Electrocardiogram, cardiac output, and blood lactate accumulation were recorded in three elite breath-hold divers diving to 40-55 m in a pressure chamber in thermoneutral (35 degrees C) or cool (25 degrees C) water. In two of the divers, invasive recordings of arterial blood pressure were also obtained during dives to 50 m in cool water. Bradycardia during the dives was more pronounced and developed more rapidly in the cool water, with heart rates dropping to 20-30 beats/min. Arrhythmias occurred, particularly during the dives in cool water, when they were often more frequent than sinus beats. Because of bradycardia, cardiac output decreased during the dives, especially in cool water (to <3 l/min in 2 of the divers). Arterial blood pressure increased dramatically, reaching values as high as 280/200 and 290/150 mmHg in the two divers, respectively. This hypertension was secondary to peripheral vasoconstriction, which also led to anaerobic metabolism, reflected in increased blood lactate concentration. The diving response of these divers resembles the one described for diving animals, although the presence of arrhythmias and large increases in blood pressure indicate a less perfect adaptation in humans.
End tidal O2 and CO2 (PETCO2) pressures, expired volume, blood lactate concentration ([Lab]), and arterial blood O2 saturation [dry breath holds (BHs) only] were assessed in three elite breath-hold divers (ED) before and after deep dives and BH and in nine control subjects (C; BH only). After the dives (depth 40-70 m, duration 88-151 s), end-tidal O2 pressure decreased from approximately 140 Torr to a minimum of 30.6 Torr, PETCO2 increased from approximately 25 Torr to a maximum of 47.0 Torr, and expired volume (BTPS) ranged from 1.32 to 2.86 liters. Pulmonary O2 exchange was 455-1,006 ml. CO2 output approached zero. [Lab] increased from approximately 1.2 mM to at most 6.46 mM. Estimated power output during dives was 513-929 ml O2/min, i.e. approximately 20-30% of maximal O2 consumption. During BH, alveolar PO2 decreased from approximately 130 to less than 30 Torr in ED and from 125 to 45 Torr in C. PETCO2 increased from approximately 30 to approximately 50 Torr in both ED and C. Contrary to C, pulmonary O2 exchange in ED was less than resting O2 consumption, whereas CO2 output approached zero in both groups. [Lab] was unchanged. Arterial blood O2 saturation decreased more in ED than in C. ED are characterized by increased anaerobic metabolism likely due to the existence of a diving reflex.
Achievements in breath-hold diving depend, amongst others, on body oxygen stores at start of dive. A diver with very high lung volumes could increase dive's duration, and attain deeper depths for a given speed. Thus, we hypothesized that extreme breath-hold divers have very high lung volumes. On eight extreme breathhold divers (age 35 + 4 years, height 179 + 7 cm, body mass 76 + 6 kg) and 9 non-diving controls (age 37 + 6 years, height 177 + 4 cm, body mass 81 + 9 kg) residual volume, vital capacity and total lung capacity (TLC) were measured with a body plethysmograph. Forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV 1 ) were measured with a spirometer. Peak expiratory flow and flow-volume loops were measured with a pneumotachograph. In divers, but not in controls, volumes and capacities were systematically and significantly (p<0.01, paired t-test) higher than predicted from their body size. Consistently, volumes and capacities were significantly higher in divers than in controls, except for residual volume. Divers' TLC was 22% higher than predicted, and 21% higher than in controls. All divers' TLC was higher than 8 L, two had it higher than 9 L. FVC and FEV 1 were significantly higher in divers than in controls. The FEV 1 /FVC ratio was the same in both groups. We conclude that extreme breath-hold divers may constitute a niche population with physiological characteristics different from those of normal individuals, facilitating the achievement of excellent diving performances.
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