Pulmonary edema after competitive breath-hold diving

During an international breath-hold diving competition, 19 of the participating divers volunteered for the present study, aimed at elucidating possible symptoms and signs of pulmonary edema after deep dives. Measurements included dynamic spirometry and pulse oximetry, and chest auscultation was performed on those with the most severe symptoms. After deep dives (25-75 m), 12 of the divers had signs of pulmonary edema. None had any symptoms or signs after shallow pool dives. For the whole group of 19 divers, average reductions in forced vital capacity (FVC) and forced expiratory volume in the first second (FEV(1)) were -9 and -12%, respectively, after deep dives compared with after pool dives. In addition, the average reduction in arterial oxygen saturation (Sa(O(2))) was -4% after the deep dives. In six divers, respiratory symptoms (including dyspnea, cough, fatigue, substernal chest pain or discomfort, and hemoptysis) were associated with aggravated deteriorations in the physiological variables (FVC: -16%; FEV(1): -27%; Sa(O(2)): -11%). This is the first study showing reduced spirometric performance and arterial hypoxemia as consequences of deep breath-hold diving, and we suggest that the observed changes are caused by diving-induced pulmonary edema. From the results of the present study, it must be concluded that the great depths reached by these elite apnea divers are associated with a risk of pulmonary edema.     

Splenic contraction during breath-hold diving in the Korean ama

Major increases of hemoglobin concentration and hematocrit, possibly secondary to splenic contraction, have been noted during diving in the Weddell seal. We sought to learn whether this component of the diving response could be present in professional human breath-hold divers. Splenic size was measured ultrasonically before and after repetitive breath-hold dives to approximately 6-m depth in ten Korean ama (diving women) and in three Japanese male divers who did not routinely practice breath-hold diving. Venous hemoglobin concentration and hematocrit were measured in nine of the ama and all Japanese divers. In the ama, splenic length and width were reduced after diving (P = 0.0007 and 0.0005, respectively) and calculated splenic volume decreased 19.5 +/- 8.7% (mean +/- SD, P = 0.0002). Hemoglobin concentration and hematocrit increased 9.5 +/- 5.9% (P = 0.0009) and 10.5 +/- 4% (P = 0.0001), respectively. In Japanese male divers, splenic size and hematocrit were unaffected by repetitive breath-hold diving and hemoglobin concentration increased only slightly over baseline (3.0 +/- 0.6%, P = 0.0198). Splenic contraction and increased hematocrit occur during breath-hold diving in the Korean ama.     

Effect of 16 weeks diving practice at two different times of day on the pulmonary function,spirometry measurements and 6-minute walk test data of healthy professional Tunisian scuba divers

The aim of this study was to investigate the effect of time of the day (TOD) and 16 weeks diving practice (16WDP) on the spirometric parameters and 6-min walk test data (6MWT) on professional Tunisian scuba divers. In randomized order, 36 health males divided into 3 groups [morning practice group) (MPG): n = 12; evening practice group (EPG): n = 12; control group (CG) n = 12] participated voluntary in this study. They performed spirometry measurements and 6MWT during two periods: [before-season (June 05–10), and after-season (October 05–10)]. Our results revealed that assessment sessions comprised the following: FVC, FEV1, FEV1/FVC and PEF. Results were analyzed by applying repeated measures analysis of variance ANOVA. The spirometric parameters were similar upon two times of day on both EPG and MPG before the season (i.e. FEV1, FVC). Likewise, our finding revealed a significant decrease in lung functions following the 16 weeks practice of scuba diving upon two times of day. Thus, this period of hyperbaric scuba diving practice lead a significant alteration of lung function parameters with decrease of percent of variation in EPG vs. CEG compared to MPG vs. CMG: (i.e. FEV1, FVC, and PEF). In conclusion, 16 weeks of hyperbaric scuba diving lead a significant change in the spirometric and 6MWT values and respiratory problem with damage on lung function in healthy adult divers older than 40 years. Professional divers are recommended to have practice diving in the morning.     

Features of glossopharyngeal breathing in breath-hold divers.

One technique employed by competitive breath-hold divers to increase diving depth is to hyperinflate the lungs with glossopharyngeal breathing (GPB). Our aim was to assess the relationship between measured volume and pressure changes due to GPB. Seven healthy male breath-hold divers, age 33 (8) [mean (SD)] years were recruited. Subjects performed baseline body plethysmography (TLC(PRE)). Plethysmography and mouth relaxation pressure were recorded immediately following a maximal GPB maneuver at total lung capacity (TLC) (TLC(GPB)) and within 5 min after the final GPB maneuver (TLC(POST)). Mean TLC increased from TLC(PRE) to TLC(GPB) by 1.95 (0.66) liters and vital capacity (VC) by 1.92 (0.56) liters (P < 0.0001), with no change in residual volume. There was an increase in TLC(POST) compared with TLC(PRE) of 0.16 liters (0.14) (P < 0.02). Mean mouth relaxation pressure at TLC(GPB) was 65 (19) cmH(2)O and was highly correlated with the percent increase in TLC (R = 0.96). Breath-hold divers achieve substantial increases in measured lung volumes using GPB primarily from increasing VC. Approximately one-third of the additional air was accommodated by air compression.     

Exercise-induced bronchoconstriction alters airway nitric oxide exchange in a pattern distinct from spirometry

Exhaled nitric oxide (NO) is altered in asthmatic subjects with exercise-induced bronchoconstriction (EIB). However, the physiological interpretation of exhaled NO is limited because of its dependence on exhalation flow and the inability to distinguish completely proximal (large airway) from peripheral (small airway and alveolar) contributions. We estimated flow-independent NO exchange parameters that partition exhaled NO into proximal and peripheral contributions at baseline, postexercise challenge, and postbronchodilator administration in steroid-naive mild-intermittent asthmatic subjects with EIB (24-43 yr old, n = 9) and healthy controls (20-31 yr old, n = 9). The mean +/- SD maximum airway wall flux and airway diffusing capacity were elevated and forced expiratory flow, midexpiratory phase (FEF(25-75)), forced expiratory volume in 1 s (FEV(1)), and FEV(1)/forced vital capacity (FVC) were reduced at baseline in subjects with EIB compared with healthy controls, whereas the steady-state alveolar concentration of NO and FVC were not different. Compared with the response of healthy controls, exercise challenge significantly reduced FEV(1) (-23 +/- 15%), FEF(25-75) (-37 +/- 18%), FVC (-12 +/- 12%), FEV(1)/FVC (-13 +/- 8%), and maximum airway wall flux (-35 +/- 11%) relative to baseline in subjects with EIB, whereas bronchodilator administration only increased FEV(1) (+20 +/- 21%), FEF(25-75) (+56 +/- 41%), and FEV(1)/FVC (+13 +/- 9%). We conclude that mild-intermittent steroid-naive asthmatic subjects with EIB have altered airway NO exchange dynamics at baseline and after exercise challenge but that these changes occur by distinct mechanisms and are not correlated with alterations in spirometry.     

Alveolar gas composition and exchange during deep breath-hold diving and dry breath holds in elite divers

End tidal O2 and CO2 (PETCO2) pressures, expired volume, blood lactate concentration ([Lab]), and arterial blood O2 saturation [dry breath holds (BHs) only] were assessed in three elite breath-hold divers (ED) before and after deep dives and BH and in nine control subjects (C; BH only). After the dives (depth 40-70 m, duration 88-151 s), end-tidal O2 pressure decreased from approximately 140 Torr to a minimum of 30.6 Torr, PETCO2 increased from approximately 25 Torr to a maximum of 47.0 Torr, and expired volume (BTPS) ranged from 1.32 to 2.86 liters. Pulmonary O2 exchange was 455-1,006 ml. CO2 output approached zero. [Lab] increased from approximately 1.2 mM to at most 6.46 mM. Estimated power output during dives was 513-929 ml O2/min, i.e. approximately 20-30% of maximal O2 consumption. During BH, alveolar PO2 decreased from approximately 130 to less than 30 Torr in ED and from 125 to 45 Torr in C. PETCO2 increased from approximately 30 to approximately 50 Torr in both ED and C. Contrary to C, pulmonary O2 exchange in ED was less than resting O2 consumption, whereas CO2 output approached zero in both groups. [Lab] was unchanged. Arterial blood O2 saturation decreased more in ED than in C. ED are characterized by increased anaerobic metabolism likely due to the existence of a diving reflex.     

Norwegian deep diving trials

In 1983 NUTEC, together with two diving companies, completed two dives with 12 divers (6 in each dive) to pressures equivalent to 350 m s.w., one dive lasted for 17 d, and the other, 24 d. The purpose of the dives was to demonstrate that the diving companies were prepared for diving to 300 m depth in the North Sea. No major medical or physiological problems arose during the dives, although all divers had minor symptoms of high pressure nervous syndrome during compressions. During decompression three decompression sickness incidents occurred, which involved pain only, and all were successfully treated. All divers went through comprehensive medical physiological examinations before and after the dives. No significant changes from values measured before diving have been found in the six divers who have so far been examined after diving, except that five of them were considerably more sensitive to CO2 after the dive than before. Several problems arose in connection with the divers' breathing equipment, thermal protection and communication, which need to be improved.     

Organization of metabolic pathways in vastus lateralis of patients with chronic obstructive pulmonary disease

The objective of this study was to determine whether patients with chronic obstructive lung disease (COPD) display differences in organization of the metabolic pathways and segments involved in energy supply compared with healthy control subjects. Metabolic pathway potential, based on the measurement of the maximal activity (V(max)) of representative enzymes, was assessed in tissue extracted from the vastus lateralis in seven patients with COPD (age 67 +/- 4 yr; FEV(1)/FVC = 44 +/- 3%, where FEV(1) is forced expiratory volume in 1 s and FVC is forced vital capacity; means +/- SE) and nine healthy age-matched controls (age 68 +/- 2 yr; FEV(1)/FVC = 75 +/- 2%). Compared with control, the COPD patients displayed lower (P < 0.05) V(max) (mol.kg protein(-1).h(-1)) for cytochrome c oxidase (COX; 21.2 +/- 2.0 vs. 28.7 +/- 2.2) and 3-hydroxyacyl-CoA dehydrogenase (HADH; 2.54 +/- 0.14 vs. 3.74 +/- 0.12) but not citrate synthase (CS; 2.20 +/- 0.16 vs. 3.19 +/- 0.5). While no differences between groups were observed in V(max) for creatine phosphokinase, phosphorylase (PHOSPH), phosphofructokinase (PFK), pyruvate kinase, and lactate dehydrogenase, hexokinase (HEX) was elevated in COPD (P < 0.05). Enzyme activity ratios were higher (P < 0.05) for HEX/CS, HEX/COX, PHOSPH/HADH and PFK/HADH in COPD compared with control. It is concluded that COPD patients exhibit a reduced potential for both the electron transport system and fat oxidation and an increased potential for glucose phosphorylation while the potential for glycogenolysis and glycolysis remains normal. A comparison of enzyme ratios indicated greater potentials for glucose phosphorylation relative to the citric acid cycle and the electron transport chain and glycogenolysis and glycolysis relative to beta-oxidation.     

Exercise performance following a carbohydrate load in chronic airflow obstruction

We evaluated the effects of a large (920 cal) liquid carbohydrate (CHO) load on the maximum exercise capacity of 18 patients with chronic airflow obstruction [forced expiratory volume at at 1 s (FEV1) = 1.27 +/- 0.48 liters; FEV1/forced vital capacity = 0.41 +/- 0.11]. Patients underwent duplicate incremental cycle ergometer exercise tests to a symptom-limited maximum following CHO and a liquid placebo in single-blind fashion. Expired gas measurements were obtained during each power output. In 12 patients arterial blood gases were measured, and in six patients venous blood was obtained for measurement of glucose, electrolytes, and osmolality. With CHO, the maximum power output decreased from 86 +/- 30 to 76 +/- 31 W (P less than 0.001), whereas the ventilation at exhaustion was nearly identical (47.6 +/- 13.2 and 46.8 +/- 12.5 l/min). Arterial partial pressure of CO2 (PaCO2) at exhaustion decreased (P less than 0.025), arterial partial pressure of O2 (PaO2) increased (P less than 0.01), and the ventilatory equivalent for CO2 (VE/VCO2) increased (P less than 0.005) with CHO. At equivalent power outputs, CHO resulted in significant increases in VE (P less than 0.001) and VCO2 (P less than 0.001); PaCO2 was unchanged, whereas PaO2 increased (P less than 0.01). CHO increased the serum glucose at rest and during exercise. No changes in serum osmolality or electrolytes occurred during exercise following CHO. After CHO loading, the majority of patients appeared to reach their limiting level of ventilation at a lower power output. In contrast, there was no significant difference in the mean maximum power output with CHO in six normal control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)     

Energetics of wet-suit diving in Japanese male breath-hold divers

The present study was undertaken to investigate energy balance in professional male breath-hold divers in Tsushima Island, Japan. In 4 divers, rectal (Tre) and mean skin (Tsk) temperatures and rate of O2 consumption (VO2) were measured during diving work in summer (27 degrees C water) and winter (14 degrees C water). Thermal insulation and energy costs of diving work were estimated. In summer, comparisons were made of subjects clad either in wet suits (protected) or in swimming trunks (unprotected), and in winter, they wore wet suits. The average Tre in unprotected divers decreased to 36.4 +/- 0.2 degrees C at the end of 1-h diving work, but in protected divers it decreased to 37.2 +/- 0.3 degrees C in 2 h in summer and to 36.9 +/- 0.1 degree C in 1.5 h in winter. The average Tsk of unprotected divers decreased to 28.0 +/- 0.6 degrees C in summer and that of protected divers decreased to 32.9 +/- 0.5 degrees C in summer and 28.0 +/- 0.3 degrees C in winter. Average VO2 increased 190% (from 370 ml/min before diving to 1,070 ml/min) in unprotected divers in summer, but in protected divers it rose 120% (from 360 to 780 ml/min) in summer and 110% (from 330 to 690 ml/min) in winter. Overall thermal insulation (tissue and wet suit) calculated for protected divers was 0.065 +/- 0.006 degree C X kcal-1 X m-2 X h-1 in summer and 0.135 +/- 0.019 degree C X kcal-1 X m-2 X h-1 in winter.(ABSTRACT TRUNCATED AT 250 WORDS)     

Regional heterothermy and conservation of core temperature in emperor penguins diving under sea ice

Temperatures were recorded at several body sites in emperor penguins (Aptenodytes forsteri) diving at an isolated dive hole in order to document temperature profiles during diving and to evaluate the role of hypothermia in this well-studied model of penguin diving physiology. Grand mean temperatures (+/-S.E.) in central body sites during dives were: stomach: 37.1+/-0.2 degrees C (n=101 dives in five birds), pectoral muscle: 37.8+/-0.1 degrees C (n=71 dives in three birds) and axillary/brachial veins: 37.9+/-0.1 degrees C (n=97 dives in three birds). Mean diving temperature and duration correlated negatively at only one site in one bird (femoral vein, r=-0.59, P<0.05; range <1 degrees C). In contrast, grand mean temperatures in the wing vein, foot vein and lumbar subcutaneous tissue during dives were 7.6+/-0.7 degrees C (n=157 dives in three birds), 20.2+/-1.2 degrees C (n=69 in three birds) and 35.2+/-0.2 degrees C (n=261 in six birds), respectively. Mean limb temperature during dives negatively correlated with diving duration in all six birds (r=-0.29 to -0.60, P<0.05). In two of six birds, mean diving subcutaneous temperature negatively correlated with diving duration (r=-0.49 and -0.78, P<0.05). Sub-feather temperatures decreased from 31 to 35 degrees C during rest periods to a grand mean of 15.0+/-0.7 degrees C during 68 dives of three birds; mean diving temperature and duration correlated negatively in one bird (r=-0.42, P<0.05). In general, pectoral, deep venous and even stomach temperatures during diving reflected previously measured vena caval temperatures of 37-39 degrees C more closely than the anterior abdominal temperatures (19-30 degrees C) recently recorded in diving emperors. Although prey ingestion can result in cooling in the stomach, these findings and the lack of negative correlations between internal temperatures and diving duration do not support a role for hypothermia-induced metabolic suppression of the abdominal organs as a mechanism of extension of aerobic dive time in emperor penguins diving at the isolated dive hole. Such high temperatures within the body and the observed decreases in limb, anterior abdomen, subcutaneous and sub-feather temperatures are consistent with preservation of core temperature and cooling of an outer body shell secondary to peripheral vasoconstriction, decreased insulation of the feather layer, and conductive/convective heat loss to the water environment during the diving of these emperor penguins.     

Lower pulmonary diffusing capacity in the prone vs. supine posture.

We evaluated the effect of prone positioning on gas-transfer characteristics in normal human subjects. Single-breath (SB) and rebreathing (RB) maneuvers were employed to assess carbon monoxide diffusing capacity (DlCO), its components related to capillary blood volume (Vc) and membrane diffusing capacity (Dm), pulmonary tissue volume (Vti), and cardiac output (Qc). Alveolar volume (Va) was significantly greater prone than supine, irrespective of the test maneuver used. Nevertheless, Dl(CO) was consistently lower prone than supine, a difference that was enhanced when appropriately corrected for the higher Va prone. When adequately corrected for Va, diffusing capacity significantly decreased by 8% from supine to prone [SB: Dl(CO,corr) supine vs. prone: 32.6 +/- 2.3 (SE) vs. 30.0 +/- 2 ml x min(-1) x mmHg(-1) stpd; RB: Dl(CO,corr) supine vs. prone: 30.2 +/- 2.2 (SE) vs. 27.8 +/- 2.0 ml x min(-1) x mmHg(-1) stpd]. Both Vc and Dm showed a tendency to decrease from supine to prone, but neither reached significance. Finally, there were no significant differences in Vti or Qc between supine and prone. We interpret the lower diffusing capacity of the healthy lung in the prone posture based on the relatively larger space occupied by the heart in the dependent lung zones, leaving less space for zone 3 capillaries, and on the relatively lower position of the heart, leaving the zone 3 capillaries less engorged.     

Cardiovascular changes during deep breath-hold dives in a pressure chamber

Ferrigno, Massimo, Guido Ferretti, Avery Ellis, DanWarkander, Mario Costa, Paolo Cerretelli, and Claes E. G. Lundgren. Cardiovascular changes during deep breath-hold dives ina pressure chamber. J. Appl. Physiol.83(4): 1282-1290, 1997.Electrocardiogram, cardiac output, andblood lactate accumulation were recorded in three elite breath-holddivers diving to 40-55 m in a pressure chamber in thermoneutral(35°C) or cool (25°C) water. In two of the divers, invasiverecordings of arterial blood pressure were also obtained during divesto 50 m in cool water. Bradycardia during the dives was more pronouncedand developed more rapidly in the cool water, with heart rates droppingto 20-30 beats/min. Arrhythmias occurred, particularly during thedives in cool water, when they were often more frequent than sinusbeats. Because of bradycardia, cardiac output decreased during thedives, especially in cool water (to <3 l/min in 2 of the divers).Arterial blood pressure increased dramatically, reaching values as highas 280/200 and 290/150 mmHg in the two divers, respectively. Thishypertension was secondary to peripheral vasoconstriction, which alsoled to anaerobic metabolism, reflected in increased blood lactateconcentration. The diving response of these divers resembles the onedescribed for diving animals, although the presence of arrhythmias andlarge increases in blood pressure indicate a less perfect adaptation inhumans.

     

Response to CO2 in novice closed-circuit apparatus divers and after 1 year of active oxygen diving at shallow depths.

Elevated arterial Pco(2) (hypercapnia) has a major effect on central nervous system oxygen toxicity in diving with a closed-circuit breathing apparatus. The purpose of the present study was to follow up the ability of divers to detect CO(2) and to determine the CO(2) retention trait after 1 year of active oxygen diving with closed-circuit apparatus. Ventilatory and perceptual responses to variations in inspired CO(2) (range: 0-5.6 kPa, 0-42 Torr) during moderate exercise were assessed in Israeli Navy combat divers on active duty. Tests were carried out on 40 divers during the novice oxygen diving phase (ND) and the experienced oxygen diving phase. No significant changes were found between the two phases for the minimal mean inspired Pco(2) that could be detected. The mean (with SD in parentheses) end-tidal Pco(2) during exposure to an inspired Pco(2) of 5.6 kPa (42 Torr) was significantly higher in the novice diving phase than in the experienced diving phase [8.1 kPa (SD 0.7), 62 Torr (SD 5) and 7.8 kPa (SD 0.6), 59 Torr (SD 4), respectively; P < or = 0.001]. One year of shallow oxygen diving activity with a closed-circuit apparatus does not affect the ability to detect CO(2) nor does it lead to increased CO(2) retention; rather, it may even bring about a decrease in this trait. This finding suggests that acquiring experience in oxygen diving with a closed-circuit apparatus at shallow depths does not place the diver at a greater risk of central nervous system oxygen toxicity due to CO(2) retention.     

Nitrogen tensions in brachial vein blood of Korean ama divers.

Intravascular bubble formation and symptoms of decompression sickness have been reported during repetitive deep breath-hold diving. Therefore we examined the pattern of blood N2 kinetics during and after repetitive breath-hold diving. To study muscle N2 uptake and release, we measured brachial venous N2 partial pressure (PN2) in nine professional Korean breath-hold divers (ama) during a 3-h diving shift at approximately 4 m seawater depth and up to 4 h after diving. PN2 was determined with the manometric Van Slyke method. Diving time and depth were recorded using a backpack computer-assisted dive longer that allowed calculating the surface-to-depth time ratio to derive the effective depth. With the assumption that forearm muscle N2 kinetics follow the general Haldanian principles of compression and decompression, i.e., forearm muscle is a single compartment with a uniform tissue PN2 equal to venous PN2, PN2 data were fitted to monoexponential functions of time. In the early phase of the diving shift, PN2 rapidly increased to 640 Torr (half time = 6 min) and then slowly declined to baseline levels (half time = 36 min) after the work shift. Peak PN2 levels approximated the alveolar PN2 derived from the effective depth. We conclude that forearm muscle N2 kinetics are well described by a Haldanian single-compartment model. Decompression sickness is theoretically possible in the ama; it did not occur because the absolute PN2 remained low due to the shallow working depth of the ama we studied.     

Diving heart rate development in postnatal harbour seals, Phoca vitulina

Harbour seals, Phoca vitulina, dive from birth, providing a means of mapping the development of the diving response, and so our objective was to investigate the postpartum development of diving bradycardia. The study was conducted May-July 2000 and 2001 in the St. Lawrence River Estuary (48 degrees 41'N, 68 degrees 01'W). Both depth and heart rate (HR) were remotely recorded during 86,931 dives (ages 2-42 d, n = 15) and only depth for an additional 20,300 dives (combined data covered newborn to 60 d, n = 20). The mean dive depth and mean dive durations were conservative during nursing (2.1 +/- 0.1 m and 0.57 +/- 0.01 min, range = 0-30.9 m and 0-5.9 min, respectively). The HR of neonatal pups during submersion was bimodal, but as days passed, the milder of the two diving HRs disappeared from their diving HR record. By 15 d of age, most of the dive time was spent at the lower diving bradycardia rate. Additionally, this study shows that pups are born with the ability to maintain the lower, more fully developed dive bradycardia during focused diving but do not do so during shorter routine dives.     

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.     

Transpulmonary pressures and lung mechanics with glossopharyngeal insufflation and exsufflation beyond normal lung volumes in competitive breath-hold divers.

Throughout life, most mammals breathe between maximal and minimal lung volumes determined by respiratory mechanics and muscle strength. In contrast, competitive breath-hold divers exceed these limits when they employ glossopharyngeal insufflation (GI) before a dive to increase lung gas volume (providing additional oxygen and intrapulmonary gas to prevent dangerous chest compression at depths recently greater than 100 m) and glossopharyngeal exsufflation (GE) during descent to draw air from compressed lungs into the pharynx for middle ear pressure equalization. To explore the mechanical effects of these maneuvers on the respiratory system, we measured lung volumes by helium dilution with spirometry and computed tomography and estimated transpulmonary pressures using an esophageal balloon after GI and GE in four competitive breath-hold divers. Maximal lung volume was increased after GI by 0.13-2.84 liters, resulting in volumes 1.5-7.9 SD above predicted values. The amount of gas in the lungs after GI increased by 0.59-4.16 liters, largely due to elevated intrapulmonary pressures of 52-109 cmH(2)O. The transpulmonary pressures increased after GI to values ranging from 43 to 80 cmH(2)O, 1.6-2.9 times the expected values at total lung capacity. After GE, lung volumes were reduced by 0.09-0.44 liters, and the corresponding transpulmonary pressures decreased to -15 to -31 cmH(2)O, suggesting closure of intrapulmonary airways. We conclude that the lungs of some healthy individuals are able to withstand repeated inflation to transpulmonary pressures far greater than those to which they would normally be exposed.     

Optimal diving behaviour for foraging in relation to body size

Overall, large animals dive longer and deeper than small animals; however, after the difference in body size is taken into account, smaller divers often tend to make relatively longer dives. Neither physiological nor theoretical explanations have been provided for this paradox. This paper develops an optimal foraging diving model to demonstrate the effect of body size on diving behaviour, and discusses optimal diving behaviour in relation to body size. The general features of the results are: (1) smaller divers should rely more heavily on anaerobic respiration, (2) larger divers should not always make longer dives than smaller divers, and (3) an optimal body size exists for each diving depth. These results explain the relatively greater diving ability observed in smaller divers, and suggest that if the vertical distribution of prey in the water column is patchy, there is opportunity for a population of diving animals to occupy habitat niches related to body size.     

Blunted muscle vasodilatation during chemoreceptor stimulation in patients with heart failure

Chemoreflex control of sympathetic nerve activity is exaggerated in heart failure (HF) patients. However, the vascular implications of the augmented sympathetic activity during chemoreceptor activation in patients with HF are unknown. We tested the hypothesis that the muscle blood flow responses during peripheral and central chemoreflex stimulation would be blunted in patients with HF. Sixteen patients with HF (49 +/- 3 years old, Functional Class II-III, New York Heart Association) and 11 age-paired normal controls were studied. The peripheral chemoreflex control was evaluated by inhalation of 10% O(2) and 90% N(2) for 3 min. The central chemoreflex control was evaluated by inhalation of 7% CO(2) and 93% O(2) for 3 min. Muscle sympathetic nerve activity (MSNA) was directly evaluated by microneurography. Forearm blood flow was evaluated by venous occlusion plethysmography. Baseline MSNA were significantly greater in HF patients (33 +/- 3 vs. 20 +/- 2 bursts/min, P = 0.001). Forearm vascular conductance (FVC) was not different between the groups. During hypoxia, the increase in MSNA was significantly greater in HF patients than in normal controls (9.0 +/- 1.6 vs. 0.8 +/- 2.0 bursts/min, P = 0.001). The increase in FVC was significantly lower in HF patients (0.00 +/- 0.10 vs. 0.76 +/- 0.25 units, P = 0.001). During hypercapnia, MSNA responses were significantly greater in HF patients than in normal controls (13.9 +/- 3.2 vs. 2.1 +/- 1.9 bursts/min, P = 0.001). FVC responses were significantly lower in HF patients (-0.29 +/- 0.10 vs. 0.37 +/- 0.18 units, P = 0.001). In conclusion, muscle vasodilatation during peripheral and central chemoreceptor stimulation is blunted in HF patients. This vascular response seems to be explained, at least in part, by the exaggerated MSNA responses during hypoxia and hypercapnia.