Sleep apnea syndrome (SAS), respiratory disorder characterized by repetitive complete or partial upper airway collapse during sleeping, is an independent cardiovascular disease (CVD) risk. However, underlying pathophysiological mechanisms are unknown. In this study, we examined the response of central hemodynamics during intermittent apnea in order to more accurately assess cardiac load. Fifteen apparently healthy men (23 ± 2years) underwent 20 bouts of 20 seconds of voluntary end expiratory apnea (apnea phase) followed by 40 seconds of voluntary breathing (rebreathing phase). Central arterial hemodynamics was evaluated from radial arterial pressure waveforms using pulse wave analysis via general transfer function. During every apnea-rebreathing cycle, central and peripheral arterial systolic pressure significantly increased during early rebreathing phase compared with during apnea phase and then returned toward baseline level. Furthermore, peripheral systolic pressure, and heart rate significantly increased throughout the 20 min of respiratory intervention. Rate-pressure product，an index of myocardial oxygen consumption, also elevated throughout the intervention. These results suggest that central blood pressure is increased temporarily by the rebreathing and that central arterial pressure might be raised throughout the repetitive intermittent apnea probably due to insufficient recovery duration.

DESCENTE SPORTS SCIENCE Vol.36/THE DESCENTE AND ISHIMOTO MEMORIAL FOUNDATION FOR THE PROMOTION SPORTS SCIENCE