Changes in cardiovascular parameters elicited during a maximal breath hold are well described. However, the impact of consecutive maximal breath holds on central hemodynamics in the post-apneic period is unknown. Eight trained apnea divers and eight control subjects performed five successive maximal apneas, separated by two minute resting interval, with face immersing in cold water. Ultrasound examinations of inferior vena cava (IVC) and the heart were carried out at times 0, 10, 20, 40, and 60 minutes after. The arterial oxygen saturation level and blood pressure, heart rate and transcutaneous partial pressures of CO₂ and O₂ were monitored continuously. At 20 minutes after breath-holds IVC diameter increased (27.6% and 16.8% for apnea divers and controls, respectively). Subsequently, pulmonary vascular resistance increased and cardiac output decreased both in apnea divers (62.8% and 21.4%, respectively) and the control group (74.6% and 17.8%, respectively). Cardiac output decrements were due to reductions in stroke volumes, in presence of reduced end-diastolic ventricular volumes. Transcutaneous partial pressure of CO₂ increased in all participants during breath-holding, returned to baseline between apneas, but remained slightly elevated during the post-dive observation period (~ 4.5%). Thus, increased right ventricular afterload and decreased cardiac output were associated with CO₂ retention and signs of peripheralization of blood volume. These results indicate that repeated apneas may cause prolonged hemodynamic changes after resumption of normal breathing, which may suggest what happens in sleep apnea syndrome.