Janet A. DiPietro
Department of Population and
Health Sciences
Johns Hopkins University
Baltimore, MD 21205
Kathleen A. Costigan
Eva K. Pressman
Division of Maternal±Fetal Medicine
Johns Hopkins School of Medicine
Baltimore, MD 21205
Antenatal Origins of
Individual Differences
in Heart Rate
Jane A. Doussard-Roosevelt
Institute of Child Study
University of Maryland at
College Park,
College Park, MD 20742
Received 11 May 1999; accepted 25 July 2000
ABSTRACT: This study examines prenatal-to-postnatal stability in heart rate and variability from
mid-gestation through the ®rst year of life. Fetal heart rate data were collected from 52 healthy
fetuses at 24, 30, and 36 weeks gestation, and again at 2 weeks and 12 months of age. Fetal heart rate
measures were stable during gestation and positively associated with neonatal and infant measures.
Maternal pulse rate and oxygen saturation were moderately associated with fetal heart rate.
Together, fetal cardiac (heart rate and variability) and maternal physiologic measures (blood
pressure and oxygen saturation) explained 40 and 48% of the variance in heart rate and variability,
respectively, at 1 year of age. These common measures of individual differences in autonomic
function are enduring characteristics that originate during fetal development. ß 2000 John Wiley
& Sons, Inc. Dev Psychobiol 37: 221±228, 2000
Keywords: fetal development; fetal heart rate; infant heart rate; infant development
``It will be seen that the infant heart rate is
suggestively lower than the fetal heart rate, and
is signi®cantly more variable.''
(Sontag & Richards, 1938, p. 25)
Documentation of the developmental trajectory of
heart rate from the prenatal to postnatal periods was
one of the many goals of the 1930s Fels studies of fetal
Correspondence to: J. A. DiPietro
ß 2000 John Wiley & Sons, Inc.
behavior, but methodological limitations obscured
discovery of within-individual consistency between
the fetus and the infant at that time. Recently, models
of antenatal programming of autonomic function and
disease in adulthood (Barker, 1995; Phillips & Barker,
1997) have contributed to a resurgence in interest in
the fetal period. Although it is clear that parturition
does not represent a signi®cant damarcation in neural
development (Als, 1982; Prechtl, 1984), relatively few
studies have attempted to document intraindividual,
prenatal-to-postnatal stability in the same domain.
These have been limited to investigations of motor
activity (DiPietro, Hodgson, Costigan, & Johnson,
1996; Groome et al., 1999; Shadmi Homburg, &
222
DiPietro et al.
Insler, 1986) and behavioral state (Groome, Swiber,
Atterbury, Bentz, & Holland, 1997). We are aware of
only two published studies which have examined
stability in heart rate. In the ®rst, correlations between
late third trimester fetal heart rate and infant heart rate
measured at multiple ages through the ®rst year were
consistently positive (r ranges from .25 to .73), although sample size did not exceed 17 at any age (Lewis,
Wilson, Ban, & Baumel, 1970). The second study
(Thomas, Haslum, MacGillivray, & Golding, 1989),
based on a nationally representative dataset of 11,000
10-year-old children, determined that normal fetal
heart rate during labor (i.e., 120±160 bpm) was
associated with signi®cantly higher heart rate during
childhood when compared to cases with heart rate
outside this range, although the magnitude of the
mean difference was small (1.4 bpm).
The focus of the current study is on the development of mean heart rate and variability from the fetus
through the ®rst year of life. Cardiac measures are
commonly used indicators of autonomic function in
developmental research (e.g., Fox, 1989; Huffman et
al., 1998; Porges, 1992; Richards, 1985). Measures
include both tonic and reactive heart rate as well as a
variety of metrics for variability, ranging from global,
time-based descriptives (e.g., standard deviation, mean squares of successive differences) to more complex
methods designed to isolate speci®c frequency components (e.g., cardiac vagal tone, RSA) (Bernston et al.,
1997). Moderate stability in measures of heart rate
and variability have been demonstrated in preterm
infants prior to term (DiPietro, Caughy, Cusson, &
Fox, 1994) and in full-term infants during infancy
(Fox, 1989; Fracasso, Porges, Lamb, & Rosenberg,
1994; Izard et al., 1991; Snidman, Kagan, Riordan, &
Shannon, 1995), although there are inconsistencies
across studies in the patterning of signi®cant relations.
Establishing stability is requisite to the orientation
that patterns of heart rate represent underlying
constitutional attributes of neural function and autonomic regulation.
Stability in fetal heart rate and variability within
individuals has been demonstrated in fetuses beginning at 20 weeks gestation (DiPietro et al., 1996;
Nijhuis et al., 1998). Factors which contribute to
baseline fetal heart rate and variability are not well
documented, although tonic maternal heart rate
(Patrick, Campbell, Carmichael, & Probert, 1982)
and sympathetic arousal induced by physical exercise
(Artal et al., 1986) exert some in¯uence. The aim
of the current study is to document prenatal-topostnatal stability in heart rate, and to evaluate
maternal contributions to these measures before and
after birth.
METHOD
Participants
Participants were 52 nonsmoking women with singleton pregnancies and their offspring. Inclusion
criteria included low-risk, uncomplicated pregnancies
with gestational age dating based on a pregnancy test
within 2 weeks of missed menstrual period and/or ®rst
trimester obstetric/ultrasound examination. Demographic and medical data were collected by interview and medical chart review. The sample consisted
of primarily healthy, well-educated, and employed
women (M maternal age ˆ 29.9 yrs (SD ˆ 3.5); M
education ˆ 16 (SD ˆ 2.6)). All infants included in
this analysis were delivered at term (M GA ˆ 39.6,
SD ˆ 1.1, range ˆ 37±41 weeks), of normal birthweight (M ˆ 3502 g, SD ˆ 470) and discharged from
the regular newborn nursery according to routine
schedules (5 min Apgar M ˆ 8.9, range ˆ 7±10).
Sixty percent (n ˆ 31) of offspring were boys.
Design and Procedures
Fetal Data Collection and Quanti®cation. Data were
collected at 24, 30, and 36 weeks gestational age.
Women were monitored in a left lateral recumbent
position while resting quietly. Maternal radial pulse
rate, blood pressure, and oxygen saturation (SpO2)
were measured at the beginning of each recording, at
20 min into the recording and again after 40 min.1
These three values were averaged. All 52 subjects
provided data at each gestational age.
Fetal heart rate was collected from a fetal
cardiotocograph (Toitu, MT320) using a single wide
array Doppler transducer positioned on the maternal
abdomen with an elastic belt. The current generation
of fetal heart rate monitors detect fetal heart motions
and quantify heart rate by processing small segments
of serial Doppler-generated waveforms using autocorrelation techniques. Data were collected during
50 min of undisturbed monitoring and digitized at
5 Hz using an A-D converter board and commercial
data collection package (LabVIEW NB, National
Instruments Corp., Austin, TX). A series of error rejection procedures, developed in our laboratory and
based on moving averages of acceptable values were
1
Pulse oxygen saturation was measured using a digit probe (Nellcor
Pulse Oximeter, Hayward, CA) and re¯ects the proportion of
hemoglobin-bound oxygen in pulsatile arterial blood.
Fetal-Infant Heart Rate
applied to remove movement artifact.2 Data were
interpolated to preserve temporal integrity but interpolated data were not used in data analyses. Fetal
heart rate and variability, computed as standard
deviation,3 were analyzed in 30 s epochs; means were
calculated for the entire 50 min recording. The mean
amount of rejected data was 6.5, 5.2, and 5.4% at 24,
30, and 36 weeks, respectively.
Postnatal Data Collection and Quanti®cation.
Forty-one neonates (79%) returned for testing at 2
weeks postnatal age (M ˆ 14.2 days postpartum,
SD ˆ 1.9); the average length of ECG recording was
8 min (SD ˆ 2.4). ECG was recorded using three
disposable electrodes triangulated on the infant chest.
The signal was ampli®ed (PhysioControl, Model
Lifepak 5, Plainview, NY) and recorded on an
instrumentation tape recorder (Vetter FM, Model C4). Because state exerts an in¯uence on heart rate,
effort was made to collect data during a consistent
period of active (i.e., REM) sleep state. Five infants
could not be recorded due to prolonged fussiness or
high motor activity, four were successfully recorded
during a period of either drowsiness or quiet wakefulness, and the remainder during predominantly
active sleep. Most of the subjects were breast-fed
(n ˆ 35), but because feeding method in infancy
affects cardiac patterns (Butte, Smith, & Garza, 1991;
DiPietro, Larson, & Porges, 1987; Zeskind, Marshall,
& Goff, 1992), analyses were conducted on both the
full sample and without the six exclusively formulafed infants. At 1 year, 35 (67%) subjects returned for
follow-up (M ˆ 53.4 weeks; SD ˆ 1.0); the average
length of ECG recording was 7 min (SD ˆ 1.6). ECG
data were ampli®ed and recorded in the same manner,
while the child was seated quietly on the parent's lap
and looking at a picture book. Data for three subjects
were unusable as a result of excessive movement
artifact. The main reasons for the relatively low
2
Distinguishing artifactual from real data is a dif®cult but critical
component in quantifying FHR early in the third trimester because
motor activity can result in poor quality signal if the fetal heart
moves beyond the Doppler ®eld. The digital data underwent a series
of error rejection procedures based on 5-point moving medians of
acceptable values. In brief, values were rejected if they were beyond
the criterion limits of 1.5±.75 of the previous median; the speci®c
values against which each prior data point was compared were
adjusted by .03 per rejected s, until attaining the criterion limits.
These algorithms were developed after comparing the polygraphic
output of the monitor of the computerized output of several hundred
records and ultimately validated against visual inspection of
7,500 min of collected polygraphic data. Details of the error
rejection program are available upon request.
3
Root mean square (RMS) deviation values were also computed as a
measure of variability but not used in this analysis in order to
maintain consistency with neonatal metrics.
223
follow-up rate involved participants moving from the
area and non availability of the testing site during
evenings and weekends. However, there were no
signi®cant differences in neonatal or demographic
characteristics between tested and untested subjects at
either age.
The ECG data were quanti®ed of¯ine by digitizing
the tape recorded data using a Vagal Tone Monitor
(Delta-Biometrics, Inc., Bethesda, MD), which detects R-waves and times sequential heart periods to the
nearest millisecond. Data were time-sampled to the
nearest millisecond (1000 Hz). Heart periods were
output to a personal computer and Mxedit software
(Delta-Biometrics) was used to display the data, edit
outliers and quantify heart rate measures. Heart rate,
variability (standard deviation of heart rate values),
and cardiac vagal tone4 using the Porges method
(Porges, 1985) were computed in 30-second epochs.
Means were calculated for the entire recording.
RESULTS
Development of Heart Rate and Variability
Descriptive measures of fetal and infant heart rate and
variability for the full sample are presented in Table 1.
Preliminary analyses revealed no effects based on
fetal sex during either the fetal or postpartum period.
T-tests were used to examine whether there were
signi®cant, or near-signi®cant, differences in the fetal
measures between the tested and untested samples at
each age. None were detected.
Stability over Time
Pearson correlation matrices for HR and HRV from 24
weeks gestation through the end of the ®rst year of life
are presented in Table 2. There is evidence of stability
in both fetal HR and fetal HRV during the last half of
gestation (r ranges from .30 to .72). Fetal and neonatal
HR and HRV measures are also positively associated;
4
Cardiac vagal tone was quanti®ed through a series of procedures
developed by Porges as follows: (1) the duration between successive
heartbeats was time sampled every 200 ms for neonates and 250 ms
for infants; (2) linear and complex trends were removed using a 21point cubic moving polynomial stepped through the heart period
data. The smooth template from this procedure was subtracted from
the dataset, providing a trend-free residual heart period series; (3)
time-series analyses were conducted to extract the component of
heart period variance in the frequency band associated with
spontaneous breathing in neonates (.30±1.30 Hz) and older infants
(.24±1.04 Hz). The natural logarithm of this variance measure
produced the vagal tone index, the statistic used to estimate cardiac
vagal tone from the amplitude of respiratory sinus arrhythmia.
224
DiPietro et al.
Table 1. Fetal and Infant Heart Rate and Variability Values
Heart rate
Heart rate variability
n
Mean
SD
Mean
SD
Fetus
24 weeks
30 weeks
36 weeks
52
52
52
146.0
139.9
138.4
5.5
6.1
7.6
3.9
5.1
5.7
.9
1.4
1.7
Infant
2 weeks
1 year
36
32
142.9
129.1
9.2
8.7
6.0
5.9
.5
.7
Note. Fetal data have been presented previously (DiPietro et al., 1998).
Table 2. Intercorrelations of Fetal, Neonatal, and Infant Heart Rate Measures
Fetal
(n ˆ 52)
24 weeks
30 weeks
36 weeks
Neonatal
(n ˆ 36)
Infant
(n ˆ 32)
Heart rate
24 weeks
30 weeks
36 weeks
Neonatal
Ð
Ð
Ð
Ð
.73***
Ð
Ð
Ð
.56***
.59***
Ð
Ð
.22 / .27a
.26 / .32*
.31*/.35*
Ð
.42**
.32*
.40**
.36*b
Heart rate variability
24 weeks
30 weeks
36 weeks
Neonatal
Ð
Ð
Ð
Ð
.68***
Ð
Ð
Ð
.30*
.61***
Ð
Ð
.02 / .03a
.18/ .28
.26/.33*
Ð
.04
.29*
.47**
.25b
a
Values in second neonatal column are correlations with bottle-fed infants (n ˆ 6) excluded.
n ˆ 26.
*p < :05. **p < :01. ***p < :001. Based on one-tailed test.
b
for these pairs, correlations >.27 are signi®cant based
on one-tailed criteria. Analyses conducted excluding
the exclusively formula-fed infants indicated that
removing this source of variance tends to increase the
magnitude of the coef®cients, also presented in Table
2. For both HR and HRV, associations from fetal to 1
year recordings are somewhat larger in magnitude
than those to the neonatal period.
Associations between the two cardiac measures
were also investigated. During gestation, fetal HRV
and HR were not correlated at any gestational age.
Postnatally, HR and HRV were negatively related (r
(36) ˆ ÿ .24 in the neonate and r (32) ˆ ÿ .73 at 1
year). Table 3 presents cross-correlations between
fetal HRV and infant HR, and fetal HR and infant
HRV. Higher fetal HR is negatively associated with
infant, but not neonatal, HRV (r ranges from ÿ .28 to
ÿ .35). Greater fetal HRV is associated with faster HR
in neonates, but slower HR at 1 year. Doppler-based
fetal HR data are not appropriate for calculating fetal
vagal tone,5 but because vagal tone is a speci®c measure of variability, associations between antenatal
heart rate measures and later vagal tone are of interest.
Correlations between fetal HR and vagal tone during
the neonatal and infant periods were similar to those
5
In the current study we have relied on standard cardiotocography to
measure heart rate. In contrast to ECG-based detection of R-waves
using high sampling rates, Doppler-generated fetal heart rate data do
not quantify interbeat intervals with the degree of precision
necessary for detection of RSA. In addition, the fetus displays fetal
breathing movements episodically, making continuous quanti®cation of RSA inappropriate. Fetal ECG data are most often collected
during the intrapartum period from scalp electrodes following
rupture of membranes. More recent techniques to collect fetal ECG
data noninvasively through transabdominal monitoring are in
development, but this technology is cumbersome, not widely
available, and has not been well implemented in mid-gestation. We
did not consider it to be a useful candidate for this longitudinal
study.
Fetal-Infant Heart Rate
Table 3. Cross correlations among fetal heart rate and
infant measures
Heart rate variability
Heart rate
24 weeks
30 weeks
36 weeks
Heart rate variability
24 weeks
30 weeks
36 weeks
Neonate
Infant
.11/.03a
.09/.08
ÿ .11/ ÿ .20
ÿ .29
ÿ .28
ÿ .35*
Heart rate
.35*/.36*a
.29*/.31*
.26/.28
ÿ .02
ÿ .29*
ÿ .28
a
Values in second neonatal column are correlations with bottlefed infants (n ˆ 6) excluded.
*p < :05, based on one-tailed test.
for HRV, although less consistent and of lower
magnitude. Associations with fetal HR at 24, 30,
and 36 weeks are r ˆ .28, .26, and ÿ .08, respectively,
in the neonate; r ˆ ÿ .15, ÿ .15, and ÿ .30 in infants.
Correlations between vagal tone and fetal HRV at each
fetal period are r ˆ ÿ .12, .20, and .17, respectively, in
the neonate; r ˆ ÿ .07, .22, and .37 at 1 year.
Associations between Maternal and
Fetal Measures
Mean values for the maternal measures for the full
sample, and results of repeated measures analysis of
variance for changes over gestation are presented in
Table 4. Blood pressure was analyzed as mean arterial
pressure (MAP), a composite measure of diastolic and
systolic components computed as: (2*diastolic) ‡
systolic) 3. Maternal pulse rate and MAP were
relatively stable during gestation (r ˆ .59 to .74 for
pulse rate; r ˆ .41 to .69 for MAP); pulse oxygenation
intracorrelations were lower (r ˆ .20 to .32). The
contemporaneous in¯uence of maternal pulse rate,
oxygenation (SpO2), and blood pressure on fetal HR
and HRV during gestation were evaluated using mixed
effects models (SAS PROC MIXED). Developmental
trends during gestation are robust for heart rate and
variability (p <.0001); similar results regarding the
change in HR and HRV over gestation, generated by
repeated measures analysis of variance but exclusive
of maternal factors, have been presented previously
(DiPietro, Costigan, Shupe, Pressman, & Johnson,
1998). Results of the mixed effects analysis for the
association between maternal physiologic and fetal
heart rate measures revealed no signi®cant relations
between fetal HRV and maternal measures (all ts<1).
Howver, fetal HR was moderately associated with
maternal pulse (t ˆ ÿ 2.09, p<.04) and oxygen saturation (t ˆ 1.93, p<.06). The association with maternal MAP approached a trend level of signi®cance
(t ˆ ÿ 1.63, p ˆ .11).
Prediction of 1 Year Fetal Heart
Rate Measures
Multiple regression was used to model the prediction
of 1-year heart rate measures from antenatal variables.
Because of the small sample size at 1 year, preliminary bivariate analyses were conducted to exclude
weak associations. Measures considered were of maternal heart rate, oxygen saturation, and blood pressure, averaged over the three time points, as well as
demographic variables including maternal age and
education level. Selection of fetal measures was gui-
Table 4. Mean maternal physiologic values by gestational age
Mean
Pulse rate (bpm)
24 weeks
30 weeks
36 weeks
Oxygen saturation (SpO2; %)
24 weeks
30 weeks
36 weeks
Mean arterial pressure (MAP; mm Hg)
24 weeks
30 weeks
36 weeks
@
p < :10; ***p < :001.
225
SD
84.8
87.4
86.2
9.1
9.9
11.0
97.9
96.8
97.1
1.0
1.8
1.0
70.8
72.0
76.7
7.1
6.9
9.9
F, Time
2.54@
11.53***
15.44***
226
DiPietro et al.
Table 5. Results of Multiple Regressions in Prediction of Infant Heart Rate from Fetal Heart
Rate (HR), Fetal Heart Rate Variability (FHRV), Maternal Mean Arterial Blood Pressure
(MAP), and Oxygen Saturation (SpO2)
B
I. Dependent measure: Infant heart rate
24 weeks FHR
.58
30 weeks FHRV
ÿ 1.81
Multiple R ˆ .48; R2 ˆ .23; F(2,29) ˆ 4.38*
Maternal MAP
ÿ .28
Maternal SpO2
ÿ 3.24
Multiple R ˆ .63; R2 ˆ .40; F(4,27) ˆ 4.45**
II. Dependent measure; Infant heart rate variability
36 weeks FHRV
.19
36 weeks FHR
ÿ .03
Multiple R ˆ .60; R2 ˆ .36; F(2,29) ˆ 8.27***
Maternal MAP
ÿ .01
Maternal SpO2
ÿ .28
Multiple R ˆ .69; R2 ˆ .48; F(4,27) ˆ 6.14***
t
pr
2.34*
ÿ 1.95@
.41*
ÿ .35
ÿ 1.35
ÿ 1.89@
ÿ .25
ÿ .34
3.67**
ÿ 2.05*
.58
ÿ .37
.75
2.07*
.14
.37
Note. @p < :10; *p < :05; **p < :01; ***p < :001.
ded by the pattern of correlations observed in Tables 3
and 4; the earliest associations to either attain a correlation of .30, or the highest correlation across gestation were used. For infant HR, 24-week fetal HR
(r ˆ .42) and 30-week fetal HRV (r ˆ ÿ .29) values
were used; for infant HRV, 36-week fetal HR
(r ˆ ÿ .35) and HRV (r ˆ .47) were used. Maternal
pulse rate, age, or education did not near signi®cance.
Both fetal measures were entered in the ®rst block,
followed by both maternal variables. The predictive
models for infant HR and HRV, including unstandardized regression coef®cients (B), t-values, and partial
correlations for each variable are presented in Table 5.
In each model, fetal HR and HRV account for
signi®cant variance in prediction of infant measures
(r2 ˆ .23 and .36 for HR and HRV, respectively).
Addition of maternal blood pressure and oxygen
saturation signi®cantly increase the explained variance
in infant HR and HRV r2 change ˆ .16, (F(4,27) ˆ 3.69,
p<.05) and r2 change ˆ .11 (F(4,27) ˆ 2.92, p <.05)
respectively.
DISCUSSION
The results of this longitudinal investigation demonstrate that individual differences in heart rate and
variability originate before birth. We have replicated
earlier ®ndings from a smaller sample of intraindividual stability in both fetal HR and HRV during the
second half of gestation (DiPietro et al., 1996) and
documented consistency in cardiac measures from the
fetus to 1-year-old infant. Together, these provide
strong support that heart rate and variability are enduring characteristics which index aspects of autonomic
function.
Our detection of signi®cant associations between
36-week fetal HR and HRV con®rm those reported in
an earlier study (Lewis et al., 1970), although the
magnitude of the correlations vary. A recent report of
preliminary data in which subjects were strati®ed into
low and high HR and HRV groups based on 36-week
fetal data did not detect stability between fetal and
neonatal HR within 3 days postpartum, but a signi®cant association was found at 2 months of age across
sleep state (Fifer et al., 1998). The time-intensive
nature of fetal data collection typically results in small
sample sizes, but convergent ®ndings across studies
using different methodologies provides con®dence in
these data. Our data further reveal that predictive
relations between fetal and postnatal HR begin by 24
weeks gestation. Positive relations with fetal HRV do
not emerge until 30 weeks gestation. This observation
is likely due to the later maturation of neuroregulatory
in¯uences on variability than those that control rate
(Martin, 1978).
Longitudinal relations were observed not only
within cardiac measures, but also across them. Fetal
HR was not associated with neonatal variability but
higher fetal HR was associated with lower HRV at 1
year. Higher fetal HRV was associated with higher
heart rate in the neonatal period, but also with lower
HR at 1 year. Since both the current data as well as
that reported by others (DiPietro et al., 1994; Fracasso
et al., 1994; Izard et al., 1991) reveal negative
postnatal within age relations between rate and
Fetal-Infant Heart Rate
variability,6 the 1 year ®ndings are expected but the
positive neonatal associations are not. Given the small
sample size, we are hesitant to propose hypotheses for
this unexpected result. However, the lack of any relation between HR and HRV during gestation indicates
that the contemporaneous associations develop after
birth. The positive relation fetal HRV and neonatal HR
may re¯ect this transition and the in¯uences of
cardioacceleratory processes during these periods.
Fetal HR and HRV explained 23% of the variance
in 1 year HR and 36% of the variance in 1 year HRV,
despite many sources of error that might have limited
our ability to detect these relations. Efforts to control
known sources of variance (i.e., method of feeding)
tended to increase the magnitude of the relations
between fetal and neonatal HR and HRV. Prominent
among these is the different methods of heart rate
detection used during prenatal and postnatal recordings. That is, fetal heart rate was quanti®ed through
Doppler detection of fetal heart motions in contrast to
detection of R-waves in the infant. Finally, collecting
ECG data in infancy is challenging and subject to
uncontrollable in¯uences of behavioral state and
motor activity during the recording, which limits the
duration of data collection feasible during infancy.
The higher individual stability in HR and HRV
observed during the fetal period may be related to
regulation provided from maternal sources, but may
also be related to the longer recording period (50 min)
as compared to the necessarily brief period of data
collection after birth (< 10 min at either age).
During gestation, higher maternal oxygen saturation was associated with lower fetal heart rate and
there was a near-signi®cant relation between maternal
and fetal heart rate. There is relatively little understanding of how maternal physiologic functioning
contributes to fetal functioning, although a robust
relation between maternal and fetal heart rate has been
documented near term using averaged values over 24hour continuous recordings (Patrick et al., 1982).
Because our measure of maternal heart rate was a
crude one based on palpated radial pulse, we would
expect more precise ascertainment of maternal HR
through continuously recorded ECG to provide more
robust relations with fetal HR; these efforts are
currently underway in our laboratory. Similarly, our
failure to ®nd relations between maternal pulse and
fetal HRV at this time should not be considered as
suf®cient evidence for lack of a relation.
In contrast to the few modest contemporaneous
relations between maternal variables and fetal func6
Typically, positive relations between heart period and variability
are reported.
227
tioning, maternal oxygen saturation and blood pressure added signi®cant unique variance to the
prediction of infant HR and HRV, increasing the
explained variance by 17 and 12%, respectively. In
particular, higher maternal SpO2 was predictive of
both lower infant heart rate and higher variability. A
relationship between increased SpO2 and decreased
fetal heart rate has been described in healthy term
pregnancies following induced hyperoxia (Polvi,
Pirhonen, & Erkkola, 1995). Higher normotensive
maternal blood pressure during pregnancy has been
correlated with greater neonatal irritability
(Chisholm, Woodson, & DaCosta-Woodson, 1978).
We believe the current results to be the ®rst to
document maternal physiologic effects on infant
autonomic functioning. Lower HR and higher variability are considered representative of higher vagal
tone; thus higher maternal perfusion or oxygen
saturation may enhance uteroplacental function and
accelerate development.
In summary, these results provide the most comprehensive report of the stability in development of HR
and HRV from the fetus to infant. They provide support for the use of cardiac measures in research of
individual differences, which is often predicated on
assumptions of constitutionality. Support is also provided for the utility of both global descriptives of heart
rate variability as well as the suf®ciency of cardiotocography in measurement of fetal heart rate. Further
elucidation of the role of intrinsic and extrinsic antenatal in¯uences on subsequent autonomic function is
key to understanding the extent and nature of the
programming of subsequent function that may occur
prior to birth.
NOTES
This research was supported by grant R01 HD27592,
National Institute of Child Health and Human Development,
awarded to the ®rst author, and by R01 HD22628 awarded to
S. W. Porges and the fourth author. The investigators wish to
thank the diligent and generous participation of our study
families, without which this research would not have been
possible.
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