Systemic and regional hemodynamic and (de)oxygenation responses across repeated breath-holds

Regional cerebral and peripheral tissue (de)oxygenation responses to breath-holding (apnea) have predominantly been examined during isolated attempts. How these responses evolve across repeated efforts remains unclear, as previous studies either averaged data across bouts or focused solely on the final repetition. Accordingly, this study mapped the (de)oxygenation dynamics across successive breath-holds. Fifteen nondivers performed three repeated maximal static breath-holds, separated by 2-min rest intervals. Systemic cardiovascular variables, gas exchange, and cerebral frontal cortex and forearm muscle (de)oxygenation were assessed. At each breath-hold onset, a transient fall in cerebral oxygenated hemoglobin (cO₂Hb) and arterial pressure occurred, coinciding with tachycardia. A cardiovascular steady state followed, which persisted until the onset of involuntary breathing movements (IBMs). At IBM onset, cO₂Hb increased only during the first attempt (Δ8 ± 5 µM, <i>P</i> < 0.001), with smaller changes in subsequent breath-holds (apnea-2, Δ3 ± 6 µM; apnea-3, Δ3 ± 5 µM, <i>P</i> ≤ 0.014). Cerebral deoxygenated hemoglobin (cHHb) increased progressively across breath-holds (apnea-1, Δ3 ± 4 µM; apnea-2, Δ5 ± 4 µM; apnea-3, Δ7 ± 5 µM, <i>P</i> ≤ 0.001), whereas arterial pressure increases were of similar magnitude (<i>P</i> ≥ 0.064). Forearm (de)oxygenation profiles were comparable across attempts (<i>P</i> ≥ 0.085). In nine subjects, a triphasic peripheral response emerged: initial rapid decline in O₂Hb and rise in HHb at breath-holding onset, a transient intermediate plateau, and further divergence near IBM onset. Breath-holds were terminated at successively lower cO₂Hb, cerebral tissue oxygen index, and end-tidal oxygen, and higher cHHb (<i>P</i> ≤ 0.034), but similar end-tidal carbon dioxide levels (<i>P</i> > 0.912). The magnitude and timing of regional (de)oxygenation responses vary greatly over repeated breath-holds. Cerebral oxygenation showed a pronounced increase during the first attempt but progressively smaller changes across subsequent bouts. In contrast, peripheral tissue oxygenation demonstrated a time-dependent decline across successive attempts.<b>NEW & NOTEWORTHY</b> In nondivers, regional cerebral (de)oxygenation responses varied greatly across repeated breath-holds, whereas peripheral tissue responses were comparable. At IBM onset, cerebral oxygenation increased significantly during the first breath-hold but showed progressively smaller changes in subsequent attempts. In the periphery, a triphasic (de)oxygenation pattern was identified. Its final phase-characterized by a further oxygenation decline-coincided with increased cerebral oxygenation, supporting the concept of sympathetically mediated vasoconstriction and selective blood redistribution toward vital organs.