Is the rate of whole-body nitrogen elimination influenced by exercise?

BACKGROUND: Because it has earlier been shown that exercise 24 or two hours pre-dive may suppress the appearance of venous gas bubbles (VGB) in connection with the dive, we studied whether exercise before or during N2 elimination would influence the rate of the latter. Nitrogen elimination was recorded in eight volunteers breathing a normoxic O2+argon mixture for two hours. The N2 washout was preceded two (Condition A) or 24 hours (Condition B) earlier, by one hour of exercise at 85% VO2max (two hours of exercise interspersed with two hours of rest). In separate experiments, exercise at -40% of VO2max was performed throughout the two-hour washout (Condition C), and control experiments (Condition D) with denitrogenation without exercise were also performed. RESULTS: There were no significant differences among conditions for the total N2 eliminated (904 +/- 196 mL). The half-times of N2 washout for A (35.2 +/- 10.8 minutes) and B (31.9 +/- 8.6 minutes) did not differ from control washouts. The rate of washout in C increased 14% compared to D (half-time: 30.4 +/- 7.6 vs. 34.5 +/- 7.8 minutes, p = 0.002), and correlated with cardiac output. CONCLUSION: Exercise 24 or two hours pre-N2 washout did not affect it, suggesting that the decreased VGB scores noted by others in dives preceded by conditions similar to A and B are not due to changes in nitrogen exchange but rather to factors related to bubble formation and/or appearance. That N2 elimination is enhanced by concomitant exercise makes physiological sense but does not necessarily explain the observation by others of a reduced risk of decompression sickness with exercise before diving.

Energy cost of breathing at depth: effect of respiratory muscle training.

INTRODUCTION: Respiratory muscle training against resistance (RRMT) increases respiratory muscle strength and endurance as well as underwater swimming endurance. We hypothesized that the latter is a result of RRMT reducing the high energy cost of breathing at depth. METHODS: Eight subjects breathed air in a hyperbaric chamber at 55 fsw, both before and after RRMT. They rested for 10 minutes, cycled on an ergometer for 10 minutes (100 W), rested for 10 minutes, and then, while still at rest, they voluntarily mimicked the breathing pattern recorded during the exercise (isocapnic simulated exercise ventilation, ISEV). RESULTS: Post-RRMT values of V(E) at rest, exercise and ISEV were not different from those recorded pre-RRMT. Pre-RRMT minute-ventilation (V(E)) during ISEV was not different from the exercise ventilation (49.98 +/- 10.41 vs. 47.74 +/- 8.44 L/minute). The end-tidal PCO2 during ISEV and exercise were not different (44.26 +/- 2.54 vs. 44.49 +/- 4.49 mmHg) or affected by RRMT. Oxygen uptake (VO2) was 0.32 +/- 0.08 L/ minute at rest, 1.78 +/- 0.15 during exercise pre-RRMT, and not different post-RRMT. During ISEV, VO2 decreased significantly from pre-RRMT to post-RRMT (0.46 +/- 0.06 vs. 0.36 +/- 0.11 L/minute). Post-RRMT delta VO2/delta V(E) was significantly lower during ISEV than pre-RRMT (0.0094 +/- 0.0021 L/L vs. 0.0074 +/- 0.0023 L/L). CONCLUSION: RRMT significantly reduced the energy cost of ventilation, measured as delta VO2/delta V(E) during ISEV, at a depth of 55 fsw. Whether this change was due to reduced work of breathing and/or increased efficiency of the respiratory muscles remains to be determined.

The underwater environment: cardiopulmonary, thermal, and energetic demands.

Water covers over 75% of the earth, has a wide variety of depths and temperatures, and holds a great deal of the earth's resources. The challenges of the underwater environment are underappreciated and more short term compared with those of space travel. Immersion in water alters the cardio-endocrine-renal axis as there is an immediate translocation of blood to the heart and a slower autotransfusion of fluid from the cells to the vascular compartment. Both of these changes result in an increase in stroke volume and cardiac output. The stretch of the atrium and transient increase in blood pressure cause both endocrine and autonomic changes, which in the short term return plasma volume to control levels and decrease total peripheral resistance and thus regulate blood pressure. The reduced sympathetic nerve activity has effects on arteriolar resistance, resulting in hyperperfusion of some tissues, which for specific tissues is time dependent. The increased central blood volume results in increased pulmonary artery pressure and a decline in vital capacity. The effect of increased hydrostatic pressure due to the depth of submersion does not affect stroke volume; however, a bradycardia results in decreased cardiac output, which is further reduced during breath holding. Hydrostatic compression, however, leads to elastic loading of the chest wall and negative pressure breathing. The depth-dependent increased work of breathing leads to augmented respiratory muscle blood flow. The blood flow is increased to all lung zones with some improvement in the ventilation-perfusion relationship. The cardiac-renal responses are time dependent; however, the increased stroke volume and cardiac output are, during head-out immersion, sustained for at least hours. Changes in water temperature do not affect resting cardiac output; however, maximal cardiac output is reduced, as is peripheral blood flow, which results in reduced maximal exercise performance. In the cold, maximal cardiac output is reduced and skin and muscle are vasoconstricted, resulting in a further reduction in exercise capacity.

Respiratory muscle training improves swimming endurance at depth.

Respiratory muscle training (RMT) has been shown to improve divers swimming endurance at 4 feet of depth; however, its effectiveness at greater depths, where gas density and the work of breathing are substantially elevated has not been studied. The purpose of this study was to examine the effects of resistance respiratory muscle training (RRMT) on respiratory function and swimming endurance at 55 feet of depth (270.5 kPa). Nine male subjects (25.9 +/- 6.8 years) performed RRMT for 30 min/day, 5 d/ wk, for 4 wks. Pre- and Post RRMT, subjects swam against a pre-determined load (70% VO2 max) until exhausted. As indices of respiratory muscle strength, maximal inspiratory and expiratory pressures were measured before and immediately following the swims pre- and post-RRMT. These measurements showed that ventilation was significantly lower during the swims and, at comparable swim duration, that the respiratory muscles were considerably less fatigued following RRMT. The reduced ventilation was due to a lower breathing frequency following RRMT. The ventilatory changes following RRMT coincided with significantly increased swimming time to exhaustion (approximately 60%, 31.3 +/- 11.6 vs. 49.9 +/- 16.0 min, pre- vs. post-RRMT, p < 0.05). These results suggest respiratory muscle fatigue limits swimming endurance at depth as well as at the surface and RRMT improves performance.

The effect of body position on inspiratory airflow in divers.

UNLABELLED: The purpose of this study was to examine the possibility that body position influences inspiratory airflow of submerged subjects. Our previous studies have suggested that for a given (negative) inspired gas pressure, exercising divers experience more dyspnea in the prone than in the upright position. METHODS: Six subjects performed maximal inspiratory efforts recorded as esophageal pressure (balloon catheter); simultaneously inspiratory flow and lung volumes were recorded. To standardize static lung load, the subjects' chest pressure centroids (representing the average water pressure on the chest) were held at a constant depth (0.33m) throughout the experiments. RESULTS: Recordings of peak inspiratory flow (PIF) showed a decrease of 25.56 +/- 4.14% (mean +/- SD, P = 0.01) from the submerged upright position mean flow of 6.19 +/- 1.48 (l/s) to the submerged prone mean flow of 4.37 +/- 0.69 (l/s). Nadiral esophageal pressure exhibited no significant differences: 5.40 +/- 4.32% (mean +/- SD, P = 0.512), from the upright mean pressure of (-) 51.70 +/- 24.09 (cm H2O) to the prone mean pressure of (-) 48.53 +/- 25.86 (cm H2O). CONCLUSIONS: The significant decrease in PIF when changing from the upright to the prone position, suggests a difference in the patency of the extra-thoracic airways. The higher water pressure exerted on the neck in the prone position may explain this difference. The similarity of pleural pressures in the two positions indicates that the differences in PIF were not due to differences in inspiratory effort.

Resistive respiratory muscle training improves and maintains endurance swimming performance in divers.

Respiratory work is increased during exercise under water and may lead to respiratory muscle fatigue, which in turn can compromise swimming endurance. Previous studies have shown that respiratory muscle training, conducted five days per week for four weeks, improved both respiratory and fin swimming endurance. This training (RRMT-5) consisted of intermittent vital capacity breaths (twice/minute) against spring loaded breathing valves imposing static and resistive loads generating average inspiratory pressures of approximately 40 cmH2O and expiratory pressures of approximately 47 cmH2O. The purpose of the present study (n = 20) was to determine if RRMT 3 days per week (RRMT-3) would give similar improvements, and if continuing RRMT 2 days per week (RRMT-M) would maintain the benefits of RRMT-3 in fit SCUBA divers. Pulmonary function, maximal inspiratory (P(insp)) and expiratory pressures (P(exp)), respiratory endurance (RET), and surface and underwater (4 fsw) fin swimming endurance were determined prior to and after RRMT, and monthly for 3 months. Pulmonary function did not significantly improve after either RRMT-3 or RMMT-5; while P(insp) (20 and 15%) and P(exp) (25 and 11%), RET (73 and 217%), surface (50 and 33%) and underwater (88 and 66%) swim times improved. VO2, VE and breathing frequency decreased during the underwater endurance swims after both RRMT-3 and RRMT-5. During RRMT-M P(insp) and P(exp) and RET and swimming times were maintained at post RRMT-3 levels. RRMT 3 or 5 days per week can be recommended to divers to improve both respiratory and fin swimming endurance, effects which can be maintained with RRMT twice weekly.

Alveolar gas composition before and after maximal breath-holds in competitive divers.

The urge to breathe, as stimulated by hypercapnia, is generally considered to cause a breath-hold diver to end the breath-hold, and pre-breath hold hyperventilation has been suggested to cause hypoxic loss of consciousness (LOC) due to the reduced urge to breathe. Competitors hyperventilate before "Static Apnea", yet only 10% surface with symptoms of hypoxia such as loss of motor control (LMC) or LOC. We hypothesized that the extensive hyperventilation would prevent hypercapnia even during prolonged breath-holding and we also recorded breaking-point end-tidal PO2 in humans. Nine breath-hold divers performed breath-holds of maximal duration according to their chosen "Static Apnea" procedure. They floated face down in a swimming pool (28 degrees C). The only non-standard procedure was that they exhaled into a sampling tube for end-expiratory air, before starting the breath-hold and before resuming breathing. Breath-hold duration was 284 +/- 25 (SD) seconds. End-tidal PCO2 was 18.9 +/- 2.0 mmHg before apnea and 38.3 +/- 4.7 mmHg at apnea termination. End-tidal PO2 was 131.7 +/- 2.7 mmHg before apnea and 26.9 +/- 7.5 mmHg at apnea termination. Two of the subjects showed LMC after exhaling into the sampling tube; their end-tidal PAO2 values were 19.6 and 21.0 mmHg, respectively. End-tidal CO2 was normocapnic or hypocapnic at the termination of breath-holds. These data suggest that the athletes rely primarily on the hypoxic stimuli, probably in interaction with CO2 stimuli to determine when to end breath-holds. The severity of hypoxia close to LOC was similar to that reported for acute hypobaric hypoxia in humans.

Negative pressure oxygen breathing and head-down tilt increase nitrogen elimination.

Negative pressure breathing (NPB) increases the rate of nitrogen elimination, which is thought to be due to an increase in cardiac output due to augmented venous return to the heart. Hyperoxia, however, decreases the rate of nitrogen elimination. The effect of hyperoxia on the increase in nitrogen elimination during NPB is not known. We hypothesized that NPB as and head down tilt (HDT), which is also thought to increase cardiac output, would counteract the detrimental effects of hyperoxia on nitrogen elimination. Nitrogen elimination was measured in 12 subjects while they lay supine breathing 100% O2 supplied at atmospheric pressure (control), -10 cm H2O (NPOB(-10)), and -15 cm H2O (NPOB(-15)). Nitrogen elimination was also measured in the subjects while they breathed 100% O2 supplied at atmospheric pressure in the supine position with a 6 degrees HDT. Over a two-hour washout period, NPOB significantly increased nitrogen elimination by more than 14%, although there was no significant difference between NPOB(-10) and NPOB(-15). HDT also significantly increased nitrogen elimination by almost 8%. Neither NPOB nor HDT significantly affected cardiac output but calf blood flow was significantly lower during NOPB(-15). Combining NPB or HDT with 100% oxygen breathing appear to be useful means of increasing nitrogen elimination and should be considered in situations where this effect may be beneficial, such as with oxygen prebreathing prior to decompression.

Effects of respiratory muscle training on respiratory CO2 sensitivity in SCUBA divers.

Typically, ventilation is tightly matched to CO2 production. However, in some cases CO2 is retained (SCUBA diving). One factor behind hypoventilation in divers may be low respiratory CO2 sensitivity. If this is due to inadequate respiratory muscle performance it might be remedied by respiratory muscle training (RMT). We retrospectively investigated respiratory CO2 sensitivity prior to and after RMT in several groups of SCUBA divers. CO2 sensitivity (slope of expired ventilation as a function of inspired PCO2) was measured with a rebreathing technique in 35 subjects with diving experience. RMT consisted of either isocapnic hyperventilation or intermittent vital capacity breaths (twice/minute) against spring loaded breathing valves imposing static and resistive loads generating average inspiratory pressures of approximately 40 cmH2O and expiratory pressures of approximately 47 cmH2O; RMT was performed 30 min/day, 3 or 5 days/week for 4 weeks. Based on pre-RMT CO2 sensitivity the subjects were divided into three groups: low sensitivity: < 2 l/min/mmHg PCO2, normal: 2-4 l/min/mmHg, and high sensitivity: > 4 l/min/mmHg of inspired PCO2. The normal group had a Pre-RMT CO2 sensitivity of 2.88 +/- 0.60 and a post RMT sensitivity of 2.51 +/- 0.88 l/min/mmHg (Mean +/- SD, n = 19, p = n.s). Response in low sensitivity subjects increased from 1.41 +/- 0.32 to 2.27 +/- 0.53 (n = 10, p = 0.002,) while in the high sensitivity group it decreased from 5.41 +/- 1.25 to 2.90 +/- 0.32 l/min/mmHg (n = 6, p = 0.003). These preliminary findings showed that 46% of the subjects had abnormal sensitivity, and suggest that RMT may normalize it in hypo- and hyper-ventilating divers. If the present results are verified, RMT may be an effective means of enhancing safety in CO2 retaining divers.

Cardiac performance in humans during breath holding.

The effects on cardiac performance of high and low intrathoracic pressures induced by breath holding at large and small lung volumes have been investigated. Cardiac index and systolic time intervals were recorded from six resting subjects with impedance cardiography in both the nonimmersed and immersed condition. A thermoneutral environment (air 28 degrees C, water 35 degrees C) was used to eliminate the cold-induced circulatory component of the diving response. Cardiac performance was enhanced during immersion compared with nonimmersion, whereas it was depressed by breath holding at large lung volume. The depressed performance was apparent from the decrease in cardiac index (24.1% in the immersed and 20.9% in the nonimmersed condition) and from changes in systolic time intervals, e.g., shortening of left ventricular ejection time coupled with lengthening of preejection period. In the absence of the cold water component of the diving response, breath holding at the large lung volume used by breath-hold divers tends to reduce cardiac performance presumably by impeding venous return.

Simulated breath-hold diving to 20 meters: cardiac performance in humans.

Cardiac performance was assessed in six subjects breath-hold diving to 20 m in a hyperbaric chamber, while nonsubmersed or submersed in a thermoneutral environment. Cardiac index and systolic time intervals were obtained with impedance cardiography and intrathoracic pressure with an esophageal balloon. Breath holding at large lung volume (80% vital capacity) decreased cardiac index, probably by increasing intrathoracic pressure and thereby impeding venous return. During diving, cardiac index increased (compared with breath holding at the surface) by 35.1% in the nonsubmersed and by 29.5% in the submersed condition. This increase was attributed to a fall in intrathoracic pressure. Combination of the opposite effects of breath holding and diving to 20 m left cardiac performance unchanged during the dives (relative to the surface control). A larger intrathoracic blood redistribution probably explains a smaller reduction in intrathoracic pressure observed during submersed compared with nonsubmersed diving. Submersed breath-hold diving may entail a smaller risk of thoracic squeeze (lesser intrathoracic pressure drop) but a greater risk of overloading the central circulation (larger intrathoracic blood pooling) than simulated nonsubmersed diving.

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.

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

Electrocardiogram, cardiac output, and blood lactate accumulation were recorded in three elite breath-hold divers diving to 40-55 m in a pressure chamber in thermoneutral (35 degrees C) or cool (25 degrees C) water. In two of the divers, invasive recordings of arterial blood pressure were also obtained during dives to 50 m in cool water. Bradycardia during the dives was more pronounced and developed more rapidly in the cool water, with heart rates dropping to 20-30 beats/min. Arrhythmias occurred, particularly during the dives in cool water, when they were often more frequent than sinus beats. Because of bradycardia, cardiac output decreased during the dives, especially in cool water (to <3 l/min in 2 of the divers). Arterial blood pressure increased dramatically, reaching values as high as 280/200 and 290/150 mmHg in the two divers, respectively. This hypertension was secondary to peripheral vasoconstriction, which also led to anaerobic metabolism, reflected in increased blood lactate concentration. The diving response of these divers resembles the one described for diving animals, although the presence of arrhythmias and large increases in blood pressure indicate a less perfect adaptation in humans.

Prostacyclin does not change during an oxygen induced increase in pulmonary blood flow in the fetal lamb.

The role of prostacyclin in mediating the increase in pulmonary blood flow caused by an increase in oxygen tension in the fetal lamb was investigated. Plasma concentrations of 6-keto-PGF1 alpha, the hydrolysis product of prostacyclin, were measured during an increase in pulmonary blood flow caused by a rise in oxygen tension in eight intrauterine fetal lambs. Fetal oxygen tension was increased by placing the pregnant ewes in a hyperbaric chamber and having them breathe 100% oxygen at three atmospheres absolute pressure. This increased fetal PaO2 from 27 +/- 3 to 60 +/- 6 torr (mean +/- S.E., p less than or equal to 0.0001) and increased the proportion of right ventricular output distributed to the fetal lungs from 6 +/- 2 to 45 +/- 7% (mean +/- S.E., p less than or equal to 0.001). However, the fetal plasma concentration of 6-keto-PGF1 alpha did not change, 186 +/- 26 to 208 +/- 40 pg/ml (mean +/- S.E.). Indomethacin decreased plasma concentrations of 6-keto-PGF1 alpha in each of three fetuses but did not decrease the proportion of right ventricular output distributed to their lungs. The increase in pulmonary blood flow caused by an increase in oxygen tension in the fetal lamb is not associated with an increase in plasma concentrations of 6-keto-PGF1 alpha. Prostacyclin does not appear to be involved in the increase in pulmonary blood flow caused by the increase in oxygen tension at birth.

CO2 chemosensitivity during immersion in humans.

Hypercapnic ventilatory response was compared in 9 seated subjects during head-out immersion in 35 degrees C (thermoneutral) water and during non-immersion in 28 degrees C (thermoneutral) room air. Using Read's CO2-rebreathing technique, minute ventilation (VE) and end-tidal (ET) PCO2 were sampled continuously for 4-5 min with a spirometer and a mass spectrometer, while the subject rebreathed a 6 L gas mixture initially containing 7% CO2 and 93% O2 in a bag-in-box system. The slope of the hypercapnic ventilatory response curve, expressed as delta VE/delta PETCO2, ranged from 0.76 to 2.49 L/min/mmHg. Immersion affected neither the slope nor the position of the hypercapnic ventilatory response curve. The rate of rise of PETCO2 during immersed CO2-rebreathing was significantly reduced (4.47 +/- 0.19 [SE] mmHg/min), as compared to the control value (5.67 +/- 0.24). It was concluded that the CO2 chemosensitivity during immersion in humans did not change and that the capacity to store CO2 in tissue might have been increased.

Perfusion of the visual cortex during pressure breathing at different high-G stress profiles.

The effects of pressure breathing for G protection (PBG) on perfusion of the visual cortex were studied in a subject during various high-G stress profiles. Blood flow velocity was measured in the posterior cerebral artery using a transcranial Doppler (TCD) ultrasound instrument. The G profiles examined included gradual and rapid onset rates. Mean cerebral blood flow velocity (MCBFV) declined with increasing +Gz with G-suit protection alone. The MCBFV increased in direct proportion with increase in +Gz acceleration with PBG. The mediating mechanisms for the effects of PBG may include improved gaseous exchange, the diminished sympathicoadrenal discharges, and cardiopulmonary reflexes. A role for TCD in further research is indicated.

Moderate hypercapnia: cardiovascular function and nitrogen elimination.

Elevated carbon dioxide concentrations frequently encountered in diving operations may have cardiovascular effects. If so, changes in nitrogen loading and elimination may be induced. To study this possibility, whole body nitrogen elimination rates were determined using a rebreathing apparatus and gas chromatographic measurement of N2 in expired gas in six subjects as they breathed mixtures of 3 and 5% CO2 with 21% O2 and a balance of Ar for 125 min. No significant differences were observed among mean N2 yields, which were 815 ml (95% confidence interval +/- 51 ml), 831 ml (+/- 38 ml), and 845 ml (+/- 57 ml) for 0, 3, and 5% CO2 mixtures, respectively. Simultaneous measurements of heart rate showed a significant increase while breathing 5% CO2 as compared to 3 and 0% CO2. The increases in heart rate were not accompanied by any significant change in cardiac output, mean arterial pressure, or tissue perfusion. We conclude that at these levels of hypercarbia, tissue perfusion is not influenced enough to cause any changes in whole-body N2 elimination.

Alveolar gas exchange during simulated breath-hold diving to 20 m.

Alveolar gas exchange, as affected by changes in pulmonary blood flow, was studied in five subjects performing breath holds lasting 75 s at the surface and during compression to 20 m in a hyperbaric chamber. After reaching the maximal depth, VO2 started to increase, compared to control, reaching a maximum of 346 +/- 66 (SE) ml (STPD).min-1.m2 (body surface area) at 50 s, i.e., early in the ascent; it exceeded the 50-s surface breath-hold value by 214 +/- 9 ml.min-1.m2. During descent, CO2 was absorbed from the alveoli into the blood, initially at 140 +/- 24 ml.min-1.m2; during ascent CO2 was transferred back into the lungs. These changes reflected compression and expansion of lung air. The increase in VO2 during the dives, which are not steady states, may be explained by an increasing cardiac output at depth. An augmented cardiac output had earlier been observed under identical conditions and explained by a drop in transthoracic pressure, enhancing venous return. Upon surfacing, the PAO2 was about 20 mmHg lower than after surface breath holds, reflecting the effects of changes in cardiac output.

Effects of inspiratory and expiratory resistance in divers' breathing apparatus.

This study was performed to determine if inspiratory breathing resistance causes greater or smaller changes than expiratory resistance. Unacceptable inspiratory resistances were also determined. Five subjects exercised at 60% of their VO2max while immersed in a hyperbaric chamber. The chamber was pressurized to either 147 kPa (1.45 atm abs, 4.5 msw, 15 fsw) or 690 kPa (6.8 atm abs, 57 msw, 190 fsw). Breathing resistance was imposed on the inspiratory or expiratory side and was as high as 0.8-1.2 kPa liter(-1) x s(-1) (8-12 cm H2O x liter(-1) x s(-1)) at a flow of 2-3 liter x s(-1) at 1 atm abs., the other side being unloaded. The subjects reacted to the imposed load by prolonging the phase of breathing that was loaded. Inspiratory breathing resistance caused greater changes than expiratory resistance in end-tidal CO2, dyspnea scores, maximum voluntary ventilation, and respiratory duty cycle. Using previously published criteria for acceptable levels of dyspnea scores and the CO2 levels, we found that an inspiratory resistance inducing a volume-averaged pressure of 1.5 kPa is not acceptable. Similarly, an expiratory resistance should not induce a volume-averaged pressure exceeding 2.0 kPa

Diving decompression fails to activate complement.

The present study evaluated complement activation during decompression after air dives in a hyperbaric chamber. Intravascular bubbles were quantified by Doppler ultrasound scoring. Eighteen subjects completed 92 dives, of which 74 produced bubbles. Complement activation was assessed by plasma C3a des Arg and red-cell-bound C3d before and after each dive. These parameters of in vivo complement activation failed to show significant activation. In vitro complement activation susceptibility tests on pre-dive sera were performed to explore their association with in vivo complement activation and intravascular bubbles. Such tests failed to identify a distinct complement-sensitive group and did not correlate with in vivo complement activation during the dives and/or intravascular bubble appearance. Two subjects developed decompression sickness but were not different from the rest of the group regarding in vitro complement sensitivity or complement activation during dives.