Sympathetic neural function has been conventionally evaluated by muscle sympathetic nerve activity (MSNA), plasma norepinephrine levels, and heart rate variability. Of these, MSNA is the only direct method for the assessment of sympathetic neural outflow to the peripheral vasculature. However, interindividual comparison of MSNA is limited to burst counting. Recently, we proposed a new quantitative and objective measure of MSNA--burst power--which enables to assess inter-individual differences in MSNA. The sympathetic nervous system regulates circulation via arterial and low-pressure baroreflexes, lung stretch reflex, chemoreflexes, and other somatic and sympathetic afferents. The open-loop gain of the arterial baroreflex system can be determined on the basis of the transfer function from the random input of arterial blood pressure to the output of MSNA using the autoregressive moving average model with an exogenous input (ARMAX). This model revealed that baroreflex-mediated sympathetic control was preserved while the reflex parasympathetic control was markedly attenuated in patients with heart failure. The lung stretch reflex, simulated by the ARMAX using the input of instantaneous ventilation and the output of MSNA, showed that instantaneous lung inflation suppressed MSNA within 1.5 sec. The magnitude or the lung stretch reflex decreased as the heart failure progressed. In patients with heart failure, the carbon dioxide chemoreflex is enhanced, as evidenced by substantial increases in both ventilation and MSNA on exposure to carbon dioxide. Thus, the use of new signal processing techniques and simultaneous assessment of MSNA and other hemodynamic and respiratory variables could provide a new insight into the dynamic function of cardiovascular and respiratory neural reflexes.