Heart rate variability (HRV) spectral analysis has been used as a tool for short-term assessment of parasympathetic (PNS) and sympathetic nervous system (SNS) control of heart rate. However, it has been suggested that the PNS and SNS indicators are superimposed on a broad-band noise spectrum in which the power spectral densities are inversely proportional to their frequency (1/f beta). In this study, we have used coarse-graining spectral analysis to extract the harmonic components for calculation of PNS and SNS indicators and to obtain the slope (beta) of the 1/f beta component to estimate fractal dimension (DF) of a trail of HRV. DF was regarded as an indicator of cardiovascular system complexity. Ten healthy young subjects (6 women and 4 men) were studied in supine rest and with sequential applications of four levels of lower body negative pressure (LBNP; -10, -20, -30, and -50 mmHg) and head-up tilt (HUT; 10, 20, 30, and 70 degrees). In the 20 tests, there were six occurrences of presyncopal symptoms that required the test to be terminated before the planned end point. At low levels of LBNP or HUT, arterial pulse pressure (PP) was not changed from rest, and calculated DF was very high (beta approximately 1.00). At the higher levels of LBNP and HUT, PP decreased. Coincident with this reduction in PP, PNS activity decreased, SNS activity increased, and DF was reduced, each with a significant linear relationship to the change in PP (PNS: r = 0.56; SNS: r = 0.57; DF: r = 0.70, P < 0.01). Each occurrence of presyncope was associated a low PNS indicator as well as DF < 2.50 (beta > or = 1.80). These data indicate that the cardiovascular system is operating at a reduced level of complexity and further suggest that reduced complexity might not be compatible with cardiovascular homeostasis.

The kinetics of oxygen uptake (VO2) were observed at the onset of submaximal cycling exercise in seven men and one woman [mean age 22.6 +/- 0.9 (SE) yr] in the upright and supine positions and the supine position with -40 mmHg lower body negative pressure (LBNP). There was no significant difference for peak VO2 and ventilatory threshold between the supine (3,081 +/- 133 and 1,954 +/- 138 ml/min, respectively) and the supine + LBNP positions (3,062 +/- 152 and 1,973 +/- 122 ml/min); however, both were reduced compared with upright exercise (3,483 +/- 200 and 2,353 +/- 125 ml/min). Kinetic analysis applied to six repetitions by each subject indicated a slowing from a mean total lag time (time required to achieve 63% of the difference in VO2 between baseline and new steady state) of 36.3 +/- 2.7 s in upright exercise to 44.1 +/- 3.5 s in the supine position. However, total lag time for the supine + LBNP position (36.0 +/- 2.8 s) did not differ from upright exercise but was significantly faster than supine exercise. These data have been interpreted in support of an O2 transport limitation to VO2 kinetics at the onset of supine exercise that is countered by LBNP, likely through a more rapid increase in perfusion to the exercising muscle at these submaximal work rates.

Lower body negative pressure (LBNP; -5 and -15 mmHg) was applied to 14 men (mean age 44 yr) to test the hypothesis that reductions in preload without effect on stroke volume or blood pressure increase selectively muscle sympathetic nerve activity (MSNA), but not the ratio of low- to high-frequency harmonic component of spectral power (P(L)/P(H)), a coarse-graining power spectral estimate of sympathetic heart rate (HR) modulation. LBNP at -5 mmHg lowered central venous pressure and had no effect on stroke volume (Doppler) or systolic blood pressure but reduced vagal HR modulation. This latter finding, a manifestation of arterial baroreceptor unloading, refutes the concept that low levels of LBNP interrogate, selectively, cardiopulmonary reflexes. MSNA increased, whereas P(L)/P(H) and HR were unchanged. This discordance is consistent with selectivity of efferent sympathetic responses to nonhypotensive LBNP and with unloading of tonically active sympathoexcitatory atrial reflexes in some subjects. Hypotensive LBNP (-15 mmHg) increased MSNA and P(L)/P(H), but there was no correlation between these changes within subjects. Therefore, HR variability has limited utility as an estimate of the magnitude of orthostatic changes in sympathetic discharge to muscle.

Short-term application of nasal continuous positive airway pressure increases heart rate variability and time and frequency domain indexes of parasympathetic activity without influencing cardiac sympathetic activity. This increase may occur reflexively, through stimulation of pulmonary mechanoreceptor afferents.