Repeated maximal breath‐holds have been demonstrated to induce bradycardia, increase haematocrit and haemoglobin and prolong subsequent breath‐hold duration by 20%. Freedivers use non‐maximal breath‐hold techniques (BHTs) to improve breath‐hold duration. The aim of this study was to investigate the cardiorespiratory and haematological responses to various BHTs. Ten healthy men (34.5 ± 1.9 years) attended five randomized experimental trials and performed a 40 min period of quiet rest or one of three BHTs followed by a maximal breath‐hold challenge during facial immersion in water at 30 or 10°C. Cardiovascular and respiratory parameters were measured continuously using finger plethysmography and breath‐by‐breath gas analysis, respectively, and venous blood samples were collected throughout. Facial immersion in cold water caused marked bradycardia (74.1 vs. 50.2 beats/min after 40 s) but did not increase breath‐hold duration compared with warm water control conditions. Facial immersion breath‐hold duration was 30.8–43.3% greater than the control duration when preceded by BHTs that involved repeated breath‐holds of constant duration ( P = 0.021), increasing duration ( P < 0.001) or increasing frequency ( P < 0.001), with no difference observed between BHTs. The increased duration of apnoea across all three BHT protocols was associated with a 6.8% increase in end‐tidal O 2 and a 13.1% decrease in end‐tidal CO 2 immediately before facial immersion. There were no differences in blood pressure, cardiac output, heart rate, haematocrit or haemoglobin between each BHT and control conditions ( P > 0.05). In conclusion, the duration of apnoea can be extended by manipulating blood gases through repeated prior breath‐holds, but changes in cardiac output and red blood cell mass do not appear essential.
What is the central question of this study?
What is the effect of three repeated breath‐hold techniques routinely used by freedivers, thought to manipulate arterial partial pressures of O 2 and CO 2, on the cardiorespiratory and haematological response to breath‐holding during facial immersion?
What is the main finding and its importance?
All three techniques increased breath‐hold by a similar duration, probably owing to the similar marked increase in end‐tidal O 2 and decrease in end‐tidal CO 2 observed in all three trials before facial immersion. These were the only cardiorespiratory changes that were consistently manipulated before the maximal breath‐hold. This would suggest that pronounced bradycardia and vasoconstriction of selective vascular beds are probably not obligatory for prolonging breath‐hold duration.