J Appl Physiol 92: 162–168, 2002;
10.1152/japplphysiol.00409.2001.
Validity of pulse oximetry during maximal exercise
in normoxia, hypoxia, and hyperoxia
YOSHIKI YAMAYA, HARM J. BOGAARD, PETER D. WAGNER,
KYUICHI NIIZEKI, AND SUSAN R. HOPKINS
Department of Medicine, University of California, San Diego, La Jolla, California 92093
Received 27 April 2001; accepted in final form 29 August 2001
Yamaya, Yoshiki, Harm J. Bogaard, Peter D. Wag-
ner, Kyuichi Niizeki, and Susan R. Hopkins. Validity
of pulse oximetry during maximal exercise in normoxia,
hypoxia, and hyperoxia. J Appl Physiol 92: 162–168, 2002;
10.1152/japplphysiol.00409.2001.—During exercise, pulse
oximetry is problematic due to motion artifact and altered
digital perfusion. New pulse oximeter technology addresses
these issues and may offer improved performance. We simul-
taneously compared Nellcor N-395 (Oxismart XLTM) pulse
oximeters with an RS-10 forehead sensor (RS-10), a D-25
digit sensor (D-25), and the Ivy 2000 (Masimo SETTM)/
LNOP-Adt digit sensor (Ivy) to arterial blood oxygen satura-
tion (SaO2) by cooximetry. Nine normal subjects, six athletes,
and four patients with chronic disease exercised to maximum
oxygen consumption (V̇O2 max) under various conditions [nor-
moxia, hypoxia inspired oxygen fraction (FIO2) ⫽ 0.125; hy-
peroxia, FIO2 ⫽ 1.0]. Regression analysis for normoxia and
hypoxic data was performed (n ⫽ 161 observations, SaO2 ⫽
73–99.9%), and bias (B) and precision (P) were calculated.
RS10 offered greater validity than the other two devices
tested (y ⫽ 1.009x ⫺ 0.52, R2 ⫽ 0.90, B⫾P ⫽ 0.3 ⫾ 2.5).
Finger sensors had low precision and a significant negative
bias (D-25: y ⫽ 1.004x ⫺ 2.327, R2 ⫽ 0.52, B⫾P ⫽ ⫺2.0 ⫾ 7.3;
Ivy: y ⫽ 1.237x ⫺ 24.2, R2 ⫽ 0.78, B⫾P ⫽ ⫺2.0 ⫾ 5.2).
Eliminating measurements in which heart rate differed by
⬎10 beats/min from the electrocardiogram value improved
precision minimally and did not affect bias substantially
(B⫾P ⫽ 0.5 ⫾ 2.0, ⫺1.8 ⫾ 8.4, and ⫺1.25⫾4.33 for RS-10,
D-25, and Ivy, respectively). Signal detection algorithms and
pulse oximeter were identical between RS-10 and D-25; thus
the improved performance of the forehead sensor is likely
because of sensor location. RS-10 should be considered for
exercise testing in which pulse oximetry is desirable.
oxygen saturation; cooximetry; patients; normal subjects;
athletes
DURING EXERCISE TESTING, it is often desirable to monitor
arterial oxygen saturation of hemoglobin (SaO2), espe-
cially in the context of pulmonary or cardiovascular
disease or when subjects are breathing hypoxic gas
mixtures as part of research protocols. Pulse oxime-
ters, because they are noninvasive and obviate the
need for arterial catheterization, are often used in this
context. In addition, many researchers investigating
pulmonary gas exchange during exercise utilize pulse
Address for reprint requests and other correspondence: S. R. Hop-
kins, Univ. of California, San Diego, Dept. of Medicine-0623, 9500
Gilman Dr., La Jolla, CA 92093-0623 (E-mail: shopkins@ucsd.edu).
162 8750-7587/02 $5.00 Copyright © 2002 the American Physiological Society
Downloaded from journals.physiology.org/journal/jappl (190.014.071.009) on August 7, 2020.
oximetry either to prescreen research subjects before
more invasive studies or in place of direct measure-
ment of SaO2 using cooximetry (3, 7, 8, 11).
Pulse oximeters use a light source and photodiode
light detector to measure the amount of light passing
through an arteriolar bed. SaO2 can be estimated non-
invasively because the light-absorbing characteristics
of hemoglobin differ between oxyhemoglobin and de-
oxyhemoglobin. Although well accepted for use in rest-
ing subjects, using pulse oximetry during exercise for
accurate measurement of SaO2 has been problematic
for several reasons. First, depending on the sensor site,
sensors are subjected to varying degrees of motion
resulting in signal corruption and thus inaccurate es-
timations of saturation (9). Furthermore, sensors
placed on the digits are even more susceptible to this
problem during cycle exercise because gripping the
handlebars results in weakening or even complete loss
of signals (17, 19). Recently developed pulse oximeters
offer potential advantages because they utilize ad-
vanced signal-processing methodologies in an attempt
to provide continuous and accurate measurements of
oxygen saturation when signals are weak (e.g., low
perfusion) or corrupted by motion artifact (1, 2, 15).
The purpose of this study was to evaluate new pulse
oximeter technologies during exercise in a variety of
study populations. We tested two devices: the Ivy 2000
(Masimo, Irvine, CA) with the LNOP-Adt finger sensor
and two Nellcor N-395 (Oxismart XL, Mallinckrodt, St.
Louis, MO) pulse oximeters equipped with either a
RS-10 forehead sensor or a D-25 digit sensor. These
devices were used in normal subjects, athletes, and
patients with either chronic obstructive pulmonary dis-
ease or chronic heart failure. We hypothesized that the
combination of motion-tolerant pulse oximeter and
RS-10 forehead sensor, because of the previously men-
tioned problems with motion artifact and digital per-
fusion during exercise, would provide the most valid
noninvasive measure of SaO2. We chose to compare
athletes and patients with normal subjects because
monitoring SaO2 in these two groups is likely to be
problematic for the athletes because of poor signal
detection caused by the diversion of large amounts of
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.
http://www.jap.org
 PULSE OXIMETRY DURING EXERCISE 163

Table 1. Subject descriptive characteristics The order of the two exercise tests was balanced in group 1,
and subjects rested for ⬃1 h between tests.
Group 1 Group 2 Group 3 Results of these preliminary tests were used to select
(n ⫽ 9) (n ⫽ 6) (n ⫽ 4) workloads that represented 30, 60, 90, and 100% of V̇O2 max in
Age 33.5 ⫾ 6.8 28.8 ⫾ 5.8 56.7 ⫾ 16.6*
Height, cm 171.0 ⫾ 3.8†‡ 173.7 ⫾ 3.9 179.7 ⫾ 9.6
Weight, kg 68.9 ⫾ 8.2 70.3 ⫾ 3.9 95.8 ⫾ 21.2*
Normoxic V̇O2 max,
l/min 3.13 ⫾ 0.56 4.12 ⫾ 0.34† 1.83 ⫾ 0.75*
Normoxic V̇O2 max,
ml 䡠 kg⫺1 䡠 min⫺1 45.6 ⫾ 8.2 58.7 ⫾ 4.0† 18.8 ⫾ 5.1*
Hypoxic (FIO2 ⫽ 0.12)
V̇O2 max, l/min 2.59 ⫾ 0.47
Hypoxic V̇O2 max,
ml 䡠 kg⫺1 䡠 min⫺1 37.2 ⫾ 6.4
Values are means ⫾ SE. V̇O2 max, maximal oxygen consumption;
FIO2, inspired oxygen fraction. * Significantly different from group 1
and 2 (P ⬍ 0.05). † Significantly different from group 1 (P ⬍ 0.05).
‡ Significantly different from group 3 (P ⬍ 0.05).

blood to working muscles during high-intensity exer-

cise and for the patients because of a potential circu-
latory compromise caused by chronic disease.
METHODS

This study was approved by the Human Subjects Commit-

tee of the University of California, San Diego. Nineteen
subjects were recruited by advertisement and, after giving
written informed consent, agreed to further study. Subjects
belonged to one of the following three groups. Group 1 was
healthy active nonsmoking adults (n ⫽ 9), group 2 was
healthy nonsmoking competitive cyclists (n ⫽ 6), and group 3
(n ⫽ 4) was patients with either chronic heart failure or
chronic obstructive pulmonary disease.
Preliminary screening. A screening history and physical
examination was performed, and female subjects were screened
for pregnancy. Maximal oxygen consumption (V̇O2 max) was
determined on an electronically braked cycle ergometer (Ex-
caliber, Quinton Instruments, Gronigen, Netherlands). After
a 5-min warm up at 25–100 W, groups 1 and 2 rode a
progressive exercise test (25–30 W/min) until they were
unable to continue. Group 3 protocol was similar except that
the work rate increment was 10–20 W/min. Heart rate was
monitored by cardiac monitor (Lifepak 6, Physio-control,
Redmond, WA). Subjects breathed through a nonrebreathing
valve (2700, Hans-Rudolph, Kansas City, MO). Expired gas
was sampled continuously from a heated mixing chamber,
and oxygen and carbon dioxide concentrations were mea-
sured (mass spectrometer-1100, Perkin-Elmer, Pomona, CA).
Expired gas flow was measured by using a pneumotach (no.
3 Fleisch) and differential pressure transducer (Validyne,
DP45-14, Northridge, CA), and electrical signals from the
mass spectrometer and pneumotach were logged at 100 Hz Fig. 1. Relationship of arterial oxygen saturation (SaO2) measured
by using a 12-bit analog-to-digital converter. Ventilation (V̇E) by pulse oximetry using the N-395/RS-10 (A), the N-395/D-25 (B),
oxygen consumption (V̇O2) and carbon dioxide production and the Ivy 2000 (C) devices compared with SaO2 measured by
(V̇CO2) were calculated by using a commercially available cooximetry. ■, Data points in which adequate pulse-rate signal
software package (Consentius Technologies, Salt Lake, UT). detection was present [heart rate measured by the device was within
V̇O2 max was calculated as the average of the four highest 10 beats/min of that measured by electrocardiogram (ECG)]; E, data
consecutive 15-s measurements of V̇O2. points in which adequate pulse-rate signal detection was not present
(heart rate measured by the device was ⱖ10 beats/min different from
All subjects fulfilled at least two of the following four
that measured by ECG). Solid lines are the lines of identity; small
criteria for V̇O2 max: 1) heart rate ⱖ age predicted maximum; dotted lines are the regression lines for all data points; large dotted
2) respiratory exchange ratio ⬎ 1.10; 3) no further increase or lines are the ⫾95% prediction limits for the regression equation (see
a decrease in V̇O2 with increasing workload; and 4) no further text for details) for all data points. Regression equations for all points
increase in heart rate despite an increase in workload. Group are y ⫽ 1.009x ⫺ 0.52 (for N-325/RS-10); y ⫽ 1.004x ⫺ 2.327 (for
1 also underwent a similar protocol, breathing 12% oxygen. N-395/D-25); y ⫽ 1.237x ⫺ 24.2 (for IVY 2000).

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164 PULSE OXIMETRY DURING EXERCISE
groups 1 and 2, and 25, 50, 75, 90, and 100% of V̇O2 max in
group 3.
Subject preparation. Under continuous electrocardiogram
(ECG) monitoring (Lifepak 6), a 20-gauge arterial cannula
was placed in the radial artery of the nondominant hand by
using a sterile technique. We followed the instruction as
supplied by the manufacturer, attaching the Ivy 2000 with
Masimo’s LNOP-Adt sensor and the Nellcor N-395 with the
D-25 digit sensor (N-395/D-25) to the digits of opposite
hands. A light-opaque shield was lightly taped over the digit
to exclude interfering ambient light. Digit placement (digits
2, 3, and 4) and hand selection (right or left) were randomized
between subjects. The Nellcor N-395 with a RS-10 forehead
sensor (N-395/RS-10) was positioned over the left eyebrow on
the forehead and secured with a terrycloth sweatband.
Data collection protocol. Each subject was seated on the
cycle ergometer and breathed through the mouthpiece for 10
min before the start of resting measurements. Data collection
consisted of duplicate 3-ml samples of arterial blood, which
were collected at rest and in the last 2 min of each exercise
level (30, 60, 90, and, in some subjects, 100% of V̇O2 max in
groups 1 and 2 and 25, 50, 75, and, in some subjects, 90–
100% of V̇O2 max in group 3). Group 1 performed the exercise
protocol in normoxia and while breathing hypoxic gas (in-
spired oxygen fraction ⫽ 0.12), group 2 exercised in normoxia
only, and group 3 exercised in both normoxia and 100%
oxygen. SaO2 by pulse oximetry was obtained by interfacing
the three devices with a portable computer and recording
data over a 30-s period simultaneously from all three devices
and synchronously with arterial blood sampling. Data in
which poor signal detection was evident (heart rate deviated
10 or more beats/min from that measured by ECG) were
identified so that analyses could be conducted with and
without these data points.
Blood-gas measurements. Arterial samples were main-
tained on ice until analyzed for hemoglobin concentration
and SaO2 using an IL 682 cooximeter (Instrumentation Lab-
oratories, Lexington, MA). Blood gas analyses were com-
pleted within 30 min of data collection. SaO2 was measured as
FO2Hb
Sa O2 ⫽ 100 ⫻
100 ⫺ 共FCOHb ⫹ FmetHb兲
where FO2Hb is the oxyhemoglobin fraction, FCOHb is the
carboxyhemoglobin fraction, and FmetHb is the methemoglo-
bin fraction.
Statistical analyses. We compared measured SaO2 by
cooximetry to each of the pulse oximeters by using linear
regression (Statview 5.0, SAS, Cary, NC). Prediction limits of
⫾95% for the prediction of SaO2 by pulse oximeter as a
function of measured SaO2 were generated for each device.
Table 2. Bias and precision of SaO2 measurement by subject group and pulse oximeter
Group 1
(Normal Subjects)
N-395/RS-10 forehead 0.4 ⫾ 3.0a,b
(n ⫽ 90)
N-395/D-25 finger ⫺1.4 ⫾ 7.9
(n ⫽ 90)
Ivy 2000 finger ⫺2.2 ⫾ 4.9
(n ⫽ 89)
Average across devices ⫺1.1 ⫾ 5.7
(n ⫽ 269)
Values are means of bias ⫾ precision (SD); n, number of observations. a Significantly different from Ivy 2000 finger (P ⬍ 0.05).
b
Significantly different from N-395/D-25 finger (P ⬍ 0.05). c Significantly different from groups 1 and 2 (P ⬍ 0.05). d Significantly different
from group 1 (P ⬍ 0.05). e Significantly different from group 3 (P ⬍ 0.05).
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The ⫾95% prediction limits can be thought of as the ⫾2 SD
limits of the least squares regression line at any point along
the regression. To examine the effect of poor signal detection,
heart rate by ECG was compared with heart rate by pulse
oximetry, and separate regression analyses were performed
after eliminating all SaO2 data in which the simultaneously
obtained heart rate deviated by ⱖ10 beats/min from that
measured by ECG. In addition, data obtained while breath-
ing 100% oxygen are on the flat part of the oxyhemoglobin
equilibrium curve. These data were not included as part of
the regression analyses and were analyzed separately. Bias
[or mean error; calculated as (SaO2 pulse-oximetry ⫺ SaO2
cooximetry)/n⫺1] and precision (SD of SaO2 pulse-oximetry ⫺
SaO2 cooximetry; the smaller the SD, the greater the preci-
sion) were calculated for each device. As for the regression
analyses, these parameters were calculated for all data
points and also after eliminating data points in which there
were poor pulse rate signal detections. Significance was ac-
cepted at P ⬍ 0.05, two-tailed. Data are presented as
means ⫾ SD.
RESULTS
Subject descriptive data are given in Table 1. As
expected, athletes had a greater V̇O2 max than healthy
normal subjects (group 1; P ⬍ 0.005) or patients (group
2; P ⬍ 0.0001). Patients were significantly older and
heavier than either the athletes (P ⬍ 0.001) or the
healthy normal subjects (P ⬍ 0.001).
SaO2 measured by pulse oximetry during exercise in
normoxia and hypoxia is compared with results ob-
tained by direct arterial blood measurements in Fig. 1
and Table 2. Figure 1 shows the correlation between
SaO2 measured by cooximetry and by pulse oximetry for
each device for all subjects. All three devices showed
significant correlations between cooximetry and pulse
oximetry values. However, there were considerable dif-
ferences between devices. The N-395/RS-10 forehead
SaO2 (Fig. 2A) was very highly correlated with SaO2
measured by using cooximetry (R2 ⫽ 0.90, P ⬍ 0.0001),
and values obtained were centered around the line of
identity (slope ⫽ 1.009, intercept ⫽ ⫺0.52). Poor pulse-
rate or arterial signal detection was evident in 13
(8.1%) measurements of SaO2 and, when these data
were eliminated, R2 increased to 0.94, although slope
and intercept of the relationship did not change appre-
ciably (slope ⫽ 0.998, intercept ⫽ 0.65).
Group 2 Group 3 Average
(Athletes) (Patients) Across Groups
⫺0.3 ⫾ 1.5b,d,e 1.1 ⫾ 1.1a,b 0.3 ⫾ 2.5a,b
(n ⫽ 41) (n ⫽ 30) (n ⫽ 161)
⫺3.1 ⫾ 7.1 ⫺2.1 ⫾ 5.2 ⫺2.0 ⫾ 7.3
(n ⫽ 38) (n ⫽ 29) (n ⫽ 157)
⫺0.4 ⫾ 4.1b ⫺3.8 ⫾ 6.9c ⫺2.0 ⫾ 5.2
(n ⫽ 41) (n ⫽ 30) (n ⫽ 160)
⫺1.3 ⫾ 5.0 ⫺1.6 ⫾ 5.4
(n ⫽ 120) (n ⫽ 89)
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 PULSE OXIMETRY DURING EXERCISE
Fig. 2. Bias and precision of SaO2 measured by pulse oximetry using
the N-395/RS-10 (A), the N-395/D-25 (B), and the Ivy 2000 (C)
devices compared with SaO2 measured by cooximetry. ■, Data points
in which adequate pulse-rate signal detection was present (heart
rate measured by the device was within 10 beats/min of that mea-
sured by ECG); E, data points in which adequate pulse-rate signal
detection was not present (heart rate measured by the device was
ⱖ10 beats/min different from that measured by ECG). Solid lines are
the lines of identity; fine dotted lines are the regression lines for all
data points.
Correlation for the Ivy 2000 finger sensor was not as
close (Fig. 2B; R2 ⫽ 0.78, P ⬍ 0.0001), and there was a
tendency for the device to underestimate SaO2, partic-
ularly under hypoxic conditions, (slope ⫽ 1.23, inter-
cept ⫽ ⫺24.2). Many of the measurements suffered
from poor pulse-rate signal detection (76 measure-
ments; 48.4%), and eliminating these measurements
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165
increased R2 to 0.87. However, even with this modifi-
cation, slope of the relationship was unchanged (1.20)
and intercept was still markedly negative (⫺19.9).
Thus adequate pulse-rate signal detection does not
prevent the problem of underestimating SaO2 in this
device.
The N-395/D-25 finger sensor utilized the same pulse
oximeter tested for the N-395/RS-10 but provided data
that were much less closely correlated with SaO2 mea-
sured by cooximetry (Fig. 2C; R2 ⫽ 0.52, P ⬍ 0.0001).
Although the N-395/D-25 finger sensor underesti-
mated SaO2 at all levels, measurements were not
greater during hypoxia than during normoxia (slope ⫽
1.004, intercept ⫽⫺2.32). Poor pulse-rate signal detec-
tion was present in 43 (26.9%) measurements, and
removal of these data from the regression improved the
strength of the relationship substantially (R2 ⫽ 0.87)
but did not significantly alter slope and intercept of the
relationship (1.04 and ⫺3.30, respectively).
Bias and precision of the SaO2 measurement from the
three devices compared with the cooximeter are given
in Table 2 and Fig. 2. Averaged over all subjects, the
N-395/RS-10 forehead device had significantly lower
bias and greater precision than the two finger probes
(precision ⫽ 2.5 for N-395/RS-10 vs. 5.2 and 7.3 for IVY
2000 and N-395/D-25, respectively). Eliminating data
points with poor pulse-rate signal detection had a min-
imal effect on these values (precision ⫽ 2.0 for N-395/
RS-10 vs. 4.3 and 8.4 for IVY 2000 and N-395/D-25,
respectively). The N-395/D-25 and N-395/RS-10 per-
formed similarly in all three subject groups, although
there were minor differences between athletes and
patients for the N-395/RS-10. However, the IVY 2000
was significantly worse in group 3 compared with ath-
letes and normal subjects.
Bias and precision SaO2 data from patients exercis-
ing in 100% oxygen are presented in Table 3. In this
data set, SaO2 approaches 100% [all partial pressure of
oxygen (PaO2) values were ⬎500 Torr]. This approach
essentially eliminates any variation in the indepen-
dent variable (i.e., SaO2 measured by cooximetry).
Therefore, any deviation of SaO2 measured by the three
devices is related to issues such as perfusion and/or
signal detection. Under these conditions, the N-395/
RS-10 forehead sensor had significantly less bias and
greater precision than the other two devices (P ⬍ 0.05).
Bias and precision of the heart rate data, which can
be used as an index of the adequacy of pulse-rate signal
detection for the different devices, are presented in
Table 4. Averaged across all subject groups, there were
significant differences between devices. The N-395/
RS-10 had significantly less bias and greater precision
of heart rate measurements compared with the other
two devices (P ⬍ 0.001), and the N-395/D-25 demon-
strated significantly less bias compared with the Ivy
2000 (P ⬍ 0.001). There were no significant differences
between subject groups for the N-395/RS-10. Both the
N-395/D-25 and Ivy 2000 significantly underestimated
the heart rate compared with the ECG measure of
heart rate. There were no significant differences in bias
between subject groups for the N-395/D-25, but the Ivy
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166 PULSE OXIMETRY DURING EXERCISE
Table 3. Bias and precision by pulse oximeter
in hyperoxia
N-395/RS-10 forehead ⫺0.24 ⫾ 0.57
(n ⫽ 27)
N-395/D-25 finger ⫺4.48 ⫾ 6.29
(n ⫽ 26)
Ivy 2000 finger ⫺5.20 ⫾ 11.11
(n ⫽ 24)
Values are means of bias ⫾ precision (SD) for group 3 only.
2000 had significantly greater bias in the athletes than
in the other two subject groups.
DISCUSSION
The N-395/RS-10 offered greater validity of SaO2 and
heart rate measurements under all conditions (nor-
moxia, hypoxia, hyperoxia) and in all subject groups
(normal subjects, athletes, patients) than the other two
devices tested. This is reflected by a higher correlation
between SaO2 measured by this device and that mea-
sured by cooximetry, a smaller ⫾95% prediction limit,
less bias, greater precision, and fewer data points with
poor pulse-rate signal detection. This is likely due to
the position of the sensor, because the identical pulse
oximeter equipped with a digital sensor (N-395/D-25)
performed substantially worse than both the forehead
sensor and the IVY 2000 pulse oximeter equipped with
a finger sensor. In general, the N-395/RS-10 performed
similarly in all three subject groups, as did the N-395/
D-25, albeit with more bias and less precision than the
N-395/RS-10. However, the Ivy 2000 performed signif-
icantly worse in the measurement of SaO2 in the pa-
tients we studied than it did in the normal subjects or
athletes.
There have been many validation studies of pulse
oximetry during exercise over the last 20 years, with
widely varying conclusions offered on the part of the
authors. For example, Powers et al. (10) tested three
devices (two finger sensors and one ear sensor) and
found standard error of estimates (SEE; numerically
similar to precision) ranging from 1.43 to 1.97%, simi-
lar to values we found with the N-395/RS-10 forehead
sensor. These authors concluded that the accuracy of
pulse oximetry was sufficient for use during exercise
testing. However, Symth et al. (14) found a SEE of 4.08
Table 4. Bias and precision of heart rate measurement by subject group and pulse oximeter
Group 1
(Normal Subjects)
N-395/RS-10 forehead ⫺2.9 ⫾ 13.0*†
(n ⫽ 90)
N-395/D-25 finger ⫺13.9 ⫾ 33.6
(n ⫽ 90)
Ivy 2000 finger ⫺20.5 ⫾ 33.6
(n ⫽ 90)
Average across devices ⫺12.5 ⫾ 29.3
(n ⫽ 270)
Values are means of bias ⫾ precision (SD). n, Number of observations. * Significantly different from Ivy 2000 finger (P ⬍ 0.05).
† Significantly different from N-395/D-25 finger (P ⬍ 0.05). ‡ Significantly different from group 1 (P ⬍ 0.01). § Significantly different from
group 3 (P ⬍ 0.01).
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and 5.39% in the two devices they evaluated during
exercise in normoxia and hypoxia (one pulse oximeter
equipped with an ear probe and the HP 47201A ear
oximeter, which analyzes light from eight wave-
lengths).
Exercise induces potential problems related to the
accuracy of pulse oximetry. For example, motion arti-
fact can interfere with arterial signal detection, and
new generation pulse oximeters such as the Masimo
Ivy 2000 and the Nellcor Oxismart incorporate ad-
vanced signal processing to deal with nonstandard
signal detection (1, 2, 15). In addition, poor perfusion
states, such as those that occur with cool skin temper-
ature, may induce significant bias (18). However, as
can be appreciated from Figs. 1 and 2, significant
measurement errors occurred even when adequate
pulse-rate signal detection was evident. Conversely,
especially with the N-395/RS-10, many data points
with poor pulse-rate signal detection still provided
reliable data. Thus this criterion alone cannot be used
to judge the quality of the data obtained by using these
devices. An estimate of the extent that a particular
device underestimates SaO2 may be obtained by the
administration of several breaths of hyperoxic gas mix-
tures (inspired oxygen fraction ⫽ 0.5–1.0) in the final
few seconds of an exercise test. This will elevate SaO2 to
⬃100%, and any systematic bias by the device will
become apparent. As can be seen in Table 3, the two
devices using finger probes substantially underesti-
mated SaO2 in patients breathing 100% oxygen by an
average of ⬃5%, which was similar to their perfor-
mance compared with cooximetry during normoxia.
We wish to emphasize that our conclusions are
strongly influenced by the setting in which the device
was used. Clearly, pulse oximeters offer several advan-
tages in the clinical setting. These devices are nonin-
vasive, easy to use, and do not require significant
analysis time or maintenance of other equipment to
obtain data. In addition, the nature of the bias of the
devices we tested is such that, when significant errors
are present, the tendency is toward underestimating
the true SaO2. Consequently, pulse oximetry offers a
conservative estimate of SaO2 during clinical exer-
cise testing and thus is likely suitable for safety
monitoring.
Group 2 Group 3 Average
(Athletes) (Patients) Across Groups
1.8 ⫾ 5.5*† 1.2 ⫾ 1.9*† ⫺0.8 ⫾ 9.8*†
(n ⫽ 30) (n ⫽ 56) (n ⫽ 176)
⫺23.4 ⫾ 37.0 ⫺18.0 ⫾ 36.1 ⫺16.9 ⫾ 35.0
(n ⫽ 30) (n ⫽ 56) (n ⫽ 176)
⫺49.9 ⫾ 41†‡§ ⫺33.1 ⫾ 29.6†‡ ⫺29.5 ⫾ 35.4†
(n ⫽ 30) (n ⫽ 56) (n ⫽ 176)
⫺23.8 ⫾ 38.4‡ ⫺16.6 ⫾ 30.3
(n ⫽ 90) (n ⫽ 168)
92 • JANUARY 2002 • www.jap.org
 PULSE OXIMETRY DURING EXERCISE
In addition to concerns related to accuracy during
exercise, which we have briefly outlined, there are
other issues to consider, such as sensor location. Finger
sensors may be easier to place and to maintain in
position in some patients. The forehead sensor offers a
potential advantage in that it avoids the digits and the
severe effects caused by gripping and motion. Also, the
forehead site may be better than the earlobe, as signals
are usually greater and the sensor can be easily se-
cured and held in place with the addition of a head-
band. However, the signal obtained from forehead sen-
sors is susceptible to contamination from venous blood
and consequently will be biased toward low readings if
central venous pressure is raised (12, 16). This was not
observed in the present study, even in patients with
heart failure. However, it may be more of a problem
with certain types of exercise, such as rowing, in which
a Valsalva maneuver is performed at the start of the
stroke. However, this may in part be prevented by the
use of a compressive headband, such as the one used in
the present study (4). The forehead sensor location may
also interfere with secure placement of some types of
headsets that support respiratory mouth pieces and
vice versa. Finally, in one of our subjects in one in-
stance, poor arterial signal acquisition occurred when
the subject altered his facial expression during maxi-
mal exercise. This was accompanied by a loss of the
pulse-rate signal and a markedly erroneous data point.
As can been seen from Fig. 1, a similarly erroneous
data point also occurred with no obvious loss of pulse-
rate signal, and it is not possible, post facto, to deter-
mine the source of this error. Potential users of these
devices should also should be aware that significant
differences in the time to detect the onset of hypoxia
have been reported with different sensor locations (6).
Because we tested healthy subjects and patients who
were ambulatory and able to complete an exercise test,
we cannot extend our findings to clinical situations
other than exercise testing. It is possible that some
devices using an ear sensor may offer similar perfor-
mance to the forehead sensor, as these might be less
susceptible to motion artifact and poor perfusion than
finger sensors. However, because we did not test any
ear sensors, we cannot comment on their performance.
When precise measurement of oxygen transport is
important, such as in answering research questions,
measurement of SaO2 alone is probably not adequate,
particularly during normoxic exercise, in which rela-
tively small changes in SaO2 are associated with large
differences in PaO2. For example, although the mean
bias for the N-395/RS-10 for all patient groups was
0.3% SaO2, the precision was ⫾2.5% SaO2. With the use
of a standard oxyhemoglobin equilibrium curve at a pH
of 7.4, a PaO2 of 40 Torr and a temperature of 37°C,
⫾2.5% SaO2 encompasses a variation of almost 40 Torr
in PaO2, assuming a normal resting PaO2 of 90 Torr.
(13). Additionally, during exercise in which SaO2 is also
affected by temperature and pH, typical changes ob-
served in maximal exercise, such as a reduction in pH
from 7.4 to 7.2 and an increase in the temperature from
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167
37 to 39.5°C, result in a ⬃4% decrement in SaO2 in the
absence of any change in PaO2.
Recently, Dempsey and Wagner (5) have offered a
standardized definition of mild exercise-induced arte-
rial hypoxemia as a fall in SaO2 to below 95% from a
normal resting value of 98%. This value is very close to
the precision of the most accurate device tested (N-395/
RS-10) and for the two finger-probe devices, both of
which had an average bias of ⫺2.0%. Many data points
could be expected to fit this definition on the basis of
nonrandom measurement error alone. Ideally, if cir-
cumstances dictated the use of pulse oximetry, it would
be desirable to validate the pulse oximetry device
against direct measures on arterial blood in a repre-
sentative sample of the study population.
In conclusion, the N-395/RS-10 forehead sensor of-
fered greater validity of SaO2 measurements under all
conditions and in all subject groups than the other two
digital oximeters tested. Bias was negligible, however,
and precision was ⫾2.5%. Both finger sensors showed
significant negative bias and underestimated SaO2 dur-
ing exercise. They also showed low precision (⬎5%).
Eliminating data points with poor pulse-rate signal
acquisition, as evidenced by an error in heart rate
measurement, did not substantially improve the per-
formance of these devices.
We would like to thank our subjects for their enthusiastic partic-
ipation and Harrieth Wagner, Nick Busan, and Jeff Struthers for
technical assistance.
This study was supported by National Center for Research Re-
sources Grant MO1 RR-00827, National Heart, Lung, and Blood
Institute Grant HL-17731, and Mallinckrodt.
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