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.

No abstract

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

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.

To test the hypothesis that vasodilation occurs because of the release of a vasoactive substance after a brief muscle contraction and to determine whether acetylcholine spillover from the motor nerve is involved in contraction-induced hyperemia, tetanic muscle contractions were produced by sciatic nerve stimulation in anesthetized dogs (n = 16), instrumented with flow probes on both external iliac arteries. A 1-s stimulation of the sciatic nerve at 1. 5, 3, and 10 times motor threshold increased blood flow above baseline (P < 0.01) for 20, 25, and 30 s, respectively. Blood flow was significantly greater 1 s after the contraction ended for 3 and 10 x motor threshold (P < 0.01) and did not peak until 6-7 s after the contraction. The elevations in blood flow to a 1-s stimulation of the sciatic nerve and a 30-s train of stimulations were abolished by neuromuscular blockade (vecuronium). The delayed peak blood flow response and the prolonged hyperemia suggest that a vasoactive substance is rapidly released from the contracting skeletal muscle and can affect blood flow with removal of the mechanical constraint imposed by the contraction. In addition, acetylcholine spillover from the motor nerve is not responsible for the increase in blood flow in response to muscle contraction.

Attenuation of sympathetic vasoconstriction (sympatholysis) in working muscles during dynamic exercise is controversial. A potential mechanism is a reduction in alpha-adrenergic-receptor responsiveness. The purpose of this study was to examine alpha(1)- and alpha(2)-adrenergic-receptor-mediated vasoconstriction in resting and exercising skeletal muscle using intra-arterial infusions of selective agonists. Thirteen mongrel dogs were instrumented chronically with flow probes on the external iliac arteries of both hindlimbs and a catheter in one femoral artery. The selective alpha(1)-adrenergic agonist (phenylephrine) or the selective alpha(2)-adrenergic agonist (clonidine) was infused as a bolus into the femoral artery catheter at rest and during mild and heavy exercise. Intra-arterial infusions of phenylephrine elicited reductions in vascular conductance of 76 +/- 4, 71 +/- 5, and 31 +/- 2% at rest, 3 miles/h, and 6 miles/h and 10% grade, respectively. Intra-arterial clonidine reduced vascular conductance by 81 +/- 5, 49 +/- 4, and 14 +/- 2%, respectively. The response to intra-arterial infusion of clonidine was unaffected by surgical sympathetic denervation. Agonist infusion did not affect either systemic blood pressure, heart rate, or blood flow in the contralateral iliac artery. alpha(1)-Adrenergic-receptor responsiveness was attenuated during heavy exercise. In contrast, alpha(2)-adrenergic-receptor responsiveness was attenuated even at a mild exercise intensity. These results suggest that the mechanism of exercise sympatholysis may involve reductions in postsynaptic alpha-adrenergic-receptor responsiveness.

1. The human spleen sequesters 200-250 mL densely packed red blood cells. Up to 50% of this viscous blood is actively expelled into the systemic circulation during strenuous exercise or simulated apnoea (breath-hold) diving. The contribution of splenic contraction to changes in the circulating volume of red blood cells (RBCV), as well as the venous concentration of white blood cells (WBC) and platelets (PLT), was investigated following repeated breath-hold apnoeas. 2. Eighteen trained apnoea divers and 18 intact and six splenectomized subjects without diving experience repeated five maximal apnoeas with face immersion in cold water, with 2 min intervals between successive attempts. Venous blood samples were taken before and between consecutive apnoeas, as well as at 0, 10 and 20 min after the last breath hold. Arterial pressure, heart rate and transcutaneous partial pressure of oxygen and carbon dioxide were monitored continuously. 3. Plasma protein concentration decreased by 5.8, 2.2 and 9% in apnoea divers, untrained and splenectomized subjects, respectively, indicating an expansion of plasma volume. The RBCV and venous concentration of WBC, corrected for changes in plasma volume, increased in both trained apnoea divers (4.9+/-1.0 and 14.9+/-3.1%, respectively) and intact subjects (1.7+/-0.8 and 7.2+/-1.8%, respectively), whereas in splenectomized subjects there was no change in RBCV and a delayed increase in WBC concentration. Furthermore, an initial lymphocytosis detected during repeated breath holds in divers and intact subjects was completely absent in splenectomized subjects. None of the groups showed significant changes in PLT concentrations. The well-recognized diving response to apnoea (bradycardia and increased blood pressure) was seen during all breath-hold attempts in all subjects. 4. Repeated breath-holds (apnoeas) contribute to increased RBCV and venous blood concentrations of WBC through splenic contraction.