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Purpose Acute breath-holding deprives the human body from oxygen. In an effort to protect the brain, the diving response is initiated, coupling several physiological responses. The aim of this study was to describe the physiological responses to apnea at the cardiac, peripheral and cerebral level. Methods 31 physically active subjects (17 male, 14 female, 23.3 ± 1.8 years old) performed a maximal static breath-hold in a seated position. Heart rate (HR), muscle and cerebral oxygenation (by means of near-infrared spectroscopy, NIRS) were continuously measured. RM MANOVA's were used to identify changes in HR, peripheral (mTOI) and cerebral (cTOI) tissue oxygenation and oxygenated (O 2 Hb) and deoxygenated (HHb) hemoglobin during apnea. Results Average apnea duration was 157 ± 41 s. HR started decreasing after 10 s (p < 0.001) and dropped on average by 27 ± 14 bpm from baseline (p < 0.001). mTOI started decreasing 10 s after apnea (p < 0.001) and fell by 8.6 ± 4.0% (p < 0.001). Following an immediate drop after 5 s (p < 0.001), cTOI increased continuously, reaching a maximal increase of 3.7 ± 2.4% followed by a steady decrease until the end of apnea. cTOI fell on average 5.4 ± 8.3% below baseline (p < 0.001). Conclusion During apnea, the human body elicits several protective mechanisms to protect itself against the deprivation of oxygen. HR slows down, decreasing O 2 demand of the cardiac muscle. The decrease in mTOI and increase in cTOI imply a redistribution of blood flow prioritizing the brain. However, this mechanism is not sufficient to maintain cTOI until the end of apnea. Keywords Breath-holding • Diving response • NIRS • Cerebral oxygenation • Peripheral oxygenation • Syncope Abbreviations bpm Beats per minute c[HHb] Deoxygenated cerebral hemoglobin concentration c[O 2 Hb] Oxygenated cerebral hemoglobin concentration cTOI Cerebral tissue oxygenation index HR Heart rate µM Micro mol. L −1 Manova Multivariate analysis of variance m[HHb] Deoxygenated muscle hemoglobin concentration m[O 2 Hb] Oxygenated muscle hemoglobin concentration mTOI Muscle tissue oxygenation index O 2 Oxygen * Jan Boone

Purpose: Acute apnea is known to induce decreases in oxyhemoglobin desaturation (SpO2) and increases in erythropoietin concentration ([EPO]). This study examined the potential of an apnea training program to induce erythropoiesis and increase hematological parameters and exercise performance. Methods: Twenty-two male subjects were randomly divided into an apnea and control group. The apnea group performed a 6-week apnea training program consisting of a daily series of 5 maximal static apneas. Before and after training, subjects visited the lab on three test days to perform 1) a ramp incremental test measuring V̇O2peak, 2) CO-rebreathing for Hb mass determination and a 3-km time trial and 3) an apnea test protocol with continuous finger SpO2 registration. Venous blood samples were drawn before and 180 minutes after the apnea test for analysis of [EPO]. Results: Minimal SpO2 reached during the apnea test protocol was 91 ±7% pre and 82 ±7% post apnea training. The apnea test protocol did not elicit an acute increase in [EPO] (p=0.685) before nor after the training program. Consequently, resting [EPO] (p=0.170), Hbmass (p=0.134), V̇O2peak (p=0.796) and 3-km cycling time trial performance (p=0.509) were not affected either. Conclusion: The apnea test and training protocol, consisting of 5 maximal static apneas, did not induce a sufficiently strong hypoxic stimulus to cause erythropoiesis and therefore did not result in an increase in resting [EPO], Hbmass, V̇O2peak or time trial performance. Longer and/or more intense training sessions inducing a stronger hypoxic stimulus are probably needed to obtain changes in hematological and exercise parameters.

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Syncope or "blackout" (BO) in breath-hold diving (freediving) is generally considered to be caused by hypoxia. However, it has been suggested that cardiac arrhythmias affecting the pumping effectivity could contribute to BO. BO is fairly common in competitive freediving, where athletes aim for maximal performance. We recorded heart rate (HR) during a static apnea (STA) competition, to reveal if arrhythmias occur. Four male freedivers with STA personal best (PB) of 349±43s, volunteered during national championships, where they performed STA floating face down in a shallow indoor pool. A non-coded Polar T31 chest strap recorded R-R intervals and a water- and pressure proof pulse oximeter arterial oxygen saturation. Three divers produced STA near their PB without problems, while one diver ended with BO at 5min17s, which was 12s beyond his PB. He was immediately brought up by safety divers and resumed breathing within 10s. All divers attained similar lowest diving HR (47±4bpm), but HR recordings displayed a different pattern for the diver ending with BO. After a short tachycardia the three successful divers developed bradycardia which became more pronounced during the second half of the apnea. The fourth diver developed pronounced bradycardia earlier, and at 2.5min into the apnea HR started alternating between approximately 50 and 140 bpm, until the diver lost consciousness. At resumed breathing, HR returned to baseline. Nadir oxygen saturation was similar for all divers. We speculate that arrhythmia could have contributed to BO, by lowering stroke volume leading to a systolic blood pressure drop, affecting brain perfusion.