The purpose of this study was 1) to answer whether the reduction in spleen size in breath-hold apnea is an active contraction or a passive collapse secondary to reduced splenic arterial blood flow and 2) to monitor the spleen response to repeated breath-hold apneas. Ten trained apnea divers and 10 intact and 7 splenectomized untrained persons repeated five maximal apneas (A1-A5) with face immersion in cold water, with 2 min interposed between successive attempts. Ultrasonic monitoring of the spleen and noninvasive cardiopulmonary measurements were performed before, between apneas, and at times 0, 10, 20, 40, and 60 min after the last apnea. Blood flows in splenic artery and splenic vein were not significantly affected by breath-hold apnea. The duration of apneas peaked after A3 (143, 127, and 74 s in apnea divers, intact, and splenectomized persons, respectively). A rapid decrease in spleen volume ( approximately 20% in both apnea divers and intact persons) was mainly completed throughout the first apnea. The spleen did not recover in size between apneas and only partly recovered 60 min after A5. The well-known physiological responses to apnea diving, i.e., bradycardia and increased blood pressure, were observed in A1 and remained unchanged throughout the following apneas. These results show rapid, probably active contraction of the spleen in response to breath-hold apnea in humans. Rapid spleen contraction and its slow recovery may contribute to prolongation of successive, briefly repeated apnea attempts.

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

Is there an ordered pattern in the recruitment of postganglionic sympathetic neurones? Using new multi-unit action potential detection and analysis techniques we sought to determine whether the activation of sympathetic vasomotor neurones during stress is governed by the size principle of recruitment. Multi-unit postganglionic sympathetic activity (fibular nerve) was collected from five male subjects at rest and during periods of elevated sympathetic stress (end-inspiratory apnoeas; 178 ± 37 s(mean ± S.D.)). Compared to baseline (0.24 ± 0.04 V), periods of elevated stress resulted in augmented sympathetic burst size (1.34 ± 0.38 V, P < 0.05). Increased burst size was directly related to both the number of action potentials within a multi-unit burst of postganglionic sympathetic activity (r = 0.88 ± 0.04, P < 0.001 in all subjects), and the amplitude of detected action potentials (r = 0.88 ± 0.06, P < 0.001 in all subjects). The recruitment of larger, otherwise silent, neurons accounted for approximately 74% of the increase in detected action potentials across burst sizes. Further, action potential conduction velocities (inverse of latencies) were increased as a function of action potential size (R 2 = 0.936, P = 0.001). As axon diameter is positively correlated with action potential size and conduction velocity, these data suggest that the principle of ordered recruitment based on neuronal size applies to postganglionic sympathetic vasomotor neurones. This information may be pertinent to our understanding of reflex-specific recruitment strategies in postganglionic sympathetic nerves, patterns of vasomotor control during stress, and the malleability of sympathetic neuronal properties and recruitment in health and disease.

During and after decompression from dives, gas bubbles are regularly observed in the right ventricular outflow tract. A number of studies have documented that these bubbles can lead to endothelial dysfunction in the pulmonary artery but no data exist on the effect of diving on arterial endothelial function. The present study investigated if diving or oxygen breathing would influence endothelial arterial function in man. A total of 21 divers participated in this study. Nine healthy experienced male divers with a mean age of 31 ± 5 years were compressed in a hyperbaric chamber to 280 kPa at a rate of 100 kPa min −1 breathing air and remaining at pressure for 80 min. The ascent rate during decompression was 9 kPa min −1 with a 7 min stop at 130 kPa (US Navy procedure). Another group of five experienced male divers (31 ± 6 years) breathed 60% oxygen (corresponding to the oxygen tension of air at 280 kPa) for 80 min. Before and after exposure, endothelial function was assessed in both groups as flow-mediated dilatation (FMD) by ultrasound in the brachial artery. The results were compared to data obtained from a group of seven healthy individuals of the same age who had never dived. The dive produced few vascular bubbles, but a significant arterial diameter increase from 4.5 ± 0.7 to 4.8 ± 0.8 mm (mean ± S.D.) and a significant reduction of FMD from 9.2 ± 6.9 to 5.0 ± 6.7% were observed as an indication of reduced endothelial function. In the group breathing oxygen, arterial diameter increased significantly from 4.4 ± 0.3 mm to 4.7 ± 0.3 mm, while FMD showed an insignificant decrease. Oxygen breathing did not decrease nitroglycerine-induced dilatation significantly. In the normal controls the arterial diameter and FMD were 4.1 ± 0.4 mm and 7.7 ± 0.2.8%, respectively. This study shows that diving can lead to acute arterial endothelial dysfunction in man and that oxygen breathing will increase arterial diameter after return to breathing air. Further studies are needed to determine if these mechanisms are involved in tissue injury following diving.