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1 Department of Kinesiology, University of Waterloo, Waterloo, Ontario N2L 3G1, Canada; and 2 Department of Physiology, University of Nijmegen, 6500 HB Nijmegen, The Netherlands
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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We hypothesized that forearm
blood flow (FBF) during moderate intensity dynamic exercise would meet
the demands of the exercise and that postexercise FBF would quickly
recover. In contrast, during heavy exercise, FBF would be inadequate
causing a marked postexercise hyperemia and sustained increase in
muscle oxygen uptake (
O2musc). Six
subjects did forearm exercise (1-s contraction/relaxation, 1-s pause)
for 5 min at 25 and 75% of peak workload. FBF was determined by
Doppler ultrasound, and O2 extraction was estimated from
venous blood samples. In moderate exercise, FBF and
O2musc increased within 2 min to steady
state. Rapid recovery to baseline suggested adequate O2
supply during moderate exercise. In contrast, FBF was not adequate
during heavy dynamic exercise. Immediately postexercise, there was an
~50% increase in FBF. Furthermore, we observed for the first time in
the recovery period an increase in
O2musc above end-exercise values. During
moderate exercise, O2 supply met requirements, but with
heavy forearm exercise, inadequate O2 supply during
exercise caused accumulation of a large O2 deficit that was
repaid during recovery.
oxygen deficit; oxygen debt; excess postexercise oxygen consumption; Doppler; aerobic metabolism; lactate
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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DURING MODERATE RHYTHMIC
EXERCISE of human forearm (12, 15, 26) or leg
(28) muscles, the blood flow adapts to a steady value that
is appropriate for the metabolic demand. Blood flow is greatly reduced
or stopped during muscle contractions and is elevated during the muscle
relaxation (15, 28). Over the complete muscle
contraction/relaxation schedule, the perfusion pressure gradient and
the vascular conductance dictate blood flow. At least for moderate work
rates, the flow appears to be adequate as the muscle achieves a
steady-state blood flow and rate of oxygen consumption (O2) (10, 12), and on
cessation of exercise, blood flow recovers quickly to the preexercise
baseline (28).
At heavier workloads, the tension developed in the muscle will probably totally occlude arterial inflow during contraction (4, 14, 27, 29). Whether the total blood flow during the limited window between contractions is adequate depends on the duration of the recovery pause and the metabolic demand of the exercise (15).
In the recovery period after exercise, the whole body
O2 recovers gradually to resting values.
The term "O2 debt" has classically been used to
describe this whole process that some investigators have called
"excess postexercise O2 consumption" (EPOC)
(22). For heavy exercise, the O2 debt exceeds
the O2 deficit incurred at the onset of exercise (1,
2). With very short-lasting exhaustive exercise, di Prampero et
al. (8) noted that O2 measured at the mouth remained at the end-exercise level for 12-35 s after stopping. Bangsbo et al. (3) examined both the
whole body and the muscle O2
(O2musc) at the onset of, and recovery from, exercise that induced exhaustion in ~3.2 min. Recovery values of O2musc declined rapidly after
exercise, but they still exceeded the calculated requirement to repay
the O2 deficit (3). In studies of
O2musc in a dog muscle preparation, the
magnitude of O2 debt was seen to be equivalent to
O2 deficit across a wide range of metabolic demands
(7).
There is reason to suspect that the exercise and recovery responses
might be different in strenuous forearm exercise compared with leg
exercise. Although the knee-extension exercise in the study of Bangsbo
et al. (3) was at a high work rate, there was no evidence
of an overshoot in the postexercise hyperemia. This contrasts with the
response to dynamic (28) and isometric heavy forearm
contractions (14, 17, 27, 29) where the blood flow is
markedly impaired during contractions (14). None of these
studies determined O2musc. In this
study, we examined the rate of change in
O2musc at the onset and end of exercise from continuous measurements of forearm blood flow (FBF) by Doppler ultrasound and repeated blood sampling to determine O2
extraction. We hypothesized that FBF during exercise would be
inadequate during heavy but not moderate exercise and that there would
be a marked postexercise hyperemia after heavy forearm exercise.
Furthermore, it was hypothesized that in response to inadequate FBF
during the exercise, the postexercise
O2musc would remain elevated in
compensation for the O2 deficit incurred during the heavy
forearm exercise. This contrasts with the moderate exercise where we
hypothesize that O2 will recover rapidly
while repaying the O2 deficit.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Six healthy young subjects (4 males, 2 females) volunteered to take part in this study after receiving full written and verbal details of the experimental procedures and signing a consent form approved by the Office of Research Ethics of the University. The average (±SE) physical characteristics were age 27.8 ± 1.8 yr, height 180 ± 3 cm, and weight 71.2 ± 6.1 kg.
Experimental design. All testing took place in the supine position with the arm extended to be at heart level. The first test for all subjects was an incremental maximal test to exhaustion. The subjects raised and lowered a bucket that was being continuously filled with water at a rate of 1 kg/min, through a distance of 5 cm by squeezing a handgrip device. This weight was raised during a period of ~0.5 s and lowered during the next ~0.5 s with a 1-s rest pause between contractions. Thus the exercise was dynamic with no static component. The test began with a load of 1 kg and continued until the subjects were not able to lift the weight. The workloads for subsequent constant load testing were picked as 25 (2.4 ± 0.3 kg) and 75% (7.1 ± 0.9 kg) of the peak workload achieved during the incremental exercise (9.4 ± 1.2 kg).
The constant load tests were conducted as two trials on each of 2 separate days. The first trial of each day was at 25%, whereas the second trial was at 75% of the peak workload. At least 30 min separated the two tests on each day. Each trial consisted of a 5-min monitoring period at rest, with data collected over the final minute of this period, a 5-min period of exercise, and a 20-min recovery after the exercise. To eliminate anticipatory responses, the subjects were not aware of the time during any trial.Data acquisition. FBF was measured beat by beat with combined pulsed Doppler ultrasound (model 500V, Multigon Industries) and echo Doppler imaging (model SSH-140A, Toshiba) (26). The mean blood velocity was digitally recorded at 100 Hz after analysis with a Doppler signal processor (26). The pulsed Doppler probe was a flat 4-MHz crystal with an angle of insonation fixed at 45° relative to the skin. The exact angle to the brachial artery from the skin was confirmed by echo Doppler imaging. Throughout one trial at each workload, the diameter of the brachial artery was obtained by Doppler imaging. Vessel diameter was measured three times at rest, at times centered on 10-s intervals during the first minute of exercise, then at 1-min intervals to the end of exercise. All measurements were obtained at the same point of the cardiac cycle at end diastole. From these measured diameter values, a curve of best fit was obtained in an attempt to minimize random variation and to allow calculation of diameter for each cardiac cycle. Instantaneous FBF was determined from the product of mean blood velocity over a cardiac cycle and the simultaneous cross-sectional area of the vessel.
Arterial blood pressure was monitored continuously with a finger-cuff photoplethysmograph device (Finapres, Ohmeda) placed on the middle finger of the nonexercising hand. The cuff was maintained at heart level. The analog signal was recorded with the other variables at 100 Hz. Mean arterial pressure was determined from 1/3 systolic + 2/3 diastolic blood pressure.Blood sampling. A catheter (21-gauge, 1-in. Angiocath) was inserted into a vein draining from deep within the forearm. A three-way stopcock was attached to allow for frequent drawing of blood into heparinized 1-ml syringes for measurement of blood gases (ABL-30, Radiometer) and of blood lactate concentration by a fluorimetric method (21). Blood was sampled over ~5 s in the latter half of a 10-s sampling interval. This was the case whether the sample interval was 10 s as in the first minute or 30 to 60 s as later in exercise or recovery. At regular intervals throughout the testing, blood samples were obtained in microcapillary tubes for determination of hematocrit. Hemoglobin concentration was calculated from measured hematocrit as 33% of the total red blood cell volume, and venous O2 content was determined by standard equations from the calculated O2 saturation and hemoglobin concentration (12).
Calculated O2musc.
The product of FBF and arteriovenous O2 content difference
(a-vDO2) was taken as the
O2musc (12). Arterial
O2 content was calculated based on the assumption that the
arterial blood was 97% saturated (as normally measured in our
laboratory by oximetry). Furthermore, as the central cardiovascular
demand of forearm exercise is minimal, it is safe to assume that
arterial O2 content was unchanged throughout the test.
Statistical analysis.
The FBF, a-vDO2, and O2musc
were plotted at the midpoint of the 10-s sample intervals.
Statistically significant differences (P < 0.05) as a
function of time within workload tests were determined by one-way,
repeated-measures ANOVA using commercially available software
(SigmaStat, SPSS). The primary focus was on the comparison with
baseline values and between the end-exercise and immediately postexercise time points. Post hoc testing was completed with a
Student-Newman-Keuls test except when the variance was not normally distributed (75% FBF only) when a Wilcoxon's rank sum test was used.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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FBF.
At the onset of 25% exercise, FBF increased rapidly (Fig.
1). One-way ANOVA plus post hoc tests
detected a statistically significant difference from baseline after 1.5 min of exercise. A plateau was reached, with flow increasing about
fourfold over the resting values. Immediately on cessation of exercise
at the 25% load, there was a small, nonsignificant, increase in FBF
above the end-exercise value only during the first 10-s sample period.
FBF during recovery remained above the preexercise baseline for 1.25 min.
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Brachial artery diameter.
Throughout the 25% exercise test, there was a small increase in
brachial artery diameter (Fig. 2), but
the diameter was only significantly greater than baseline in the first
minute after exercise. During the 75% test, brachial artery diameter
increased significantly above baseline by 25 s, and it remained
greater until the end of measurements at the completion of recovery
monitoring. Also, immediately after the 75% exercise test, diameter
was significantly elevated above the end-exercise value for the first 2 min of recovery.
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a-vDO2. During the first 2 min of exercise at the 75% load, the a-vDO2 was greater than for the 25% load (Fig. 1). Over the final 3 min of exercise, there were no differences between the a-vDO2 for the two exercise loads. The a-vDO2 declined rapidly on cessation of exercise, with a return to preexercise baseline by 1.5 min in the 25% exercise load tests. In the 75% load tests, the a-vDO2 declined below baseline, not returning to preexercise values until 15 min after the end of exercise.
O2musc.
In both the 25 and 75% exercise load tests, the
O2musc was significantly elevated above
baseline by 35 s of exercise. Furthermore, O2musc continued to increase over the
first 2-3 min of exercise to an apparent plateau (Fig. 1). In the
case of the 25% test, the O2musc was
not different between the end-exercise value and that observed in the
first samples in recovery. The O2musc was no longer significantly elevated above preexercise baseline after
only 25 s of recovery in the 25% tests.
O2musc increased significantly above the
end-exercise values at 10 and 20 s of recovery. O2musc remained elevated above baseline
for the first minute of recovery.
Lactate concentration.
The lactate concentration in venous blood increased from just under 1 mmol/l at rest to ~1.8 mmol/l during the 25% exercise load test and
to 3.2 mmol/l during the 75% test. Return to preexercise levels was
delayed until 15 min after exercise in both tests (Fig. 3).
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Mean arterial blood pressure.
The small increases in mean arterial blood pressure during the 25%
exercise tests were not significantly different from the baseline (Fig.
4). During the 75% exercise test, mean
arterial pressure was significantly elevated above baseline by 25 s and did not return to baseline until 2 min after the end of exercise.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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To the best of our knowledge, this is the first time that
O2musc has been observed to increase
during the recovery period to values above those measured at the end of
dynamic exercise. Consistent with our hypothesis, FBF during the heavy
forearm exercise was inadequate for the demands of metabolism and waste
removal. This was indicated by a marked and prolonged postexercise
hyperemia. Our results differ from those presented by Bangsbo et al.
(3) for knee-extension exercise that caused exhaustion in
3.2 min. They did not see an overshoot in blood flow, nor did they see an elevation in O2musc after exercise.
There were differences in experimental design that might account for
the findings as considered below. The current results for the heavy
exercise, but not for the moderate exercise, also differ from those
reported for one set of experiments with dog muscle where the time
course of O2musc at the onset of
exercise mirrored that in recovery (7). Our findings,
similar to those of Bangsbo et al. (3), showed a marked
asymmetry with a long recovery time for
O2musc after heavy exercise.
Furthermore, our results are consistent with another set of animal
experiments where the peak O2musc was
influenced by the type of muscle contraction such that insufficient time for perfusion restricted O2 supply (4).
Critique of methodology. Combined pulsed and echo Doppler techniques allow for continuous beat-by-beat quantitative determination of FBF (26, 28). In this study, the immediate increase in FBF on cessation of heavy exercise was a function of removal of the high resistance to flow during the contractions. Indeed, we observed (data not shown) that the flow on each complete cardiac cycle that occurred between contractions was identical to that measured in the first 10-20 s of recovery. This confirms previous reports of the beat-by-beat variation in flow to an exercising muscle (15, 26, 28). The thermodilution method as used by Bangsbo et al. (3) is an intermittent approach to the study of muscle blood flow. These authors did not show data until ~30 s after the completion of their exercise challenge and may have missed important information about the magnitude of postexercise hyperemia. In our study, FBF was still markedly elevated above the mean end-exercise value at 30 s of recovery. These data suggest that the metabolic challenge of exercise relative to the muscle perfusion was probably greater in the current experiments than in those of Bangsbo et al. (3).
One factor that might contribute to the relatively greater flow deficit in the current experiments compared with the experiments of Bangsbo et al. (3) is the type of muscle contraction. In their experiments, the subjects performed knee-extension exercise at ~60 per minute. This required ~0.5 s for extension and a similar time for passive recovery. Our subjects performed a handgrip that required ~0.5 s to lift the weight and 0.5 s to lower the weight followed by a 1-s relaxation. That is, even though both exercises were dynamic with no static component and the duty cycle was similar in the two studies, the duration of a contraction was longer in our experiments. This might have been an important factor in restricting blood flow relative to metabolic demand. In this study, as in our previous report (12), we did not believe we could justify insertion of an arterial catheter simply to confirm that saturation did not vary from 97%. Given the minimal change in central cardiovascular response, there is no reason to believe that arterial saturation might change as it does in some individuals during very heavy exercise (6). In the estimation of a-vDO2, venous O2 content is the greatest uncertainty in this study, because it is impossible to isolate the blood from only the exercising muscle and totally exclude the possibility of skin or nonworking muscle contributions with human subjects (5). An additional concern with the calculation ofO2musc by the product of blood flow
(measured continuously) and a-vDO2 (measured intermittently) is the matching of these two variables. Blood was drawn
over the final 5 s of each time period. Given the short distance
from the exercising muscle to the sample site, this might be expected
to be representative of the O2 extraction at the midpoint of the 10-s windows that were analyzed in the first minute of exercise
and recovery. However, it is appropriate to examine the outcome if the
arrival of blood was delayed by one full sample period. It can be
appreciated from Fig. 1 that for the 75% exercise challenge, the
O2musc would still be elevated above the
end-exercise value even if O2musc was
calculated as the product of the FBF during the first 10-s period
matched with the a-vDO2 of the second 10-s sample period.
Such a large mismatch is unlikely, but even if it did occur, the
outcome and interpretation of our data would not be changed.
FBF and O2musc.
Our observations of achievement of steady state for FBF and
O2musc during the 25% exercise load are
consistent with recent reports at the onset of moderate intensity arm
(12) and leg exercise (10). In agreement with
experiments that investigated the response of isolated dog muscle
(7), our data showed that recovery
O2musc had a similar time course to that
at the onset of light-intensity exercise. Calculated O2
debt (16.1 ± 1.6 ml O2) did not differ from the
O2 deficit incurred at the onset of exercise (15.3 ± 1.4 ml O2). There was a greater total FBF above baseline
during recovery (206 ± 20 ml) than there was FBF deficit at the
onset of exercise (112 ± 21 ml, P < 0.05),
suggesting that supply of O2 was not the crucial regulatory factor.
O2musc at the onset of and recovery from
heavy knee-extension exercise. There are some important differences in
the results. First, we observed a marked and sustained
postexercise hyperemia, whereas Bansbo et al. (3)
did not. As considered above, this might have been a consequence of
their intermittent method of measurement or differences between leg and
arm exercise. Even though we employed dynamic muscle contractions with
a 1-s pause between contractions, the pattern of FBF after 75%
exercise resembled that after heavy isometric exercise (14, 17,
27, 29) where there is essentially no flow through the
contracting muscle during contraction (14). A second major
difference between our high-intensity exercise and that studied by
Bangsbo et al. (3) was that
O2musc increased in our study from ~50
ml/min during exercise to ~70 ml/min immediately after exercise.
O2musc then declined slowly to baseline
over the next 10-15 min. It was not possible to compute deficit
and debt for FBF and O2musc because of
uncertainty in the "steady-state" value during exercise.
Exploration of muscle metabolism by magnetic resonance spectroscopy to
determine intramuscular phosphocreatine and pH during the
high-intensity exercise could provide important insight into metabolic
control. Previous investigations of human forearm or leg muscles have
shown progressive depletion of phosphocreatine as work rate increased,
but it is not known how blood flow was affected in these studies
(18, 30).
It is appropriate to examine whether our values of FBF and
O2musc are realistic in terms of
metabolic potential. In single leg knee-extension exercise, values of
at least 250 ml · 100 g
1 · min1 have been observed for
peak blood flow and 363 ml · kg1 · min1 for peak
O2 (23). We do not have
magnetic resonance imaging data to provide an accurate assessment of
active muscle mass in our subjects. If the active forearm muscle mass
was less than 500 g (from an average total forearm volume of
~1,100 ml), then peak FBF would be ~150 ml · 100 g1 · min1 and the
O2 peak would be ~140
ml · kg1 · min1. The values
for peak blood flow for forearm exercise would be expected to be less
than those for single leg ergometry for several reasons. The most
important reason is that the peak blood flow occurred after stopping
the forearm exercise, because even though mean arterial pressure was
higher during exercise, each contraction caused vascular occlusion.
Furthermore, with the arm at heart level rather than below, as with the
leg exercise, perfusion pressure was lower in the arm exercise. It
remains to be determined if forearm and leg blood flow responses could
be equivalent if tested under similar conditions.
O2 extraction. Calculated O2 extraction (a-vDO2) reflected the change in venous O2 content. In the early phase of the 75% exercise load, there was greater O2 extraction compared with the 25% load, suggesting a greater metabolic demand. Throughout the final 3 min of exercise, O2 extraction was the same at the lower and higher intensities of exercise. This finding is consistent with the observations of others (3, 13, 16, 23) who have shown that venous O2 content rarely drops below 50 ml/l during strenuous exercise of a small muscle mass. With intermittent handgrip exercise, blood flow occurs almost exclusively during the pause between contractions. Thus flow rate was quite high during the pause, and this might have contributed to reduced O2 extraction.
On cessation of the 25% exercise load, the O2 extraction returned to baseline values within 90 s and remained at this level throughout the remainder of the recovery period. In contrast, O2 extraction during the recovery after the 75% exercise load declined to values below baseline within 30 s. Until the 15-min point of recovery, the O2 extraction was less than baseline, indicating an excess of blood flow relative to O2 requirement. The mechanism responsible for this hyperemia was at least in part related to the local metabolic state as evidenced by the sustained increase in venous blood lactate concentration. On the other hand, for the 25% exercise load, venous blood lactate remained elevated slightly above baseline values throughout the first 5 min of recovery, whereas FBF returned to baseline.Venous blood lactate. As expected, the increase in venous blood lactate from the forearm during the 25% exercise load was less than during the 75% exercise load. This observation is consistent with other suggestions of inadequate O2 delivery during the heavier exercise. Venous lactate remained elevated at approximately the end-exercise value for the first 3-4 min of recovery after both the 25 and 75% exercise tasks. Given the very high FBF in the recovery after the 75% exercise task, this suggests a very high venous lactate outflow from muscle and interstitial sources.
Brachial artery diameter, blood pressure, and blood flow. During the 25% exercise load tests, there was only a small, nonsignificant, increase in brachial artery diameter so that the major contributor to the threefold increase in FBF was an increase in blood velocity. Immediately after the 25% exercise load, there was a small significant increase in diameter. The brachial artery diameter response to the 75% exercise load was an exaggeration of the response to the lower-intensity exercise.
It seems to us that the most likely explanation for the dilation of the brachial artery, a main conduit vessel supplying the exercising forearm, is an upstream transmission of dilatory stimuli released by the exercising muscles (24). In line with our previous observations (25), greater dilation occurred with the heavier work rate. Additional factors to consider include release of nitric oxide and/or prostacyclin in response to increases in blood flow velocity stimulating the endothelial cells via increased shear stess (11). Removal of sympathetic restraint that existed during the exercise (20) or a myogenic response to the decrease in arterial pressure after exercise (19) should also be considered as potential explanations for the conduit artery response. The marked increase in arterial blood pressure during the 75% exercise load indicates that this type of exercise did induce a severe local strain. As with sustained isometric contractions, the 75% load caused at least relative muscle ischemia and the accumulation of metabolites that stimulated the muscle chemoreflex to bring about a sympathetic nervous system-mediated increase in vascular resistance. As indicated above, this sympathetic response might have influenced the conduit vessels as well as the resistance vessels (i.e., arterioles) that are further downstream.Perspectives
Consistent with our hypotheses, we found that the blood flow response to moderate exercise was adequate to meet the metabolic demands with little need for a postexercise hyperemia. On the other hand, the metabolic demand of repeated higher-intensity contractions could not be met by oxidative mechanisms because of the major impairment to total blood flow during the muscular contraction. This has implications for many tasks in an industry that requires repeated application of high levels of muscular force (9). It is apparent from our data that major deficits can occur in blood flow andO2musc that will cause muscle fatigue with the potential to cause injury. Appropriate work-to-rest schedules could be developed based on the duration and intensity of the work task.
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ACKNOWLEDGEMENTS |
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The authors are grateful to D. Northey for excellent technical assistance.
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FOOTNOTES |
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This research was supported by the Natural Sciences and Engineering Research Council of Canada and a NATO Collaborative Project Grant.
Address for reprint requests and other correspondence: R. L. Hughson, Dept. of Kinesiology, Univ. of Waterloo, Waterloo, Ontario N2L 3G1, Canada (E-mail: hughson{at}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 29 September 2000; accepted in final form 25 January 2001.
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REFERENCES |
|---|
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
|
|---|
1.
Asmussen, E.
Aerobic recovery after anaerobiosis in rest and work.
Acta Physiol Scand
11:
197-210,
1946.
2.
Bahr, R,
and
Sejersted OM.
Effect of intensity of exercise on excess postexercise O2 consumption.
Metabolism
40:
836-841,
1991[ISI][Medline].
3.
Bangsbo, J,
Gollnick PD,
Graham TE,
Juel C,
Kiens B,
Mizuno M,
and
Saltin B.
Anaerobic energy production and O2 deficit-debt relationship during exhaustive exercise in humans.
J Physiol (Lond)
422:
539-559,
1990
4.
Brechue, WF,
Barclay JK,
O'Drobinak DM,
and
Stainbsy WN.
Differences between VO2 maxima of twitch and tetanic contractions are related to blood flow.
J Appl Physiol
71:
131-135,
1991
5.
Corcondilas, A,
Koroxenidis GT,
and
Shepherd JT.
Effect of a brief contraction of forearm muscles on forearm blood flow.
J Appl Physiol
19:
142-146,
1964
6.
Dempsey, JA,
Hanson PE,
and
Henderson KS.
Exercise induced arterial hypoxemia in healthy persons at sea level.
J Physiol (Lond)
355:
161-175,
1984
7.
di Prampero, PE,
and
Margaria R.
Relationship between O2 consumption, high energy phosphates and the kinetics of the O2 debt in exercise.
Pflügers Arch
304:
11-19,
1968[ISI][Medline].
8.
di Prampero, PE,
Peeters L,
and
Margaria R.
Alactic O2 debt and lactic acid production after exhausting exercise in man.
J Appl Physiol
34:
628-632,
1973
9.
Fransson-Hall, C,
Byström S,
and
Kilbom A.
Characteristics of forearm-hand exposure in relation to symptoms among automobile assembly line workers.
Am J Ind Med
29:
15-22,
1996[ISI][Medline].
10.
Grassi, B,
Poole DC,
Richardson RS,
Knight DR,
Erickson BK,
and
Wagner PD.
Muscle O2 uptake kinetics in humans: implications for metabolic control.
J Appl Physiol
80:
988-998,
1996
11.
Hecker, M,
Mulsch A,
Bassenge E,
and
Busse R.
Vasoconstriction and increased flow: two principal mechanisms of shear stress-dependent endothelial autacoid release.
Am J Physiol Heart Circ Physiol
265:
H828-H833,
1993
12.
Hughson, RL,
Shoemaker JK,
Tschakovsky M,
and
Kowalchuk JM.
Dependence of muscle VO2 on blood flow dynamics at the onset of forearm exercise.
J Appl Physiol
81:
1619-1626,
1996
13.
Jensen-Urstad, M,
and
Ahlborg G.
Is the high lactate release during arm exercise due to a low training status?
Clin Physiol
12:
487-496,
1992[ISI][Medline].
14.
Kagaya, A,
and
Homma S.
Brachial arterial blood flow during static handgrip exercise of short duration at varying intensities studied by a Doppler ultrasound method.
Acta Physiol Scand
160:
257-265,
1997[ISI][Medline].
15.
Kagaya, A,
and
Ogita F.
Blood flow during muscle contraction and relaxation in rhythmic exercise at different intensities.
Ann Physiol Anthrop
11:
251-256,
1992[Medline].
16.
Koskolou, MD,
Calbet JAL,
Rådegran G,
and
Roach RC.
Hypoxia and the cardiovascular response to dynamic knee-extensor exercise.
Am J Physiol Heart Circ Physiol
272:
H2655-H2663,
1997
17.
Lind, AR,
and
McNicol GW.
Local and central circulatory responses to sustained contractions and the effect of free or restricted arterial inflow on post-exercise hyperaemia.
J Physiol (Lond)
192:
575-593,
1967
18.
McCann, DJ,
Molé PA,
and
Caton JR.
Phosphocreatine kinetics in humans during exercise and recovery.
Med Sci Sports Exerc
27:
378-389,
1995[ISI][Medline].
19.
Mohrman, DE,
and
Sparks HV.
Myogenic hyperemia following brief tetanus of canine skeletal muscle.
Am J Physiol
227:
531-535,
1974.
20.
O'Leary, DS,
Robinson ED,
and
Butler JL.
Is active skeletal muscle functionally vasoconstricted during dynamic exercise in conscious dogs?
Am J Physiol Regulatory Integrative Comp Physiol
272:
R386-R391,
1997
21.
Phillips, SM,
Green HJ,
MacDonald MJ,
and
Hughson RL.
Progressive effect of endurance training on VO2 kinetics at the onset of submaximal exercise.
J Appl Physiol
79:
1914-1920,
1995
22.
Roth, DA,
Stanley WC,
and
Brooks GA.
Induced lactacidemia does not affect postexercise O2 consumption.
J Appl Physiol
65:
1045-1049,
1988
23.
Rowell, LB,
Saltin B,
Kiens B,
and
Christensen NJ.
Is peak quadriceps blood flow in humans even higher during exercise with hypoxemia?
Am J Physiol Heart Circ Physiol
251:
H1038-H1044,
1986
24.
Segal, SS.
Cell-to-cell communication coordinates blood flow control.
Hypertension
23:
1113-1120,
1994
25.
Shoemaker, JK,
MacDonald MJ,
and
Hughson RL.
Time course of brachial artery diameter responses to rhythmic handgrip exercise in humans.
Cardiovasc Res
35:
125-131,
1997
26.
Shoemaker, JK,
Pozeg ZI,
and
Hughson RL.
Forearm blood flow by Doppler ultrasound during rest and exercise: tests of day-to-day repeatability.
Med Sci Sports Exerc
28:
1144-1149,
1996[ISI][Medline].
27.
Sjogaard, G,
Savard G,
and
Juel C.
Muscle blood flow during isometric activity and its relation to fatigue.
Eur J Appl Physiol
57:
327-335,
1988.
28.
Walloe, L,
and
Wesche J.
Time course and magnitude of blood flow changes in the human quadriceps muscles during and following rhythmic exercise.
J Physiol (Lond)
405:
257-274,
1988
29.
Wesche, J.
The time course and magnitude of blood flow changes in the human quadriceps muscles following isometric contraction.
J Physiol (Lond)
377:
445-462,
1986
30.
Yoshida, T,
and
Watari H.
31P-nuclear magnetic resonance spectroscopy study of the time course of energy metabolism during exercise and recovery.
Eur J Appl Physiol
66:
494-499,
1993.
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) and 75%
(
) peak load for 5 min and during recovery. FBF was
significantly different from baseline from 2 min 25 s to 6 min
15 s during the 25% tests and from 1 min 25 s to the end of
measurement during the 75% tests (P < 0.05 by 1-way,
repeated-measures ANOVA). a-vDO2 was different from baseline from
45 s to 5 min 15 s in the 25% tests and from 25 s to 5 min and 6 min 30 s to 15 min in the 75% tests.
