The compensatory responses of the respiratory system to simulated central hypervolemia (CHV) were investigated in 14 normal subjects. The central hypervolemia was caused by a short-time passive head-down tilt (HDT, -30°, 30 min). The results show that CHV increased the mechanical respiratory load and the airway resistance, slowed the inspiratory flow, increased the duration of the inspiratory phase, reduced the respiratory rate, but not changed the minute ventilation. CHV induced a significant rise in inspiratory swings of alveolar pressure (184%), based on the inspiratory occlusion pressure measurement. These changes indicate a compensatory increase in the inspiratory muscle contraction force. A stable level of minute ventilation during CHV was an effect of increased EMG activity of parasternal muscles more than twice (P<0.01). A contribution of the diaphragm and scalene muscles to ventilation during spontaneous breathing in HDT was reduced. An increase of genioglossus contractile activity during HDT contributed to the stabilization of airway patency. These results suggest that a coordinated modulation of inspiratory muscles activity allows preserving a constant level of minute ventilation during a short-time intrathoracic blood volume expansion. The mechanisms of respiratory load compensation seem to be mediated by afferent information from the lung and respiratory muscle receptors and from the segmentary reflexes and intrinsic properties of the muscle fibers.