Autonomic and cardiovascular responses to chemoreflex stress in apnoea divers

Sleep apnoea, with repeated periods of hypoxia, results in cardiovascular morbidity and concomitant autonomic dysregulation. Trained apnoea divers also perform prolonged apnoeas accompanied by large lung volumes, large reductions in cardiac output and severe hypoxia and hypercapnia. We tested the hypothesis that apnoea training would be associated with decreased cardiovagal and sympathetic baroreflex gains and reduced respiratory modulation of muscle sympathetic nerve activity (MSNA; microneurography). Six trained divers and six controls were studied at rest and during asphyxic rebreathing. Despite an elevated resting heart rate (70 ± 14 vs. 56 ± 10 bpm; p = 0.038), divers had a similar cardiovagal baroreflex gain (−1.22 ± 0.47 beats/mmHg) as controls (−1.29 ± 0.61; NS). Similarly, though MSNA burst frequency was slightly higher in divers at rest (16 ± 4 bursts/min vs. 10 ± 5 bursts/min, p = 0.03) there was no difference in baseline burst incidence, sympathetic baroreflex gain (−3.8 ± 2.1%/mmHg vs. −4.7 ± 1.7%/mmHg) or respiratory modulation of MSNA between groups. Resting total peripheral resistance (11.9 ± 2.6 vs. 12.3 ± 2.2 mmHg/L/min) and pulse wave velocity (5.82 ± 0.55 vs. 6.10 ± 0.51 m/s) also were similar between divers and controls, respectively. Further, the sympathetic response to asphyxic rebreathing was not different between controls and divers (−1.70 ± 1.07 vs. −1.74 ± 0.84 a.u./% desaturation). Thus, these data suggest that, unlike patients with sleep apnoea, apnoea training in otherwise healthy individuals does not produce detectable autonomic dysregulation or maladaption.