Sympathetic vasoconstriction of muscle vascular beds is important in the regulation of systemic blood pressure. However, vasoconstriction during exercise can also compromise blood flow support of muscle metabolism. This study tested the hypothesis that local factors in exercising muscle blunt vessel responsiveness to sympathetic vasoconstriction. We performed selective infusions of three doses of tyramine into the brachial artery (n= 8) to evoke endogenous release of noradrenaline (norepinephrine) at rest and during moderate and heavy rhythmic handgrip exercise. In separate experiments, tyramine was administered during two doses of adenosine infusion (n= 7) and two doses of sodium nitroprusside (SNP) infusion (n= 8). Vasoconstrictor effectiveness across conditions was assessed as the percentage reduction in forearm vascular conductance (FVC), calculated from invasive blood pressure and non‐invasive Doppler ultrasound blood flow measurements at the brachial artery. Tyramine evoked a similar dose‐dependent vasoconstriction at rest in all three groups, with the highest dose resulting in a 42‐46 % reduction in FVC. This vasoconstriction was blunted with increasing exercise intensity (e.g. tyramine high dose percentage reduction in FVC; rest −43.4 ± 3.7 %, moderate exercise −27.5 ± 2.3 %, heavy exercise −16.7 ± 3.6 %; P < 0.05). In contrast, tyramine infusion resulted in a greater percentage reduction in FVC during both doses of adenosine vs. rest (P < 0.05). Finally, percentage change in FVC was greater during low dose SNP infusion vs. rest (P < 0.05), but not different from rest at the high dose of SNP infusion (P= 0.507). A blunted percentage reduction in FVC during endogenous noradrenaline release in exercise but not vasodilator infusion indicates that sympathetic vasoconstriction is blunted in exercising muscle. This blunting appears to be exercise intensity‐dependent.

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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