Abstract-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. Key Words: baroreflex Ⅲ breath-hold diving Ⅲ chemoreflex Ⅲ diving response Ⅲ sympathetic nervous system . "I nvoluntary" sleep apnea episodes trigger sympathetically mediated blood pressure surges 1 and predispose to cardiovascular and cerebrovascular morbidity and mortality. [2][3][4] The state of affairs is disturbing, because healthy people, including underwater hockey players, synchronized swimmers, and elite breath-hold divers practice "voluntary" apnea on a regular basis. Freestyle swimmers may hold their breath throughout 50-m sprint competitions. Elite breath-hold divers can hold their breath for several minutes. In these unique individuals, arterial oxygen saturation may decrease to Ͻ50%, whereas alveolar carbon dioxide partial pressure increases substantially. 5 Typically, diving fish-catching competitions last for 5 hours with cumulative apnea duration of Ϸ1 hour.Breath holding elicits complex cardiovascular adaptations even before relevant changes in arterial blood gases occur. The response includes bradycardia, reduced cardiac output, and peripheral vasoconstriction through sympathetic activation. 6,7 The so-called diving response seems to conserve oxygen. 8 -10 Breath holding without water immersion also increases sympathetic vasomotor tone. [11][12][13][14][15][16][17][18][19]20 and hypercapnia 16,18 provide additional stimuli to the sympathetic nervous system through central and peripheral chemoreflex mechanisms. However, in untrained individuals, breath-hold duration is too short to elicit a relevant decrease in arterial oxygen saturation. 21 We tested the hypothesis that the sympathetic vasomotor response to maximal breath holding is increased in apnea divers compared with control subjects. Methods Study PopulationWe recruited 43 young white subjects. Twenty two were active apnea divers. Within the preceding months, they participated in Ն7 diving competitions and Ն70 training sessions, each consisting of 30 to 40 maximal apneas, separated by variable interapneic periods. Matched, untrained subjects served as controls. All of the participants were healthy nonsmokers and ingested no medications. The

Diving-induced acute alterations in cardiovascular function such as arterial endothelial dysfunction, increased pulmonary artery pressure (PAP) and reduced heart function have been recently reported. We tested the effects of acute antioxidants on arterial endothelial function, PAP and heart function before and after a field dive. Vitamins C (2 g) and E (400 IU) were given to subjects 2 h before a second dive (protocol 1) and in a placebo-controlled crossover study design (protocol 2). Seven experienced divers performed open sea dives to 30 msw with standard decompression in a non-randomized protocol, and six of them participated in a randomized trial. Before and after the dives ventricular volumes and function and pulmonary and brachial artery function were assessed by ultrasound. The control dive resulted in a significant reduction in flow-mediated dilatation (FMD) and heart function with increased mean PAP. Twenty-four hours after the control dive FMD was still reduced 37% below baseline (8.1 versus 5.1%, P = 0.005), while right ventricle ejection fraction (RV-EF), left ventricle EF and endocardial fractional shortening were reduced much less (∼2-3%). At the same time RV end-systolic volume was increased by 9% and mean PAP by 5%. Acute antioxidants significantly attenuated only the reduction in FMD post-dive (P < 0.001), while changes in pulmonary artery and heart function were unaffected by antioxidant ingestion. These findings were confirmed by repeating the experiments in a randomized study design. FMD returned to baseline values 72 h after the dive with pre-dive placebo, whereas for most cardiovascular parameters this occurred earlier (24-48 h). Right ventricular dysfunction and increased PAP lasted longer. Acute antioxidants attenuated arterial endothelial dysfunction after diving, while reduction in heart and pulmonary artery function were unchanged. Cardiovascular changes after diving are not fully reversed up to 3 days after a dive, suggesting longer lasting negative effects.

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These findings indicate that, in moderately trained athletes, postexercise hypotension is associated primarily with reduced cardiac output because of reduced stroke volume, suggesting venous pooling. In addition, the occurrence of hypotension is more frequent in trained subjects with lower cardiopulmonary fitness level or higher resting SBP.