Hydrostatic pressure-induced changes in central hemodynamics modulate respiratory regulation and cerebral hemodynamics under the orthostatic stress, but its regulatory function in athletes undergoing repeated sprint and jump training is unknown. In 10 college male volleyball players and 7 healthy subjects, low body negative pressure (LBNP -45mmHg) method was used. To characterize the respiratory controller, we induced hypercapnia by changing the inspiratory CO2 fraction, and estimated the linear end-tidal PCO2-minute ventilation relation, and cerebrovascular reactivity to CO2 by transcranial doppler ultrasonography. A decrease in central blood volume by LBNP was shown to reset the controller element leftward with a change in the respiratory operating point only in the control subjects, but no such significant change was observed in athletes. Cerebrovascular reactivity was significantly higher in athletes than in controls. These findings indicate the possibility of acquired adaptive capacity of both respiratory and cerebral circulatory regulatory systems to orthostatic stress through training.
