This study examined the physiological responses of ten elite divers to normal breathing (BHn), glossopharyngeal inhalation (BHi), and complete exhalation (BHe) prior to five maximal breath-hold (BH) efforts. Breath-hold time (BHT), hemological variables, mean arterial pressure (MAP), other hemodynamic indices, and diaphragmatic activity (DA) were recorded. During BHs, phases were identified as easy-going (EPh: minimal DA), struggling (SPh: increased DA), PhI (MAP transition), PhII (MAP stabilization), and PhIII (steep MAP increase). BHi significantly extended BHT (309.14 ± 12.91s) compared to BHn (288.77 ± 10.99s) and BHe (151.18 ± 10.94s) (P = 0.001). BHT, EPh, and SPh in BHi increased by 7.05%, 2.57%, and 11.08% over BHn, respectively. PhIII appeared earlier in BHe than in other conditions (P < 0.001) and accounted for 47.07%, 44.96%, and 60.18% of BHT in BHn, BHi, and BHe, respectively. SPh comprised 47.10%, 46.01%, and 45.13% of BHT in BHn, BHi, and BHe, respectively, with SPh onset coinciding with PhIII onset in BHn and BHi but not in BHe. Bradycardia was more pronounced in BHe, maintaining better stroke volume. No significant differences in red blood cells or maximal MAP were noted across conditions. Glossopharyngeal inhalation improves BHT and extends EPh and SPh durations. PhIII onset is linked to SPh in BHn and BHi but not in BHe. BHe triggers an earlier MAP rise, leading to stronger parasympathetic responses. Despite similar maximal MAP across conditions, the higher BHT and tissue hypoxemia in BHi and BHn suggest MAP is a key limiting factor in apnoea.
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