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1 Department of Kinesiology, We hypothesized that near-infrared spectroscopy
(NIRS) measures of hemoglobin and/or myoglobin
O2 saturation
(IR-SO2)
in the vascular bed of exercising muscle would parallel changes in
femoral venous O2 saturation
(SfvO2)
at the onset of leg-kicking exercise in humans. Six healthy subjects
performed transitions from rest to 48 ± 3 (SE)-W two-legged kicking
exercise while breathing 14, 21, or 70% inspired
O2.
IR-SO2 was
measured over the vastus lateralis muscle continuously
during all tests, and femoral venous and radial artery blood samples
were drawn simultaneously during rest and during 5 min of exercise. In
all gas-breathing conditions, there was a rapid decrease in both
IR-SO2 and
SfvO2 at the onset of moderate-intensity
leg-kicking exercise. Although SfvO2 remained at
low levels throughout exercise,
IR-SO2
increased significantly after the first minute of exercise in both
normoxia and hyperoxia. Contrary to the hypothesis, these data show
that NIRS does not provide a reliable estimate of hemoglobin
and/or O2 saturation as
reflected by direct femoral vein sampling.
hemoglobin; myoglobin; tissue oxygenation; oxygen consumption
QUANTITATIVE ESTIMATES of
O2 supply to skeletal muscle at
the onset of exercise are difficult to obtain in humans. It is possible to make direct measurements of O2
content in venous and arterial blood. When combined with measurements
of blood flow made via Doppler (9) or thermodilution (6), indications
of O2 supply and utilization can
be provided.
Because of the difficulties with sampling of arteriovenous blood, it
would be beneficial to have a noninvasive method to continuously determine the relative O2
saturation
(SO2)
in exercising muscle at the onset of exercise. Near-infrared
spectroscopy (NIRS) utilizes the principle that the absorbance of light
by oxygenated and deoxygenated hemoglobin (Hb) and myoglobin (Mb)
differs at different near-infrared wavelengths (4). NIRS has been used
to estimate relative
SO2 in
human muscle (2, 7, 10, 13, 14, 35). Previous research in both animals
(14) and humans (10) has shown close correlations between measures of
tissue oxygenation determined via NIRS and venous
SO2 as work
rate increased during exercise. Costes et al. (5)
showed that, for steady-state cycling exercise, femoral venous
O2 saturation
(SfvO2) parallelled relative oxygenation changes measured via NIRS in hypoxia but not normoxia.
The temporal response of NIRS measurements at exercise onset has not
been validated by measures of venous effluent
SO2.
The purpose of the present study was to assess the oxygenation in human
skeletal muscle at the onset of submaximal leg-kicking exercise in
normoxia, hyperoxia, and hypoxia by using noninvasive reflectance NIRS.
The results in each gas-breathing condition were compared with
simultaneous measures of
SO2 of
venous blood draining the exercising leg. We hypothesized that the
noninvasive NIRS measurements would parallel those from direct blood sampling.
Six healthy volunteers [2 men, 4 women; age 25 ± 1 (SE) yr; height, 175 ± 3 cm; and weight, 68 ± 4 kg] participated in this study. They were not engaging in any
regular endurance-training exercise. After receiving a full written and
oral description of the experimental protocol, all subjects gave
written consent on forms approved by the University of Waterloo Office
of Human Research and Animal Care.
Exercise protocol.
Subjects reported to the laboratory on three occasions for training on
the kicking ergometer and to assist in learning the exercise mode. The
kicking ergometer is a specially designed piece of exercise equipment
that allows electrically braked exercise of both the quadricep and
hamstring muscles in an alternating kicking fashion. Subjects remained
in the seated position for all tests, with a hip angle of 120° and
with knee extension and flexion between 90 and 135°. The kicking
frequency, between 44 and 50 kicks per leg per minute, was maintained
via feedback from a meter attached to the ergometer. The fourth visit
to the laboratory involved a progressive kicking test to exhaustion or
functional limitation in hypoxic (14%
O2) conditions. The work-rate
protocol for this progressive test was a 15-W/min ramp. The progressive test was stopped when the subject could no longer maintain the kicking
frequency or needed accessory muscle assistance, as assessed by the
investigator. The gas-exchange and work-rate data from the ramp test
were used to estimate the subjects' ventilatory threshold
(Tvent) and peak
O2 consumption
(
ABSTRACT
Top
Abstract
Introduction
Methods
Results
Discussion
References
INTRODUCTION
Top
Abstract
Introduction
Methods
Results
Discussion
References
METHODS
Top
Abstract
Introduction
Methods
Results
Discussion
References
O2). These values were
then used to select individual work rates for the step tests of each subject.
Blood samples. Femoral venous and radial arterial blood were sampled during the exercise transitions to obtain measurements of blood gas and metabolic responses. On the testing day, subjects reported to the laboratory one-half hour before testing and had catheters inserted in the femoral vein and radial artery.
A 1.5-in. plastic radial artery catheter (20-gauge Angiocath; Becton-Dickinson, Sandy, UT) was inserted into the left radial artery under local anesthetic (lidocaine HCl, 2%; Astra, Mississauga, ON). Patency was maintained with a pressurized flush system (0.9% NaCl + heparin sodium 500 IU/500 ml NaCl; ~15 ml/h). Subjects lay supine, and a 16-cm plastic catheter (16 gauge; Arrow, Reading, PA) was inserted 2 cm below the inguinal ligament into the left femoral vein under local anesthetic (see above). In one subject, the femoral catheter was inserted in the right femoral vein. In all cases, the catheter was fixed to the skin and kept patent by intermittent flushes with normal saline. The position of the catheter was confirmed, by means of ultrasound imaging, to be within the femoral vein ~3 cm distal to the inguinal ligament in a subset of the subjects (n = 2). After the usual gas-accommodation period, 1-ml venous blood samples were collected in heparinized syringes two times during rest; at 20 and 40 s during the first minute of exercise; and at the first, third, and fifth minute of the exercise transition. Arterial blood samples (1 ml each) were collected in heparinized syringes two times during rest, and during the first, third, and fifth minutes of the exercise transition. The blood samples were immediately agitated gently and stored in an ice bath. Within 1 h of collection, all whole blood samples were analyzed for hematocrit, PO2, and PCO2 by using selective electrodes in a blood-gas electrolyte analyzer (NovaStat Profile Plus 9, Waltham, MA). The analyzer was calibrated at regular intervals during the analyses. SO2 and content were obtained from the output of the analysis system after application of standard equations.NIRS data collection.
Tissue SO2
(IR-SO2)
was determined via NIRS with a commercially available unit (model
CWS-2000 Runman, NIM, Philadelphia, PA). Reflected light
was measured percutaneously at two specific wavelengths (760 and 850 nm). The lamp intensity was set at 6 V for all tests, and the time
constant for the unit was set to the shortest response time (15 s). The
sensor was positioned lengthwise 10-12 cm above the knee over the
right vastus lateralis in five subjects and over the
left vastus lateralis in one subject. The sensor was
protected from skin moisture by a clear plastic wrap. An elastic strap
was placed around the thigh and over the sensor to prevent displacement
and the detection of ambient room light. The average depth of
penetration of near-infrared (NIR) light in skeletal muscle is
estimated to be 2.5-3.0 cm (4). Two separate outputs were obtained
from the NIRS unit and were sampled at 100 Hz on a dedicated computer
system. The output containing the difference in the two received
wavelengths (760 
850 nm) was monitored as an index of relative
Hb and Mb deoxygenation, and the output containing the sum of the two
received wavelengths (760 + 850 nm) was monitored as an index of
changes in tissue blood volume (3). The signals were averaged over 20 s
preceding the venous blood sample times to obtain values for both
channels twice at rest, at 20 and 40 s after the onset of exercise, and
during minutes 1, 3, and
5 thereafter.
850 nm),
IR-SO2 was
expressed on a relative scale as a percentage of individual calibration
under each gas condition, with 100% saturation equal to the resting
saturation in each gas condition and 0% saturation arbitrarily set to
the full-scale negative deflection used in instrument calibration. For
the sum channel (760 + 850 nm), tissue blood volume was expressed on a
relative scale as a percentage of individual calibration under each gas
condition, with 0% change in blood volume equal to the resting value
in each gas condition, and 100% increase in blood volume was equal to the full-scale negative deflection. Because the calibration was relative to rest for each gas, it was not possible to compare IR-SO2
measures between gas conditions, but correlations between IR-SO2 and
SfvO2
were possible. The results obtained with respect to tissue
SO2 were
obtained on the opposite leg from the femoral venous blood samples to
minimize interference with blood sampling.
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Statistical analysis. The main effects of gas breathing (3 levels of the variable) and time (7 levels of the variable) on the SfvO2 and arterial SO2 (SaO2) responses were analyzed by a repeated-measures two-way ANOVA because comparisons between gas-breathing conditions were possible for blood-sample data. Any significant (P < 0.05) interactions from the two-way ANOVA were further analyzed with the Student-Newman-Keuls post hoc test. Because all NIRS measures were expressed as relative values, the effects of time on IR-SO2 and changes in tissue blood volume were analyzed by a one-way ANOVA. Correlations between IR-SO2 and SfvO2 were analyzed by linear regression. The correlation coefficients (r) were determined. The level of significance for the main effects and interactions was set at P < 0.05. 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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During the incremental kicking test in hypoxia,
subjects reached a peak kicking workload of 122 ± 11 W,
which corresponded to O2 of
1,878 ± 142 ml/min and a heart rate of 150 ± 8 beats/min. The
Tvent during the incremental
kicking tests was determined to be 1,368 ± 94 ml/min (Table
1).
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SaO2 was significantly elevated in
hyperoxic gas breathing and was reduced in hypoxic gas breathing at all
time points during the test, and there was no change from rest to
exercise in normoxia and hyperoxia. The
SaO2 during the hypoxic gas-breathing
condition was lower during exercise than during rest for all time
points (Table 2). The
SfvO2 was lower
in hypoxia and higher in hyperoxia relative to normoxia at all time
points during the test. At the onset of exercise, there was a
significant decrease in
SfvO2 relative to rest by 20 s in normoxia and hypoxia and by 40 s of exercise in
hyperoxia (Table 2 and Fig. 2).
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Because of the calibration method used here, it was not possible to compare muscle IR-SO2 between gases. IR-SO2 remained constant over the 4 min of rest and decreased by 20 s after the onset of exercise in all gas-breathing conditions. In hypoxia, IR-SO2 reached a minimum value by 40 s into the exercise and remained at a lower level throughout the exercise. In hyperoxia and normoxia, IR-SO2 reached a minimum level at 40 s after the onset of exercise and increased again at 3 and 5 min (Table 2 and Fig. 2). In hyperoxia, the IR-SO2 was not different from rest by 5 min of exercise.
In all gas-breathing conditions, measurements of
IR-SO2 were
significantly correlated with
SfvO2
when considering the time period from rest to 40 s after the onset of
exercise (normoxia, r = 0.53;
hyperoxia, r = 0.57; hypoxia,
r = 0.61). If the total exercise time
period was considered, measures of
IR-SO2 were
significantly correlated with
SfvO2 in
hypoxia (r = 0.42) but not in
hyperoxia (r = 0.05) or in normoxia
(r = 0.02) (Fig.
3).
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There was a decrease in the NIRS tissue blood-volume signal at the
onset of exercise in all gas-breathing conditions. This initial
decrease was followed by an increase as the exercise continued (Table 2
and Fig. 4), so that, at 5 min, tissue
blood volume was elevated with respect to rest in normoxia and equal to
rest in hyperoxia and hypoxia.
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DISCUSSION |
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Abstract
Introduction
Methods
Results
Discussion
References
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IR-SO2 and SfvO2 both decreased at the onset of exercise in all gas-breathing conditions. After the first minute of exercise, there was a marked separation in the response of the two measures, with IR-SO2 increasing again in hyperoxia and normoxia, whereas SfvO2 continued to decrease to a plateau in all three gas-breathing conditions. These findings extend those of Costes et al. (5), who studied steady-state exercise in humans in normoxia and hypoxia, and are in contrast to validation studies in humans with ramped exercise of the forearm (10) and in animals with stimulated contractions (14).
Validity of IR-SO2. This study employed reflectance spectroscopy and, because we do not know the photon pathways, only trends in muscle SO2, not absolute changes, could be determined. Although there are limitations, this methodology has been advocated for use in physiological and clinical studies (3, 13, 14). The correlation coefficients between IR-SO2 and venous effluent SO2 obtained in this study (r = 0.53-0.61) over the transition from rest to 40 s of exercise were similar to those reported during leg exercise in humans (r = 0.55) (5) and were lower than those reported in two previous studies (r = 0.97) (14) and (r = 0.92) (10). Furthermore, when the entire exercise period was considered, the correlation coefficients dropped to only r = 0.02 and 0.05 in normoxia and hyperoxia, respectively. This indicates that SfvO2 does not account for the entire NIRS signal observed at the onset of leg exercise in humans. In both the present study and that of Costes et al. (5), leg exercise was used to evaluate the measurement of tissue SO2. It is possible that NIRS is only valid for exercise of small muscle mass, such as that used in previous validation studies (10, 14). The choice of protocol may also have influenced the results. In previous studies (10, 14), ramp protocols were employed, and good correlations between venous effluent and IR-SO2 were obtained.
The IR-SO2 signal represents a weighted average of arterial, capillary, and venous Hb SO2, as well as contributions from intracellular Mb SO2 (4). The exact proportions of these components cannot be determined. In the present study, we know that the SaO2 did not change at the onset of exercise in normoxia and hyperoxia but decreased in hypoxia. These differences in SaO2 were probably small contributors to the NIRS signal. It is possible that there were changes in the proportional contribution of arterial blood to the total sample volume. Another possible contributor to the NIRS signal is Mb SO2. On the basis of proton magnetic resonance spectroscopy to determine Mb SO2, Chance et al. (3) extrapolated from dog studies to suggest that a maximum of 25% of the NIRS signal comes from Mb, with the balance from Hb. A subsequent study by Mancini et al. (10) reported very little Mb desaturation in humans until maximal exercise. In contrast, Richardson et al. (12) observed 50-60% Mb desaturation at only 50% of maximalO2. Bellardini et
al. (1) suggested that
O2 desaturation, measured with
NIRS, was caused by loss of O2
from Hb (for steady-state exercise below the lactate threshold) and was
caused by O2 loss from Mb (for exercise above the lactate threshold). In the present study,
subjects were working at or below their
Tvent by the end of 6 min of
kicking exercise in each gas condition (Table 1). On the basis of these previous investigations, Mb O2
desaturation would not be expected to have a major influence on
IR-SO2
signal changes. However, the possibility of Mb desaturation at the
onset of exercise has not been previously examined. The transient
decline in
IR-SO2 for normoxia and hyperoxia could represent a reduction in Mb
SO2 at the
onset of exercise.
It is possible that the venous blood sampled in this study did not
accurately represent exercising muscle
SO2 because
of contamination by blood originating from nonexercising tissues.
SfvO2
represents the sum of all blood returning from the exercising leg,
whereas the NIRS signal originates in the exercising muscle only (3). In previous studies which have shown a significant correlation between
IR-SO2 and
venous SO2,
the venous effluent was obtained from a deep forearm vein that drained
the exercising muscle (10) and from a vein that drained only the
electrically simulated muscle of dogs (14). In both the present study
and the work of Costes et al. (5), the venous effluent
was obtained in the femoral vein. The
SfvO2 showed a
decrease in saturation to a plateau in all gas conditions, and
contamination from nonexercising muscle would be expected to increase,
not decrease, the
SO2 of the
effluent blood. For this reason, we conclude that
SfvO2
accurately represented the venous
SO2 in the
exercising muscle in the present experiments, and we cannot account for
the differences in temporal responses of
SfvO2 and
IR-SO2 at
the onset of exercise in different gas-breathing conditions.
The type of exercise used in the present study may have influenced the
results.
IR-SO2 and
venous blood samples were obtained from opposite legs, and it is
possible that there was a systematic difference in the
O2 availability in the two legs.
However, this is highly unlikely, because the subjects had practiced
the kicking exercise, and feedback was provided to maintain kicking
frequency and work by both exercising legs.
Hypoxia vs. normoxia and hyperoxia. In hypoxia, IR-SO2 was significantly correlated with SfvO2 at all time points, whereas this correlation was only significant during rest and the initial onset of exercise in hyperoxia and normoxia (Table 2 and Fig. 3). These differences in correlation observed in hypoxia vs. normoxia and hyperoxia could be caused by several factors. It is possible that there was a systematic error in the placement and operation of the probe in different gas-breathing conditions. However, the order of the trials was randomized, and all were performed on the same day, with no movement of the probe between trials. Therefore, it is very unlikely that such an error could account for the observed differences between gas conditions.
Changes in tissue blood volume monitored via NIRS in this study indicate that, at the onset of exercise, there is a transient decrease in tissue blood volume, which reached significance in hyperoxia. This decrease was followed by increases over time to result in tissue blood volume greater than that at rest at end exercise in normoxia and equal to that at rest in hypoxia and hyperoxia. These changes in the tissue blood volume signal were observed in all gas-breathing conditions. They may represent a redistribution of blood in the exercising leg, with expulsion of blood by the muscle pump early in exercise and a progressive increase in volume as capillary beds open and vascular units are recruited. Alternatively, changes in penetration depth or muscle geometry at the onset of exercise could have contributed to the signal. However, observation of these trends in all gas-breathing conditions suggests that changes in blood volume cannot explain the differences in correlation observed between IR-SO2 and SfvO2 in the gas conditions. Variations in skin or muscle blood flow may have contributed to the different correlations observed in different gas conditions. However, skin blood flow did not influence the NIRS difference signal in previous research (7, 10). In a previous study by Costes et al. (5), a gradual drift toward reoxygenation was also observed in normoxic but not hypoxic exercise, and it was postulated that differences in blood flow might account for the variability of results in different gas-breathing conditions. In the present study, total LBF was measured simultaneously with NIRS measurements via Doppler ultrasound technology, and it was determined that the LBF increased similarly at exercise onset in all conditions; therefore, LBF cannot explain the IR-SO2 signal differences observed here. Measured steady-state blood flows to one leg, 40 s after the onset of exercise in normoxia (3,105 ± 195 ml/min), hypoxia (3,005 ± 295 ml/min), and hyperoxia (3,025 ± 210 ml/min), and at the end of exercise in normoxia (3,720 ± 197 ml/min), hypoxia (4,011 ± 262 ml/min), and hyperoxia (3,728 ± 223 ml/min), were not different among gas-breathing conditions. Whether Mb desaturation in the hypoxic tests contributes to the NIRS signal has not been previously examined. There have been reports from tests in normoxia that the Mb O2 contribution to the total NIRS signal is small, at least until very heavy exercise (3, 10). However, Richardson et al. (12) found 51% Mb desaturation in normoxia and 60% in hypoxia at moderate workloads. The pattern of decline followed by recovery of the IR-SO2 signal toward resting levels in the normoxic and hyperoxic tests might indicate a desaturation of Mb O2 at the onset of exercise, followed by reoxygenation in the steady-state exercise, with no detectable change in venous effluent SO2. In hypoxia, the lowered exercise arterial oxygenation might have prevented this reoxygenation, but the observations of Richardson et al. (12) in normoxia and hypoxia make this explanation unlikely.Conclusions. In this study, there were systematic differences in both normoxia and hyperoxia in the temporal relationships for estimates of tissue oxygenation obtained from direct venous sampling (SfvO2) and from indirect NIRS (IR-SO2). None of the potential technical limitations that we considered seems likely to have contributed to the temporal patterns or to differences between gas-breathing conditions. Rather, we are left with the conclusion that NIRS does not provide an accurate assessment of venous blood oxygenation during leg exercise, at least when arterial PO2 is at normal or elevated levels. Even in hypoxia, the correlation was low. Further determinations of tissue Mb O2 saturation at the onset of exercise are necessary to validate the use of NIRS for this purpose and to determine the role of O2 availability at the onset of large muscle mass exercise.
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ACKNOWLEDGEMENTS |
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We thank the subjects who participated in the study. Excellent technical support was provided by D. Northey, S. M. Phillips, H. Naylor, M. Chambers, S. M. Grant, B. Roy, M. E. Tschakovsky, and S. Jiroutek.
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FOOTNOTES |
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This work was supported by the Natural Science and Engineering Council of Canada. M. MacDonald was a recipient of an National Sciences and Engineering Research Council Postgraduate Scholarship and an Ontario Graduate Scholarship.
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
Address for reprint requests: R. L. Hughson, Dept. of Kinesiology, Univ. of Waterloo, Waterloo, Ontario, Canada N2L 3G1 (E-mail: hughson{at}healthy.uwaterloo.ca).
Received 9 April 1998; accepted in final form 6 November 1998.
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Top
Abstract
Introduction
Methods
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Discussion
References
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), hyperoxia (
), and hypoxia (
). Values are means ± SE for 6 subjects. Time 0, start
of exercise.