Background : In sleep apnea syndrome, arterial oxygen saturation(SaO2) decreases at a variable rate and to a variable degree for a given apneic period from patient to patient, and various kinds of cardiac arrythmia are known to occur. Factors supposed to affect arterial oxygen desaturation during apnea are duration of apnea, lung voulume at which apnea occurs, and oxygen consumption rate of the subject. The lung serves as preferential oxygen source during apnea, and there have been many reports related with the influence of lung volume on SaO2 during apnea, but there are few, if any, studies about the influence of oxygen consumption rate of an individual on SaO2 during breath holding or about the profile of arterial oxygen resaturation after breathing resumed. Methods : To investigate the changes of SaO2 and heart rate(HR) during breath holding(BH) and rebreathing(RB) and to evaluate the physiologic factors responsible for the changes, lung volume measurements, and arterial blood gas analyses were performed in 17 healthy subjects. Nasal airflow by thermistor, SaO2 by pulse oxymeter and ECG tracing were recorded on Polygraph(TA 4000, Gould, U.S.A.) during voluntary BH & RB at total lung capacity(TLC), at functional residual capacity(FRC) and at residual volume(RV), respectively, for the study subjects. Each subject's basal metabolic rate(BMR) was assumed on Harris-Benedict equation. Results: The time needed for SaO2 to drop 2% from the basal level during breath holding(T2%) were 70.1±14.2 sec(mean±standard deviation) at TLC, 44.0±11.6 sec at FRC, and 33.2±11.1 sec at RV(TLC vs. FRC, p<0.05; FRC vs. RV, p<0.05). On rebreathing after SaO2 decreased 2%, further decrement in SaO2 was observed and it was significantly greater at RV(4.3±2.1) than at TLC(1.4±1.0)(p<0.05) or at FRC(1.9±1.4)(p<0.05). The time required for SaO2 to return to the basal level after RB(Tr) at TLC was not significantly different from those at FRC or at RV. T2% had no significant correlation either with lung volumes or with BMR respectively. On the other hand, T2% had significant correlation with TLC/BMR(r=0.693, p<0.01) and FRC/BMR (r=0.615, p<0.025) but not with RV/BMR(r=0.227, p>0.05). The differences between maximal and minimal HR(ΔHR) during the BH-RB manuever were 27.5±9.2/min at TLC, 26.4±14.0/min at RV, and 19.1±6.0/min at FRC which was significantly smaller than those at TLC(p<0.05) or at RV(p<0.05). The mean difference of 5 p-p intervals before and after RB were 0.8±0.10 sec and 0.72±0.09 sec at TLC(p<0.001), 0.82±0.11 sec and 0.73±0.09 sec at FRC(p<0.025), and 0.77±0.09 sec and 0.72±0.09 sec at RV(p<0.05). Conclusion Healthy subjects showed arterial desaturation of various rates and extent during breath holding at different lung volumes. When breath held at lung volume greater than FRC, the rate of arterial desaturation significantly correlated with lung volume/basal metabolic rate, but when breath held at RV, the rate of arterial desaturation did not correlate linearly with RV/BMR. Sinus arrythmias occurred during breath holding and rebreathing manuever irrespective of the size of the lung volume at which breath holding started, and the amount of change was smallest when breath held at FRC and the change in vagal tone induced by alteration in respiratory movement might be the major responsible factor for the sinus arrythmia.