Larger splenic emptying correlate with slower EPOC kinetics in healthy men and women during supine cycling.

PURPOSE: The present study investigated whether larger splenic emptying augments faster excess post-exercise O2 consumption (EPOC) following aerobic exercise cessation. METHODS: Fifteen healthy participants (age 24 ± 4, 47% women) completed 3 laboratory visits at least 48-h apart. After obtaining medical clearance and familiarizing themselves with the test, they performed a ramp-incremental test in the supine position until task failure. At their final visit, they completed three step-transition tests from 20 W to a moderate-intensity power output (PO), equivalent to [Formula: see text]O2 at 90% gas exchange threshold, where data on metabolic, cardiovascular, and splenic responses were recorded simultaneously. After step-transition test cessation, EPOCfast was recorded, and the first 10 min of the recovery period was used for further analysis. Blood samples were collected before and immediately after the end of exercise. RESULTS: In response to moderate-intensity supine cycling ([Formula: see text]O2 = ~ 2.1 L·min-1), a decrease in spleen volume of ~ 35% (p = 0.001) was observed, resulting in a transient increase in red cell count of ~ 3-4% (p = 0.001) in mixed venous blood. In parallel, mean blood pressure, heart rate, and stroke volume increased by 30-100%, respectively. During recovery, mean τ[Formula: see text]O2 was 45 ± 18 s, the amplitude was 2.4 ± 0.5 L·min-1, and EPOCfast was 1.69 L·O2. Significant correlations were observed between the percent change in spleen volume and (i) EPOCfast (r = - 0.657, p = 0.008) and (ii) τ[Formula: see text]O2 (r = - 0.619, p = 0.008), but not between the change in spleen volume and (iii) [Formula: see text]O2 peak (r = 0.435, p = 0.105). CONCLUSION: Apparently, during supine cycling, individuals with larger spleen emptying tend to have slower [Formula: see text] O2 recovery kinetics and a greater EPOCfast.

No differences in splenic emptying during on-transient supine cycling between aerobically trained and untrained participants.

PURPOSE: The role of splenic emptying in O2 transport during aerobic exercise still remains a matter of debate. Our study compared the differences in spleen volume changes between aerobically trained and untrained individuals during step-transition supine cycling exercise at moderate-intensity. We also examined the relationship between spleen volume changes, erythrocyte release, and O2 uptake parameters. METHODS: Fourteen healthy men completed all study procedures, including a detailed medical examination, supine maximal O2 uptake ([Formula: see text] max.) test, and three step-transitions from 20 W to a moderate-intensity power output, equivalent to [Formula: see text] uptake at 90% gas exchange threshold. During these step-transitions pulmonary [Formula: see text], near-infrared spectroscopy of the vastus lateralis, and cardiovascular responses were continuously measured. In parallel, minute-by-minute ultrasonic measurements of the spleen were performed. Blood samples were taken before and immediately after step-transition cycling. RESULTS: On average, [Formula: see text] max. was 10 mL kg min-1 (p = 0.001) higher in trained compared to their aerobically untrained peers. In response to supine step-transition cycling, the splenic volume was significantly reduced, and the largest reduction (~ 106 to 115 mL, ~ 38%, p = 0.001) was similar in both aerobically trained and untrained individuals. Erythrocyte concentration and platelet count transiently increased after exercise cessation, with no differences observed between groups. However, the vastus lateralis deoxygenation amplitude was 30% (p = 0.001) greater in trained compared to untrained individuals. No associations existed between: (i) spleen volumes at rest (ii) spleen volume changes (%), (iii) resting hematocrit and oxygen uptake parameters. CONCLUSION: Greater splenic emptying and subsequent erythrocyte release do not lead to a slower [Formula: see text], regardless of individual [Formula: see text] max. readings.

Influence of oxygen enriched gases during decompression on bubble formation and endothelial function in self-contained underwater breathing apparatus diving: a randomized controlled study.

AIM: To assess the effect of air, gas mixture composed of 50% nitrogen and 50% oxygen (nitrox 50), or gas mixture composed of 1% nitrogen and 99% oxygen (nitrox 99) on bubble formation and vascular/endothelial function during decompression after self-contained underwater breathing apparatus diving. METHODS: This randomized controlled study, conducted in 2014, involved ten divers. Each diver performed three dives in a randomized protocol using three gases: air, nitrox 50, or nitrox 99 during ascent. The dives were performed on three different days limited to 45 m sea water (msw) depth with 20 min bottom time. Nitrogen bubbles formation was assessed by ultrasound detection after dive. Arterial/endothelial function was evaluated by brachial artery flow mediated dilatation (FMD) before and after dive. RESULTS: Nitrox 99 significantly reduced bubble formation after cough compared with air and nitrox 50 (grade 1 vs 3 and vs 3, respectively, P=0.026). Nitrox 50 significantly decreased post-dive FMD compared with pre-dive FMD (3.62 ± 5.57% vs 12.11 ± 6.82% P=0.010), while nitrox 99 did not cause any significant change. CONCLUSION: Nitrox 99 reduced bubble formation, did not change post-dive FMD, and decreased total dive duration, indicating that it might better preserve endothelial function compared with air and nitrox 50 dive protocols.

2D speckle tracking echocardiography of the right ventricle free wall in SCUBA divers after single open sea dive.

The presence of circulating gas bubbles and their influence on pulmonary and right heart hemodynamics was reported after uncomplicated self-contained underwater breathing apparatus (SCUBA) dive(s). Improvements in cardiac imaging have recently focused great attention on the right ventricle (RV). The aim of our study was to evaluate possible effects of a single air SCUBA dive on RV function using 2D speckle tracking echocardiography in healthy divers after single open sea dive to 18 meters of seawater, followed by bottom stay of 47 minutes with a direct ascent to the surface. Twelve experienced male divers (age 39.5 ± 10.5 years) participated in the study. Echocardiographic assessment of the right ventricular function (free wall 2 D strain, tricuspid annular planes systolic excursion [TAPSE], lateral tricuspid annular peak systolic velocity [RV s`] and fractional area change [FAC]) was performed directly prior to and 30, 60, 90 and 120 minutes after surfacing. Two-dimensional strain of all three segments of free right ventricular wall showed a significant increase in longitudinal shortening in post-dive period for maximally 26% (basal), 15.4% (mid) and 16.3% (apical) as well as TAPSE (11.6%), RV FAC (19.2%), RV S` (12.7%) suggesting a rise in systolic function of right heart. Mean pulmonary arterial pressure (mean PAP) increased post-dive from 13.3 mmHg to maximally 23.5 mmHg (P = .002), indicating increased RV afterload. Our results demonstrated that single dive with significant bubble load lead to increase in systolic function and longitudinal strain of the right heart in parallel with increase in mean PAP.

Blood pooling in extrathoracic veins after glossopharyngeal insufflation.

PURPOSE: Trained breath-hold divers hyperinflate their lungs by glossopharyngeal insufflation (GPI) to prolong submersion time and withstand lung collapse at depths. Pulmonary hyperinflation leads to profound hemodynamic changes. METHODS: Thirteen divers performed preparatory breath-holds followed by apnea with GPI. Filling of extrathoracic veins was determined by ultrasound and magnetic resonance imaging and peripheral extravasation of fluid was assessed by electrical impedance. Femoral vein diameter was measured by ultrasound throughout the easy-going and struggle phase of apnea with GPI in eight divers in a sub-study. RESULTS: After GPI, pulmonary volume increased by 0.8 ± 0.6 L above total lung capacity. The diameter of the superior caval (by 36 ± 17%) and intrathoracic part of the inferior caval vein decreased (by 21 ± 16%), while the diameters of the internal jugular (by 53 ± 34%), hepatic (by 28 ± 40%), abdominal part of the inferior caval (by 28 ± 28%), and femoral veins (by 65 ± 50%) all increased (P < 0.05). Blood volume of the internal jugular, the hepatic, the abdominal part of the inferior caval vein, and the combined common iliac and femoral veins increased by 145 ± 115, 80 ± 88, 61 ± 60, and 183 ± 197%, respectively. In the sub-study, femoral vein diameter increased by 44 ± 33% in the easy-going phase of apnea with GPI, subsequently decreasing by 20 ± 16% during the struggle phase. Electrical impedance remained unchanged over the thigh and forearm, thus excluding peripheral fluid extravasation. CONCLUSIONS: GPI leads to heart and pulmonary vessel compression, resulting in redistribution of blood to extrathoracic capacitance veins proximal to venous valves. This is partially reversed by the onset of involuntary breathing movements.

Depth of SCUBA Diving Affects Cardiac Autonomic Nervous System.

The present study investigated the influence of SCUBA dives with compressed air at depths of 10 and 20 m on ECG-derived HRV parameters in apparently healthy individuals. We hypothesized that cardiac sympathetic activity (measured by HRV parameters) adapts proportionally to diving depth, and that both time- and frequency-domain parameters are sensitive enough to track changes in cardiac ANS function during diving activities and subsequently during the recovery period. Eleven healthy middle-aged recreational divers (nine men and two women, age 43 ± 8, all nonsmokers) volunteered to participate in the present study. The participants (all open-circuit divers) were equipped with dry suits and ECG Holter devices and were later randomly assigned to dive pairs and depths (10 m vs. 20 m), and each participant served as his or her own control. No interaction effects (diving depth x time epoch) were found for the most commonly used HRV markers. More precisely, in response to two different diving protocols, a significant post hoc effect of time was observed for HR and SDNN, as these parameters transiently decreased during the dives and returned to baseline after ascent (p < 0.001). The ULF, VLF (p < 0.003), TP, and LF parameters decreased significantly during the dives, while HF significantly increased (p < 0.003). SCUBA diving apparently challenges the cardiac ANS, even in healthy individuals. The observed changes reveal possible underwater methods of influencing the parasympathetic activity of the heart depending on the depth of the dive. These results identify autonomic nervous system markers to track the cardiovascular risk related to diving and point to the possibility of tracking cardiovascular system benefits during underwater activities in selected patients.

Effects of Oxygen Prebreathing on Bubble Formation, Flow-Mediated Dilatation, and Psychomotor Performance during Trimix Dives.

Introduction: This research was performed to examine the effects of air and oxygen prebreathing on bubble formation, flow-mediated dilatation, and psychomotor performance after scuba dives. Methods: Twelve scuba divers performed two dives using a gas mixture of oxygen, nitrogen, and helium (trimix). In a randomized protocol, they breathed air or oxygen 30 min before the trimix dives. Venous bubble formation, flow-mediated dilatation, and psychomotor performance were evaluated. The participants solved three psychomotor tests: determining the position of a light signal, coordination of complex psychomotor activity, and simple arithmetic operations. The total test solving time, minimum single-task solving time, and median solving time were analyzed. Results: The bubble grade was decreased in the oxygen prebreathing protocol in comparison to the air prebreathing protocol (1.5 vs. 2, p < 0.001). The total test solving times after the dives, in tests of complex psychomotor coordination and simple arithmetic operations, were shorter in the oxygen prebreathing protocol (25 (21-28) vs. 31 (26-35) and 87 (82-108) vs. 106 (90-122) s, p = 0.028). Conclusions: In the oxygen prebreathing protocol, the bubble grade was significantly reduced with no change in flow-mediated dilatation after the dives, indicating a beneficial role for endothelial function. The post-dive psychomotor speed was faster in the oxygen prebreathing protocol.

Effect of repetitive SCUBA diving on humoral markers of endothelial and central nervous system integrity.

During SCUBA diving decompression, there is a significant gas bubble production in systemic veins, with rather frequent bubble crossover to arterial side even in asymptomatic divers. The aim of the current study was to investigate potential changes in humoral markers of endothelial and brain damage (endothelin-1, neuron-specific enolase and S-100ß) after repetitive SCUBA diving with concomitant assessment of venous gas bubble production and subsequent arterialization. Sixteen male divers performed four open-water no-decompression dives to 18 msw (meters of sea water) lasting 49 min in consecutive days during which they performed moderate-level exercise. Before and after dives 1 and 4 blood was drawn, and bubble production and potential arterialization were echocardiographically evaluated. In addition, a control dive to 5 msw was performed with same duration, water temperature and exercise load. SCUBA diving to 18 msw caused significant bubble production with arterializations in six divers after dive 1 and in four divers after dive 4. Blood levels of endothelin-1 and neuron-specific enolase did not change after diving, but levels of S-100ß were significantly elevated after both dives to 18 msw and a control dive. Creatine kinase activity following a control dive was also significantly increased. Although serum S-100ß levels were increased after diving, concomitant increase of creatine kinase during control, almost bubble-free, dive suggests the extracranial release of S-100ß, most likely from skeletal muscles. Therefore, despite the significant bubble production and sporadic arterialization after open-water dives to 18 msw, the current study found no signs of damage to neurons or the blood-brain barrier.

The Influence of Oral Cannabidiol on 24-h Ambulatory Blood Pressure and Arterial Stiffness in Untreated Hypertension: A Double-Blind, Placebo-Controlled, Cross-Over Pilot Study.

INTRODUCTION: Studies reveal that cannabidiol may acutely reduce blood pressure and arterial stiffness in normotensive humans; however, it remains unknown if this holds true in patients with untreated hypertension. We aimed to extend these findings to examine the influence of the administration of cannabidiol on 24-h ambulatory blood pressure and arterial stiffness in hypertensive individuals. METHODS: Sixteen volunteers (eight females) with untreated hypertension (elevated blood pressure, stage 1, stage 2) were given oral cannabidiol (150 mg every 8 h) or placebo for 24 h in a randomised, placebo-controlled, double-blind, cross-over study. Measures of 24-h ambulatory blood pressure and electrocardiogram (ECG) monitoring and estimates of arterial stiffness and heart rate variability were obtained. Physical activity and sleep were also recorded. RESULTS: Although physical activity, sleep patterns and heart rate variability were comparable between groups, arterial stiffness (~ 0.7 m/s), systolic blood pressure (~ 5 mmHg), and mean arterial pressure (~ 3 mmHg) were all significantly (P < 0.05) lower over 24 h on cannabidiol when compared to the placebo. These reductions were generally larger during sleep. Oral cannabidiol was safe and well tolerated with no development of new sustained arrhythmias. CONCLUSIONS: Our findings indicate that acute dosing of cannabidiol over 24 h can lower blood pressure and arterial stiffness in individuals with untreated hypertension. The clinical implications and safety of longer-term cannabidiol usage in treated and untreated hypertension remains to be established.

Effects of successive air and nitrox dives on human vascular function.

SCUBA diving is regularly associated with asymptomatic changes in cardiac, pulmonary and vascular function. The aim of this study was to evaluate the changes in vascular/endothelial function following SCUBA diving and to assess the potential difference between two breathing gases: air and nitrox 36 (36% oxygen and 64% nitrogen). Ten divers performed two 3-day diving series (no-decompression dive to 18 m with 47 min bottom time with air and nitrox, respectively), with 2 weeks pause in between. Arterial/endothelial function was assessed using SphygmoCor and flow-mediated dilation measurements, and concentration of nitrite before and after diving was determined in venous blood. Production of nitrogen bubbles post-dive was assessed by ultrasonic determination of venous gas bubble grade. Significantly higher bubbling was found after all air dives as compared to nitrox dives. Pulse wave velocity increased slightly (~6%), significantly after both air and nitrox diving, indicating an increase in arterial stiffness. However, augmentation index became significantly more negative after diving indicating smaller wave reflection. There was a trend for post-dive reduction of FMD after air dives; however, only nitrox diving significantly reduced FMD. No significant differences in blood nitrite before and after the dives were found. We found that nitrox diving affects systemic/vascular function more profoundly than air diving by reducing FMD response, most likely due to higher oxygen load. Both air and nitrox dives increased arterial stiffness, but decreased wave reflection suggesting a decrease in peripheral resistance due to exercise during diving. These effects of nitrox and air diving were not followed by changes in plasma nitrite.

A no-decompression air dive and ultrasound lung comets.

INTRODUCTION: Increased accumulation of extravascular lung water after repetitive deep trimix dives was recently reported. This effect was evident 40 min post-dive, but in subsequent studies most signs of this lung congestion were not evident 2-3 h post-dive, indicating no major negative effects on respiratory gas exchange following deep dives. Whether this response is unique for trimix dives or also occurs in more frequent air dives is presently unknown. METHODS: A single no-decompression field dive to 33 m with 20 min bottom time was performed by 12 male divers. Multiple ultrasound lung comets (ULC), bubble grade (BG), and single-breath lung diffusing capacity (DLCO) measurements were made before and up to 120 min after the dive. RESULTS: Median BG was rather high with maximal values observed at 40 min post-dive [median 4 (4-4)]. Arterialization of bubbles from the venous side was observed only in one diver lasting up to 60 min post-dive. Despite high BG, no DCS symptoms were noted. DLCO and ULC were unchanged after the dive at any time point (DLCO(corr) was 33.6 +/- 1.9 ml x min(-1) mmHg(-1) pre-dive, 32.7 +/- 3.8 ml x min(-1) x mmHg(-1) at 60 min post-dive, and 33.2 +/- 5.3 ml x min(-1) x mmHg(-1) at 120 min post-dive; ULC count was 4.1 +/- 1.9 pre-dive, 4.9 +/- 3.3 at 20 min post-dive, and 3.3 +/- 1.9 at 60 min post-dive. DISCUSSION: These preliminary findings show no evidence of increased accumulation of extravascular lung water in male divers after a single no-decompression air dive at the limits of accepted Norwegian diving tables.

Acute flywheel exercise does not impair the brachial artery vasodilation in healthy men of varying aerobic fitness.

BACKGROUND: The cardiovascular response to variable load exercise on a flywheel ergometer is still unknown. OBJECTIVE: This study examined the effects of flywheel exercise on cardiovascular response and brachial artery vasodilation capacity in healthy, active men. METHODS: In this cross-sectional study, nineteen men (20-57 years old) completed three laboratory visits, including a ramp exercise test to determine their maximal oxygen uptake JOURNAL/blpmo/04.03/00126097-202106000-00008/inline-graphic1/v/2021-04-27T091817Z/r/image-tiff max, and exercise intervention on a flywheel ergometer set at 0.075 kg·m2 moment of inertia. After the ramp test cessation, all participants were allocated into aerobically untrained (n = 10) and trained (n = 9) groups. Throughout the flywheel exercise, cardiovascular demands were continuously monitored via Finapres, while a pre/postflow-mediated dilation (FMD) assessment was performed using ultrasound imaging. RESULTS: There were no differences observed between the groups in their anthropometrics, age or resting brachial artery diameter, while the JOURNAL/blpmo/04.03/00126097-202106000-00008/inline-graphic2/v/2021-04-27T091817Z/r/image-tiff max was ~15% higher (P = 0.001) in trained compared to aerobically untrained group. The cardiovascular response to the flywheel exercise was similar between the groups, with peak mean arterial pressure and heart rate readings reaching ~160 mmHg and ~140 bpm, respectively. The flywheel exercise did not impair the FMD (%) response, which was comparable between the groups (P = 0.256). When these data were pooled, the regression analysis showed an inverse relationship among FMD (%), age (ß = -0.936, P = 0.001) and JOURNAL/blpmo/04.03/00126097-202106000-00008/inline-graphic3/v/2021-04-27T091817Z/r/image-tiffmax. (ß = -0.359, P = 0.045). CONCLUSION: Although aerobic fitness alone does not directly explain the FMD response to flywheel exercise, aerobically untrained individuals, as they get older, tend to have lower brachial artery FMD.

Spleen emptying does not correlate with faster oxygen kinetics during a step-transition supine cycling.

This manuscript quantified spleen volume changes and examined the relationship between those changes and oxygen uptake kinetics during supine cycling. Ten volunteers (age = 22 ± 3), completed 3 step transitions from 20 W to their power output at 90% gas exchange threshold. Ultrasonic measurements of the spleen were performed each minute. The largest spleen volume reduction was 105 mL (p = 0.001). No associations existed between i) spleen volumes at rest; and ii) spleen volume changes (%) and tau pulmonary oxygen uptake (τV̇O2p). Larger resting spleen volume and greater emptying do not correlate with a faster τV̇O2p. Novelty: Greater splenic contractions do not augment τV̇O2p, irrespective of spleen emptying and subsequent erythrocyte release.

Glossopharyngeal insufflation induces cardioinhibitory syncope in apnea divers.

Apnea divers increase intrathoracic pressure voluntarily by taking a deep breath followed by glossopharyngeal insufflation. Because apnea divers sometimes experience hypotension and syncope during the maneuver, they may serve as a model to study the mechanisms of syncope. We recorded changes in hemodynamics and sympathetic vasomotor tone with microneurography during breath holding with glossopharyngeal insufflation. Five men became hypotensive and fainted during breath holding with glossopharyngeal insufflation within the first minute. In four divers, heart rate dropped suddenly to a minimum of 38 ± 4 beats/min. Therefore, cardioinhibitory syncope was more common than low cardiac output syncope.

Central chemoreflex sensitivity and sympathetic neural outflow in elite breath-hold divers.

Repeated hypoxemia in obstructive sleep apnea patients increases sympathetic activity, thereby promoting arterial hypertension. Elite breath-holding divers are exposed to similar apneic episodes and hypoxemia. We hypothesized that trained divers would have increased resting sympathetic activity and blood pressure, as well as an excessive sympathetic nervous system response to hypercapnia. We recruited 11 experienced divers and 9 control subjects. During the diving season preceding the study, divers participated in 7.3 +/- 1.2 diving fish-catching competitions and 76.4 +/- 14.6 apnea training sessions with the last apnea 3-5 days before testing. We monitored beat-by-beat blood pressure, heart rate, femoral artery blood flow, respiration, end-tidal CO(2), and muscle sympathetic nerve activity (MSNA). After a baseline period, subjects began to rebreathe a hyperoxic gas mixture to raise end-tidal CO(2) to 60 Torr. Baseline MSNA frequency was 31 +/- 11 bursts/min in divers and 33 +/- 13 bursts/min in control subjects. Total MSNA activity was 1.8 +/- 1.5 AU/min in divers and 1.8 +/- 1.3 AU/min in control subjects. Arterial oxygen saturation did not change during rebreathing, whereas end-tidal CO(2) increased continuously. The slope of the hypercapnic ventilatory and MSNA response was similar in both groups. We conclude that repeated bouts of hypoxemia in elite, healthy breath-holding divers do not lead to sustained sympathetic activation or arterial hypertension. Repeated episodes of hypoxemia may not be sufficient to drive an increase in resting sympathetic activity in the absence of additional comorbidities.

Restoration of hemodynamics in apnea struggle phase in association with involuntary breathing movements.

Involuntary breathing movements (IBM) that occur in the struggle phase of maximal apneas produce waves of negative intrathoracic pressure. This could augment the venous return, increasing thereby the cardiac output and gas exchange, and release the fresh blood from venous pools of spleen and liver. To test these hypotheses we used photoplethysmography and ultrasound for assessment of hemodynamics and spleen size before, during and after maximal dry apneas at large lung volume in 7 trained divers. During the easy-going phase cardiac output was reduced about 40%, due to reduction in stroke volume and in presence of reduced inferior vena cava venous return, while the spleen contracted for about 60 ml. Towards the end of the struggle phase, in presence of intense IBM, the spleen volume further decreased for about 70 ml, while cardiac output and caval flow almost renormalized. In conclusion, IBM coincide with splenic volume reduction and restoration of hemodynamics, likely facilitating the use of the last oxygen reserves before apnea cessation.

High-grade bubbles in left and right heart in an asymptomatic diver at rest after surfacing.

INTRODUCTION: Most decompression procedures induce the formation of asymptomatic venous gas bubbles. They can be classified as "silent bubbles," which are asymptomatic compared to paradoxical arterialization of venous gas emboli, which can lead to serious neurologic damage. The penetration of such gas bubbles into the arterial circulation is due to pulmonary barotrauma, intrapulmonary (I-P) passage after massive bubble formation ("chokes"), or intracardiac shunting. Venous gas bubbles can be monitored and graded with echocardiographic scanning. CASE: We believe this is the first case to be reported of a recreational diver who, after surfacing from a dive, developed grade 5 ("white-out") venous gas bubbles in the right heart with evidence of I-P shunt at rest without any symptoms of decompression sickness. Grade 4 gas bubbles were found on the left side of the heart, indicating significant I-P shunting even at rest. CONCLUSION: We observed venous bubbles crossing through the I-P shunt during post-dive recovery at rest in a diver who developed "white out" of venous bubbles. Previously, the maximum bubble grade 5 had been observed in experimental animals, but not in humans. Moreover, a significant bubble grade was found on the left side of the heart, indicating a need for further studies to investigate the mechanisms of post-dive changes in peripheral and central circulation.

Spleen and cardiovascular function during short apneas in divers.

We investigated the spleen volume changes as related to the cardiovascular responses during short-duration apneas at rest. We used dynamic ultrasound splenic imaging and noninvasive photoplethysmographic cardiovascular measurements before, during, and after 15-20 s apneas in seven trained divers. The role of baroreflex was studied by intravenous bolus of vasodilating drug trinitrosan during tidal breathing. The role of lung volume was studied by comparing the apneas at near-maximal lung volume with apneas after inhaling tidal volume, with and without cold forehead stimulation. In apneas at near maximal lung volume, a 20% reduction in splenic volume (P = 0.03) was observed as early as 3 s after the onset of breath holding. Around that time the heart rate increased, the mean arterial pressure abruptly decreased from 89.6 to 66.7 mmHg (P = 0.02), and cardiac output decreased, on account of reduction in stroke volume. Intravenous application of trinitrosan resulted in approximately 6-mmHg decrement in mean arterial pressure, while the splenic volume decreased for approximately 13%. In apneas at low lung volume, the early splenic contraction was also observed, 10% without and 12% with cold forehead stimulation, although the mean arterial pressure did not change or even increased, respectively. In conclusion, the spleen contraction is present at the beginning of apnea, accentuated by cold forehead stimulation. At large, but not small, lung volume, this initial contraction is probably facilitated by downloaded baroreflex in conditions of decreased blood pressure and cardiac output.

Cerebral and peripheral hemodynamics and oxygenation during maximal dry breath-holds.

The effects of maximal apneas on cerebral and brachial blood flow and oxygenation are unknown in humans. Middle cerebral artery blood velocity (MCAV), cerebral and muscle oxygenation (Sc(O2) and Sm(O2)) and brachial blood flow (BBF) were measured during apneas in breath-hold divers (BHD) and non-divers (ND). Brain oxyhemoglobin (O(2)Hb) was maintained in both groups until the end of apnea, whereas deoxyhemoglobin increased more in BHD. Therefore, Sc(O2) decreased more in BHD due to longer apnea duration and smaller initial MCAV increase. MCAV increased significantly more in BHD versus ND at the end of apnea. Cerebral desaturation for approximately 13% occurred at the end of apnea in BHD despite increased cerebral oxygen delivery for approximately 50%. Larger reduction in muscle O(2)Hb was found in BHD, with similar peripheral vasoconstriction. These data indicate that BHD have decreased Sc(O2) at the end of breath-hold despite large increases in MCAV. This is partly due delayed initial cerebral vasodilation. This study provides further evidence for the oxygen-conserving effect in elite divers.