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.

Phrenic long-term depression evoked by intermittent hypercapnia is modulated by serotonergic and adrenergic receptors in raphe nuclei.

Intermittent hypercapnia evokes prolonged depression of phrenic nerve activity (phrenic long-term depression, pLTD). This study was undertaken to investigate the role of 5-HT and α2-adrenergic receptors in the initiation of pLTD. Adult male urethane-anesthetized, vagotomized, paralyzed, and mechanically ventilated Sprague-Dawley rats were exposed to a protocol of acute intermittent hypercapnia (AIHc; 5 episodes of 15% CO2 in air, each episode lasting 3 min). The experimental group received microinjection of the selective 5-HT1A receptor agonist 8-hydroxy-2-(dipropylamino)tetralin hydrobromide (8-OH-DPAT), the broad-spectrum 5-HT antagonist methysergide, or the α2-adrenergic antagonist yohimbine, whereas the control group received microinjection of 0.9% saline into the caudal raphe region. Peak phrenic nerve activity (pPNA) and burst frequency ( f) were analyzed during baseline (T0), during 5 hypercapnic episodes (THc1-THc5), and at 15, 30, and 60 min after the end of the last hypercapnic episode. In the control group, pPNA decreased 60 min after the end of the last hypercapnic episode compared with baseline values, i.e., pLTD developed ( P = 0.023). In the 8-OH-DPAT group, pPNA significantly decreased at T15, T30, and T60 compared with baseline values, i.e., pLTD developed ( P = 0.01). In the methysergide and yohimbine groups, AIHc did not evoke significant changes of the pPNA at T15, T30, and T60 compared with baseline values. In conclusion, activation of 5-HT1A receptors accentuated induction of pLTD, whereas blockade of α2-adrenergic receptors prevented development of pLTD following AIHc in anesthetized rats. These results suggest that chemical modulation of 5-HT and α2-adrenergic receptors in raphe nuclei affects hypercapnia-induced pLTD, offering important insights in understanding the mechanisms involved in development of respiratory plasticity. NEW & NOTEWORTHY Hypercapnia is a concomitant feature of many breathing disorders, including obstructive sleep apnea. In this study, acute intermittent hypercapnia evoked development of phrenic long-term depression (pLTD) 60 min after the last hypercapnic episode that was preserved if the selective 5-HT1A receptor agonist 8-hydroxy-2-(dipropylamino)tetralin hydrobromide was microinjected in the caudal raphe region before the hypercapnic stimulus. This study highlights that both 5-HT and adrenergic receptor activation is needed for induction of pLTD in urethane-anesthetized rats following intermittent hypercapnia exposure.

Intermittent hypercapnia-induced phrenic long-term depression is revealed after serotonin receptor blockade with methysergide in anaesthetized rats.

NEW FINDINGS: What is the central question of this study? Intermittent hypercapnia is a concomitant feature of breathing disorders. Hypercapnic stimuli evoke a form of respiratory plasticity known as phrenic long-term depression in experimental animals. This study was performed to investigate the putative role of serotonin receptors in the initiation of phrenic long-term depression in anaesthetized rats. What is the main finding and its importance? Phrenic nerve long-term depression was revealed in animals pretreated with the serotonin broad-spectrum antagonist, methysergide. This study highlights that serotonin receptors modulate respiratory plasticity evoked by acute intermittent hypercapnia in anaesthetized rats. This study was performed to test the hypothesis that intermittent hypercapnia can evoke a form of respiratory plasticity known as long-term depression of the phrenic nerve (pLTD) and that 5-HT receptors play a role in the initiation of pLTD. Adult male urethane-anaesthetized, vagotomized, paralysed, mechanically ventilated Sprague-Dawley rats were exposed to an acute intermittent hypercapnia protocol. One group received i.v. injection of the non-selective 5-HT receptor antagonist methysergide and another group received i.v. injection of the selective 5-HT1A receptor antagonist WAY-100635 20 min before exposure to intermittent hypercapnia. A control group received i.v. injection of saline. Peak phrenic nerve activity and respiratory rhythm parameters were analysed at baseline (T0), during each of five hypercapnic episodes, and 15, 30 and 60 min (T60) after the last hypercapnia. Intravenous injection of methysergide before exposure to acute intermittent hypercapnia induced development of amplitude pLTD at T60 (decreased by 46.1 ± 6.9%, P = 0.003). Conversely, in control and WAY-100635-pretreated animals, exposure to acute intermittent hypercapnia did not evoke amplitude pLTD. However, a long-term decrease in phrenic nerve frequency was evoked both in control (42 ± 4 breaths min(-1) at T0 versus 32 ± 5 breaths min(-1) at T60; P = 0.036) and in methysergide-pretreated animals (42 ± 2 breaths min(-1) at T0 versus 32 ± 3 breaths min(-1) at T60; P = 0.028). In WAY-100635 pretreated animals, frequency pLTD was prevented. These results suggest that 5-HT receptors modulate respiratory plasticity induced by acute intermittent hypercapnia in anaesthetized rats.

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.

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.

Long-lasting exercise involvement protects against decline in V̇O2max and V̇O2 kinetics in moderately active women.

We studied the effects of age on different physiological parameters, including those derived from (i) maximal cardiopulmonary exercise testing (CPET), (ii) moderate-intensity step transitions, and (iii) tensiomyography (TMG)-derived variables in moderately active women. Twenty-eight women (age, 19 to 53 years), completed 3 laboratory visits, including baseline data collection, TMG assessment, maximal oxygen uptake test via CPET, and a step-transition test from 20 W to a moderate-intensity cycling power output (PO), corresponding to oxygen uptake at 90% gas exchange threshold. During the step transitions, breath-by-breath pulmonary oxygen uptake, near infrared spectroscopy derived muscle deoxygenation (ΔHHb), and beat-by-beat cardiovascular response were continuously monitored. There were no differences observed between the young and middle-aged women in their maximal oxygen uptake and peak PO, while the maximal heart rate (HR) was 12 bpm lower in middle-aged compared with young (p = 0.016) women. Also, no differences were observed between the age groups in τ pulmonary oxygen uptake, ΔHHb, and τHR during on-transients. The first regression model showed that age did not attenuate the maximal CPET capacity in the studied population (p = 0.638), while in the second model a faster τ pulmonary oxygen uptake, combined with shorter TMG-derived contraction time (Tc) of the vastus lateralis (VL), were associated with a higher maximal oxygen uptake (∼30% of explained variance, p = 0.039). In conclusion, long lasting exercise involvement protects against a maximal oxygen uptake and τpulmonary oxygen uptake deterioration in moderately active women. Novelty: Faster τ pulmonary oxygen uptake and shorter Tc of the VL explain 33% of the variance in superior maximal oxygen uptake attainment. No differences between age groups were found in τ pulmonary oxygen uptake, τΔHHb, and τHR during on-transients.

Independent influence of age on heart rate recovery after flywheel exercise in trained men and women.

The present study examined whether differences in the heart rate recovery following flywheel exercise cessation were associated with differences in maximal oxygen uptake ([Formula: see text]O2 max.), age and sex in trained adults. Eleven men (age range 22-49 years, [Formula: see text]O2 max. = 43.6 ± 7.6 mL kg min-1) and ten women (age range 20-53 years, [Formula: see text]O2 max. = 38.0 ± 5.7 mL kg min-1) were randomly assigned to complete a squat-exercise on the flywheel ergometer set at three different moments of inertia, while their cardiovascular responses were continuously monitored. During the flywheel exercise the mean arterial pressure rose by ~ 35 to 40% (p = .001), and the increment was more robust in men than women. The cardiac index was two-fold greater across both sexes compared to the baseline (p = .001), while the rise in heart rate (~ 144 bpm) was more pronounced in women to compensate for their load-dependent stroke index decline (p = .001). The load-independent time-course changes in heart rate recovery markers were comparable between the sexes. When these indicators were pooled, a stepwise regression revealed age as the only relevant predictor of both fast and slow components of the heart rate recovery (~ 30% of the shared variance explained, p = .014). The present data suggest that the heart rate recovery declines with age, irrespective of sex, or well-preserved cardiorespiratory fitness in moderately-trained adults.

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.

A Randomized Crossover Trial on the Acute Cardiovascular Demands During Flywheel Exercise.

In a randomized crossover trial, we examined whether age plays a role in the mean arterial pressure (MAP) response during a vigorous flywheel exercise of varying load. We hypothesized that the magnitude of increase in the MAP during the flywheel exercise would increase in proportion to advancing age, thereby imposing a significant challenge to the cardiovascular system. A total of 30 participants of both sexes (age range from 20-55 y, 37% women) underwent a detailed medical examination, and their maximal oxygen uptake was determined. They performed a squat exercise (2 sets × 7 repetitions) on a flywheel ergometer at three randomly assigned moments of inertia set at 0.025, 0.05, and 0.075 kg m2, while the cardiovascular response was continuously recorded via a Task force monitor. Compared to the resting values, robust rises in the MAP were observed during all three flywheel loads, reaching the highest value of 179 ± 4 mmHg (p = 0.001) during the highest load. In parallel, the cardiac index (cardiac output normalized by the body surface area) was two-fold greater during all the flywheel loads compared to rest, and at a high load, exclusively, the total peripheral resistance increased by 11% (p = 0.001). The rise in heart rate compensated for a load-dependent drop in the stroke index (stroke volume normalized by the body surface area). In our study population, no correlations were observed between the relative increase in the MAP and the participants' age for the three flywheel loads. The present findings suggest that the larger moments of inertia impose a substantial burden to the cardiovascular system, without apparent associated age-differences of the relative magnitude of MAP rise throughout the exercise.

Microinjection of methysergide into the raphe nucleus attenuated phrenic long-term facilitation in rats.

Exposure to acute intermittent hypoxia (AIH) evokes persistent increase in respiratory activity that lasts up to 60 min after hypoxic episodes have ceased. This persistent increase in phrenic nerve activity (PNA) is known as phrenic long-term facilitation (LTF). AIH-induced phrenic LTF in anesthetized rats is serotonin dependant. The present study was performed to determine whether microinjection of methysergide (4 mM, 20 +/- 5 nl), a broad spectrum 5-HT receptor antagonist, into the caudal raphe nuclei influences phrenic LTF. Peak integrated PNA and respiratory frequency were recorded at 15, 30, and 60 min after five 3-min episodes of normocapnic hypoxia in urethane-anesthetized, vagotomized, paralyzed and ventilated male Sprague-Dawley rats. In control animals, phrenic nerve amplitude was elevated 66.7 +/- 8.6% from baseline 1 h after episodic hypoxia, indicating phrenic LTF. Experimental microinjections of methysergide prior to AIH exposure attenuated phrenic LTF (amplitude increase 2.62 +/- 2.9% over baseline). We conclude that methysergide microinjections into the caudal raphe region attenuated phrenic LTF induced by AIH, indicating involvement of 5-HT receptor activation at a supraspinal level.

Peripheral chemoreflex regulation of sympathetic vasomotor tone in apnea divers.

OBJECTIVES: Involuntary apnea episodes in obstructive sleep apnea patients result in selective potentiation of peripheral chemoreceptor regulation of sympathetic vasomotor tone. Breath-hold diving is associated with repeated "voluntary" apnea episodes and massive arterial oxygen desaturation, which could also perturb chemoreflex function. METHODS: We measured ventilation, heart rate, blood pressure, cardiac stroke volume, and muscle sympathetic nerve activity (MSNA) during isocapnic hypoxia in 11 breath-hold divers and eleven matched control subjects. The study was carried out at least 1 month after intense apnea training. RESULTS: Baseline MSNA frequency was 30 +/- 4 bursts/min in control subjects and 31 +/- 7 bursts/min in divers (ns). During hypoxia MSNA frequency and total activity increased similarly in both groups (30 and 66% in controls and 27 and 60% in divers, respectively). MSNA remained increased after termination of hypoxia and approached baseline measurements after 20 min. Hypoxia-induced stimulation of minute ventilation was similar in both groups, although in divers it was maintained by higher tidal volumes and lower breathing frequency compared with control subjects. In both groups, hypoxia-induced tachycardia drove an increase in cardiac output whereas total peripheral resistance decreased. Blood pressure remained unchanged. INTERPRETATION: We conclude that after the end of intensive training/competition periods, apnea divers show normal peripheral chemoreflex regulation of ventilation and sympathetic vasomotor tone. Although voluntary apnea may not lead to sustained changes in sympathetic nervous system regulation, we cannot exclude the possibility that repeated sympathetic activation elicited by voluntary apnea imposes a burden on the cardiovascular system.

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.

Changes in platelet size and spleen volume in response to selective and non-selective beta-adrenoceptor blockade in hypertensive patients.

1. The spleen contains approximately one-third of all the body's platelets. These platelets are relatively larger and haemostatically more active than platelets in the systemic circulation and can be released into the systemic circulation by stimulation of alpha-adrenoceptors or inhibition of beta-adrenoceptors. In the present study, we evaluated the effects of selective (bisoprol) and non-selective (carvedilol) beta-blockers agents on mean platelet volume (MPV) and spleen size in hypertensive patients at rest and after exercise. 2. Blood pressure, heart rate, platelet count, MPV and spleen volume were measured in 18 newly diagnosed hypertensive patients, as well as in nine healthy control subjects, subjected to treadmill exercise test at their first visit and, for the hypertensive group, after 15 and 30 days of treatment with the selective beta(1)-adrenoceptor antagonist bisoprolol 5 mg/day (n = 9) or the non-selective alpha(1)-, beta(1)- and beta(2)-adrenoceptor antagonist carvedilol 25 mg/day (n = 9). 3. Increases in resting MPV values with concomitant decreases in spleen volume were found after 15 and 30 days treatment with either bisoprolol or carvedilol. The pronounced decrease in splenic volume after exercise and the increased MPV and platelet counts seen at first visit were halved after 15 and 30 days of treatment with either drug. 4. We conclude that in hypertensive patients treated with either selective or non-selective beta-blockers, the spleen contracts and MPV increases, which may increase the risk of atherothrombosis.

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.

Expression of endothelial selectin ligands on human leukocytes following dive.

The fact that impaired endothelial-dependent vasodilatation after scuba diving often occurs without visible changes in the endothelial layer implies its biochemical origin. Since Lewisx(CD15) and sialyl-Lewisx(CD15s) are granulocyte and monocyte carbohydrate antigens recognized as ligands by endothelial selectins, we assumed that they could be sensitive markers for impaired vasodilatation following diving. Using flow cytometry, we determined the CD15 and CD15s peripheral blood mononuclear cells of eight divers, 30 mins before and 50 mins after a single dive to 54 m for 20 mins bottom time. The number of gas bubbles in the right heart was monitored by ultrasound. Gas bubbles were seen in all eight divers, with the average number of bubbles/cm2 1.9+/-1.9. The proportion of CD15+monocytes increased 2-fold after the dive as well as the subpopulation of monocytes highly expressing CD15s. The absolute number of monocytes was slightly, but not significantly, increased after the dive, whereas the absolute number of granulocytes was markedly elevated (up to 61%). There were no significant correlations between bubble formation and CD15+monocyte expression (r=-0.56; P=0.17), as well as with monocytes highly expressing CD15s (r=0.43; P=0.29). This study suggests that biochemical changes induced by scuba diving primarily activate existing monocytes rather than increase the number of monocytes at a time of acute arterial endothelial dysfunction.

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.