Cardiovascular Regulation During Apnea in Elite Divers

Involuntary apnea during sleep elicits sustained arterial hypertension through sympathetic activation; however, little is known about voluntary apnea, particularly in elite athletes. Their physiological adjustments are largely unknown. We measured blood pressure, heart rate, hemoglobin oxygen saturation, muscle sympathetic nerve activity, and vascular resistance before and during maximal end-inspiratory breath holds in 20 elite divers and in 15 matched control subjects. At baseline, arterial pressure and heart rate were similar in both groups. Maximal apnea time was longer in divers (1.7 +/- 0.4 versus 3.9 +/- 1.1 minutes; P < 0.0001), and it was accompanied by marked oxygen desaturation (97.6 +/- 0.7% versus 77.6 +/- 13.9%; P < 0.0001). At the end of apnea, divers showed a > 5-fold greater muscle sympathetic nerve activity increase (P < 0.01) with a massively increased pressor response compared with control subjects (9 +/- 5 versus 32 +/- 15 mm Hg; P < 0.001). Vascular resistance increased in both groups, but more so in divers (79 +/- 46% versus 140 +/- 82%; P < 0.01). Heart rate did not change in either group. The rise in muscle sympathetic nerve activity correlated with oxygen desaturation (r(2)=0.26; P < 0.01) and with the increase in mean arterial pressure (r(2)=0.40; P < 0.0001). In elite divers, breath holds for several minutes result in an excessive chemoreflex activation of sympathetic vasoconstrictor activity. Extensive sympathetically mediated peripheral vasoconstriction may help to maintain adequate oxygen supply to vital organs under asphyxic conditions that untrained subjects are not able to tolerate voluntarily. Our results are relevant to conditions featuring periodic apnea. (Hypertension. 2009; 53: 719-724.)