has a very different feature compared with repeated, high-intensity cycling exercise. Whereas cycling challenges both the
central and peripheral circulatory capacities, the forearm model
focuses on potential peripheral limitations. Thus any improvements in
exercise performance that occur with whole body exercise might be
further enhanced if cardiac output increases in conjunction with the
altered peripheral factors identified in this study (15). The extent to which O2 transport contributes to muscle
O2 at the onset of submaximal exercise
is still being debated (9, 11).
Limitations to the methodology. Limitations to the methodology used in the present study include both instrumental constraints as well as theoretical limitations of the model. As previously shown in our laboratory (20), and confirmed by Rådegran (18), Doppler ultrasound is a highly reliable and accurate method for determining both MBV and conduit artery diameter at rest and during exercise. The estimation accuracy of FBF in the present study may have been limited by the lack of repeated data collections; however, FBF variability was similar to that previously observed using these methods (18, 20).
In the present study, venous blood was sampled from a single deep forearm vein. Possible limitations to this include the assumption that the blood sampled from this vein accurately reflected the metabolic rate of the muscles of interest and that the distribution of venous return from the forearm was not altered with changes in flow. The patterns of change seen in the arteriovenous O2 content difference and venous O2 content were consistent with previously published patterns (11).FBF. Blood flow adapts in the transition from rest to forearm or leg exercise in a two-phase pattern. The rapid increase in blood flow observed within the first 15-20 s of exercise is a consequence of the action of the muscle pump emptying veins and allowing a greater pressure gradient in combination with a limited vasodilation (19, 23). Subsequent increases in flow are primarily a consequence of further vasodilation in response to release of local vasoactive metabolites (such as K+ and H+, as shown in this study) and, possibly, endothelial factors (14). During this adaptive phase, blood flow distribution is coordinated to deliver more blood flow to metabolically active sites.
It is important to note in the present experiments that a relatively steady FBF was not achieved until ~2 min after the onset of exercise. These data are consistent with a negative feedback control mechanism. Even though FBF appeared to be relatively steady, it is obvious from the marked postexercise hyperemia that FBF was inadequate during exercise. During high-intensity exercise, FBF was unable to meet the demands because of periodic compression and occlusion of blood vessels with each contraction. Indeed, on stopping the last contraction, the high value of FBF (~600 ml/min; Fig. 1) indicates how high flow was during the muscle relaxation phases in the latter part of exercise. Figure 5 shows the beat-by-beat values for MBV throughout the entire protocol. It is apparent in all tests that individual beat values achieved the same high velocity in the pause between contractions as in the period immediately after exercise. FBF recovered during the 5-min period between exercise bouts, but it did not return to resting baseline values. Thus, just before the start of the second exercise bout, FBF was approximately twice the value from before the first bout. The two-phase pattern of blood flow adaptation was also less obvious at the start of the second bout of exercise, possibly due to the elevation of resting flow and the increased vasodilation that may have existed in the exercising muscle vascular bed. The elevated FBF can be attributed, at least in part, to the vasodilatory effect of a significant reduction in pH, measured in venous blood, along with the significant elevation in [La] and the slight increase in
PCO2. Venous plasma K+ was
significantly reduced before the start of the second exercise bout.
This might have been a consequence of increased washout caused by the
higher FBF. Whereas this would, to some extent, counter the
vasodilatory properties, it is obvious that it did not achieve total
compensation, and thus FBF remained elevated.
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Metabolic consequences of altered O2 transport.
The more rapid increase in muscle O2
that we found in the second exercise bout would mean that a greater
proportion of the total ATP resynthesis occurred through oxidative
metabolism. Consequently, utilization of phosphocreatine stores and
anaerobic glycolysis should contribute less. We do not have information
on the phosphocreatine stores in the present study. It might be
anticipated that these stores were not completely recovered before the
onset of the second exercise bout, but their final levels are unknown.
Although we do not have intracellular measurements of
[La], we do have information from venous blood that
indicates production was probably decreased in the second compared with
the first exercise bout. Previous investigations of the effects of
warm-up exercise have reported either no effect on (8), or
a reduction in, blood [La] compared with exercise
without a warm-up (12). However, these studies did not
measure [La] in blood as it left the exercising muscle,
and many factors could have impacted systemic venous blood
[La]. Because the total muscle mass being exercised was
quite small, our finding of no change in arterialized blood
[La] was expected.
O2, which was a
consequence of a 25.1% increase in FBF and a 3.7% increase in
arteriovenous O2 content difference. These relative
contributions indicate that the major factor that influenced muscle
O2 was the increase in FBF. Indeed, the
relatively small changes in the local acid-base environment had only a
small contribution to increased O2 extraction. We used the
mean values of venous blood pH and PCO2 to
estimate the 50% saturation of hemoglobin by O2
(P50). For exercise test 1 (pH = 7.38, PCO2 = 49.5 Torr), the P50 was
27.7 Torr, whereas, for test 2 (pH = 7.36, PCO2 = 51.0 Torr), the P50 was
28.3 Torr. The difference might be greater if the effect of
temperature was included. The slightly but significantly greater
O2 extraction seen at the 30-s point of test 2 probably reflects the small shift of the O2-hemoglobin
dissociation curve as well as better distribution of blood flow to the
exercising muscle fibers. The relatively low O2 extraction
from the blood, despite the heavy workload, probably reflects the rapid
transit of red blood cells across the muscle due to very high FBF
during the pause between contractions.
These results from small muscle mass exercise might have important
implications for other conditions in which O2 transport could be less than optimal at the onset of exercise, including exercise
with beta-blockers (10) or in patients with impaired cardiac performance (1, 4, 5, 13). Factors that limit O2 transport cause greater stress on the phosphocreatine
stores and anaerobic glycolysis during the rest-to-exercise transition. However, at least for heavy exercise, factors that can promote improved
O2 transport or O2 release to the exercising
muscles should result in less depletion of phosphocreatine and lower
concentrations of muscle and blood lactate (10).
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ACKNOWLEDGEMENTS |
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We thank David Northey for excellent technical assistance.
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FOOTNOTES |
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This study was supported by the Natural Sciences and Engineering Research Council of Canada (NSERC). M. J. MacDonald and H. L. Naylor were recipients of NSERC Post Graduate Scholarships.
Address for reprint requests and other correspondence: R. L. Hughson, Dept. of Kinesiology, Univ. of Waterloo, Waterloo, Ontario, Canada N2L 3G1 (E-mail: hughson{at}healthy.uwaterloo.ca).
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.
Received 7 March 2000; accepted in final form 26 July 2000.
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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 S. M. Sostaric, t. l. S. L. Skinner, M. J. Brown, T. Sangkabutra, I. Medved, T. Medley, S. E. Selig, I. Fairweather, D. Rutar, and M. J. McKenna Alkalosis increases muscle K+ release, but lowers plasma [K+] and delays fatigue during dynamic forearm exercise J. Physiol., January 1, 2006; 570(1): 185 - 205. [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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J. J. Hamann, H. A. Kluess, J. B. Buckwalter, and P. S. Clifford Blood flow response to muscle contractions is more closely related to metabolic rate than contractile work J Appl Physiol, June 1, 2005; 98(6): 2096 - 2100. [Abstract] [Full Text] [PDF]
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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]
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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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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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M. Burnley, A. M. Jones, R. L. Hughson, N. Tordi, and S. Perrey Interpreting VO2 kinetics in heavy exercise revisited J Appl Physiol, June 1, 2003; 94(6): 2548 - 2550. [Full Text] [PDF]
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N. Tordi, S. Perrey, A. Harvey, and R. L. Hughson Oxygen uptake kinetics during two bouts of heavy cycling separated by fatiguing sprint exercise in humans J Appl Physiol, February 1, 2003; 94(2): 533 - 541. [Abstract] [Full Text] [PDF]
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Y. Fukuba, N. Hayashi, S. Koga, and T. Yoshida VO2 kinetics in heavy exercise is not altered by prior exercise with a different muscle group J Appl Physiol, June 1, 2002; 92(6): 2467 - 2474. [Abstract] [Full Text] [PDF]
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) and second bouts (
) of
high-intensity handgrip exercise. Exercise started at time
0. Values are means ± SE; n = 6. Note that
the first 
