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Central chemoreflex sensitivity and sympathetic neural outflow in elite breath-hold divers

¹Department of Physiology, University of Split School of Medicine, Split, Croatia; ²Franz-Volhard Clinical Research Center, Max Delbrück Center, Charité Campus Buch, and HELIOS Klinikum Berlin, Berlin, Germany; ³Department of Neurology, Clinical Hospital Split, Split, Croatia; ⁴Autonomic Dysfunction Service, Vanderbilt University, Nashville, Tennessee; and ⁵Department of Anesthesiology, Mayo Clinic College of Medicine, Rochester, New York

Submitted 7 August 2007 ; accepted in final form 5 November 2007

Repeated hypoxemia in obstructive sleep apnea patients increases sympathetic activity, thereby promoting arterial hypertension. Elite breath-holding divers are exposed to similar apneic episodes and hypoxemia. We hypothesized that trained divers would have increased resting sympathetic activity and blood pressure, as well as an excessive sympathetic nervous system response to hypercapnia. We recruited 11 experienced divers and 9 control subjects. During the diving season preceding the study, divers participated in 7.3 ± 1.2 diving fish-catching competitions and 76.4 ± 14.6 apnea training sessions with the last apnea 3–5 days before testing. We monitored beat-by-beat blood pressure, heart rate, femoral artery blood flow, respiration, end-tidal CO₂, and muscle sympathetic nerve activity (MSNA). After a baseline period, subjects began to rebreathe a hyperoxic gas mixture to raise end-tidal CO₂ to 60 Torr. Baseline MSNA frequency was 31 ± 11 bursts/min in divers and 33 ± 13 bursts/min in control subjects. Total MSNA activity was 1.8 ± 1.5 AU/min in divers and 1.8 ± 1.3 AU/min in control subjects. Arterial oxygen saturation did not change during rebreathing, whereas end-tidal CO₂ increased continuously. The slope of the hypercapnic ventilatory and MSNA response was similar in both groups. We conclude that repeated bouts of hypoxemia in elite, healthy breath-holding divers do not lead to sustained sympathetic activation or arterial hypertension. Repeated episodes of hypoxemia may not be sufficient to drive an increase in resting sympathetic activity in the absence of additional comorbidities.

ultrasound; muscle sympathetic nerve activity; apnea; human

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