Oxygen-conserving effects of apnea in exercising men

We sought to determine whether apnea-induced cardiovascular responses resulted in a biologically significant temporary O-2(-) conservation during exercise. Nine healthy men performing steady-state leg exercise carried out repeated apnea (A) and rebreathing (R) maneuvers starting with residual volume +3.5 liters of air. Heart rate (HR), mean arterial pressure (MAP), and arterial O-2 saturation (Sa(O2); pulse oximetry) were recorded continuously. Responses (Delta HR, Delta MAP) were determined as differences between HR and MAP at baseline before the maneuver and the average of values recorded between 25 and 30 s into each maneuver. The rate of O-2 desaturation (Delta SaO(2)/Delta t) was determined during the same time interval. During apnea, Delta SaO(2)/Delta t had a significant negative correlation to the amplitudes of Delta HR and Delta MAP (r(2) = 0.88, P < 0.001); i.e., individuals with the mast prominent cardiovascular responses had the slowest Delta SaO(2)/Delta t. Delta HR and Delta MAP were much larger during A (-44 +/- 8 beats/min, +49 +/- 4 mmHg, respectively) than during R maneuver (+3 +/- 3 beats/min, +30 +/- 5 mmHg, respectively). Delta SaO(2)/Delta t during A and R maneuvers was -1.1 +/- 0.1 and -2.2 +/- 0.2% units/s, respectively, and nadir Sao, values were 58 +/- 4 and 42 +/- 3% units, respectively. We conclude that bradycardia and hypertension during apnea are associated with a significant temporary O-2 conservation and that respiratory arrest, rather than the associated hypoxia, is essential for these responses.