Limited information exists concerning arterial blood pressure (BP) changes in underwater breath-hold diving. Simulated chamber dives to 50 m of freshwater (mfw) reported very high levels of invasive BP in two divers during static apnea (SA), whereas a recent study using a noninvasive subaquatic sphygmomanometer reported unchanged or mildly increased values at 10 m SA dive. In this study we investigated underwater BP changes during not only SA but, for the first time, dynamic apnea (DA) and shortened (SHT) DA in 16 trained breath-hold divers. Measurements included BP (subaquatic sphygmomanometer), ECG, and pulse oxymetry (arterial oxygen saturation, SpO₂, and heart rate). BP was measured during dry conditions, at surface fully immersed (SA), and at 2 mfw (DA and SHT DA), whereas ECG and pulse oxymetry were measured continuously. We have found significantly higher mean arterial pressure (MAP) values in SA (∼40%) vs. SHT DA (∼30%). Postapneic recovery of BP was slightly slower after SHT DA. Significantly higher BP gain (mmHg/duration of apnea in s) was found in SHT DA vs. SA. Furthermore, DA attempts resulted in faster desaturation vs. SA. In conclusion, we have found moderate increases in BP during SA, DA, and SHT DA. These cardiovascular changes during immersed SA and DA are in agreement with those reported for dry SA and DA.

We investigated whether the involuntary breathing movements (IBM) during the struggle phase of breath holding, together with peripheral vasoconstriction and progressive hypercapnia, have a positive effect in maintaining cerebral blood volume. The central hemodynamics, arterial oxygen saturation, brain regional oxyhemoglobin (bHbO(2)), deoxyhemoglobin, and total hemoglobin changes and IBM were monitored during maximal dry breath holds in eight elite divers. The frequency of IBM increased (by approximately 100%), and their duration decreased ( approximately 30%), toward the end of the struggle phase, whereas the amplitude was unchanged (compared with the beginning of the struggle phase). In all subjects, a consistent increase in brain regional deoxyhemoglobin and total hemoglobin was also found during struggle phase, whereas bHbO(2) changed biphasically: it initially increased until the middle of the struggle phase, with the subsequent relative decline at the end of the breath hold. Mean arterial pressure was elevated during the struggle phase, although there was no further rise in the peripheral resistance, suggesting unchanged peripheral vasoconstriction and implying the beneficial influence of the IBM on the cardiac output recovery (primarily by restoration of the stroke volume). The IBM-induced short-lasting, sudden increases in mean arterial pressure were followed by similar oscillations in bHbO(2). These results suggest that an increase in the cerebral blood volume observed during the struggle phase of dry apnea is most likely caused by the IBM at the time of the hypercapnia-induced cerebral vasodilatation and peripheral vasoconstriction.

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Marked bradycardia occurs at the end of breath‐hold dives. However, vagal modulation of heart rate (HR) during maximal static (SA) and dynamic (DA) underwater apneas is not well‐known. HR, HR variability (SD1) and arterial oxygen saturation (SpO2) were analyzed at the immersed baseline and at initial‐, mid‐ and end‐apnea (each 30 s) of maximal underwater SA and DA in nine breath‐hold divers. DA lasted 78±8 s and SA 225±20 s (mean±SEM) and resulted in similar decreases in SpO2 (78±3 and 75±3 %, p=0.352, respectively). Initially, DA increased HR from 80±5 to 122±5 bpm (p<0.001), followed by decrease in HR at mid‐apnea and end‐apnea (101±6 and 80±8 bpm). During SA, HR decreased at mid‐apnea (from 78±4 to 66±3 bpm, p=0.004) but did not decrease further at end‐apnea phase. SD1 decreased at the initial phase of DA (from 28±5 to 10±4 ms, p=0.005) being lower compared with SA (24±4 ms, p=0.005). At the end of DA and SA, SD1 tended to increase above the baseline (67±16 and 66±10 ms, p=0.088 and p=0.093, respectively) and did not differ from each other (p=0.804). We concluded that apnea blunts the effects of exercise on HR variability at the end of DA when despite the higher HR. This indicates complex interplay between vagal and sympathetic responses to apnea and exercise. Supported by TEKES, Finland, Paavo Nurmi Foundation, Finland and Croatian Ministry of Science.