The fetal cardiovascular system is precisely regulated during development. We used power spectral analysis to define heart rate and peak velocity amplitude variability in the human fetus during conditions of maternal spontaneous and stop breathing. Recordings were made from the floating loop of the umbilical artery using a Toshiba SHH140A pulsed-Doppler velocimeter with a 6 MHz transvaginal probe. Ten velocity time series were recorded during spontaneous breathing from 8 fetus at week 10 (n=2), 11(n=3) and 12(n=3). Ten non-matched velocity time series were recorded during stop breathing from 8 fetus at week 10 (n=5), 11(n=1), and 12(n=2). Ultrasound spatial peak temporal average was less than 100m W/cm2. Velocimeter wall filters were 70 or 100 Hz. Doppler forward flow audio signals were recorded at 44KHz for > 16 seconds. Peak velocity, mean velocity and instantaneous heart rate were determined for each time series. Mean heart rate and mean velocity were determined for each velocity time series. Peak velocity and heart rate variability time series were de-trended via low-order polynomial fit to remove DC-drift, and power spectra analyzed using FFT. To compensate for mean heart rate differences between fetus, we normalized spectral frequency axes for each fetus by heart rate. This unitless frequency axis ranged from zero (DC) to 1(heart rate). To compensate for mean-velocity (or mean heart rate) differences, we computed the ratio of spectral power in 10 pre-set bands (0.1 increments of normalized frequency) to total spectral power. The average power ratios for heart rate variability during stop breathing were 3%, 15%, 27%, 26%, 16%, 8%, 3%, <1%, <1%, and <1% respectively, in each band. During spontaneous maternal breathing, these ratios shifted 4%, 16%, 21%, 22%, 22%, 10%, 2%, <1%, <1%, and <1%, respectively. The average power ratios for peak-velocity variability during stop breathing were 27%, 26%, 19%, 15%, 7%, 3%, 1%, <1%, <1%, and <1%, respectively. During spontaneous maternal breathing these ratios shifted to 23%, 40%, 14%, 10%, 6%, 3%, 1%,,<1%, <1%, and <1%, respectively. These are new tools for analysis of the homeostasis in the early human fetus. We speculate that cardiovascular alteration associated with maternal fetal pathology changes these measures and may lead to earlier clinical diagnosis and therapy.