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.

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

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.

Cerebral blood flow velocity and cranial fluid volume decrease during +Gz acceleration.

Cerebral blood flow (CBF) velocity and cranial fluid volume, which is defined as the total volume of intra- and extracranial fluid, were measured using transcranial Doppler ultrasonography and rheoencephalography, respectively, in humans during graded increase of +Gz acceleration (onset rate: 0.1 G/s) without straining maneuvers. Gz acceleration was terminated when subjects' vision decreased to an angle of less than or equal to 60 degrees, which was defined as the physiological end point. In five subjects, mean CBF velocity decreased 48% from a baseline value of 59.4 +/- 11.2 cm/s to 31.0 +/- 5.6 cm/s (p<0.01) with initial loss of peripheral vision at 5.7 +/- 0.9 Gz. On the other hand, systolic CBF velocity did not change significantly during increasing +Gz acceleration. Cranial impedance, which is proportional to loss of cranial fluid volume, increased by 2.0 +/- 0.8% above the baseline value at the physiological end point (p<0.05). Both the decrease of CBF velocity and the increase of cranial impedance correlated significantly with Gz. These results suggest that +Gz acceleration without straining maneuvers decreases CBF velocity to half normal and probably causes a caudal fluid shift from both intra- and extracranial tissues.

Dead space in the breathing apparatus; interaction with ventilation.

Dead space in breathing apparatus may cause increased ventilation and/or CO2 retention. Interactions between ventilation and dead space were tested in the breathing apparatus of three divers: a full face mask with an oro-nasal cup (AGA), a full face mask without an oro-nasal cup (EXO-26) but designed to minimize dead space, and one mouthpiece. Experiments were performed at three depths; 0, 30 and 45 m seawater (msw). The breathing gas was air except at 30 msw where it was 36 O2 in N2. Five certified SCUBA divers were exercised at three levels (0, 50 and 100 W). Ventilation and gas exchange were measured. The dead space in the AGA mask was not influenced by either depth or exercise (mean 0.201). The mean dead space of the EXO-26 was 0.341, but it increased with exercise (p < 0.001) and decreased with depth (p < 0.03). Since the dead space can vary with ventilation levels it is not sufficient to test breathing apparatus only at rest as is required by the US National Institute of Occupational Safety and Health. The mean ventilation with the EXO-26 was higher than with the AGA by 10% at 50 W (p < 0.05) and by 12% (p < 0.01) at 100 W. The same comparison for end-tidal CO2 showed mean increase by 0.30 kPa at the 100-W workload (P < 0.05); changes at other workloads were not statistically significant. Comparisons of the mean inspired PCO2 to the maximum values considered acceptable by various organizations showed that the mouthpiece was always acceptable, the AGA mask was marginally acceptable or better, while sometimes the EXO-26 was not acceptable.

Physiologically and subjectively acceptable breathing resistance in divers' breathing gear.

To determine acceptable levels of breathing resistance in divers' gear, 6 subjects were exposed to varying levels of breathing resistance under demanding and realistic conditions. The immersed air-breathing subjects exercised in the prone position at 60% of their maximum oxygen uptake for 25 min in a hyperbaric chamber at 1.45 and 6.8 atm abs (145 and 690 kPa, 4.5 and 57 msw, 15 and 190 fsw). The breathing resistance ranged from minimal to 8-12 cmH2O (0.8-1.2 kPa).liter-1.s at flow rates of 2-3 liter/s. The higher resistance levels interfered with the respiration in terms of end-tidal PCO2 and dyspnea scores. There were considerable individual differences, and changes in one parameter were typically not paralleled by changes in the other. None of maximal voluntary ventilation, forced expiratory volume, expiratory reserve volume, vital capacities, or oxygen uptake was influenced by resistance. We set the maximum allowable end-tidal PCO2 at 60 mmHg and maximum dyspnea score at 1.0 on a scale from 0 (none) to 3 (severe). Based on these criteria we concluded that the external work of breathing should not exceed 1.5-2.0 J/liter in the ventilation range 30 to 75 liter/min BTPS.

CO2 retention with minimal symptoms but severe dysfunction during wet simulated dives to 6.8 atm abs.

During wet dives in a hyperbaric chamber to 6.8 atm abs (690 kPa), air breathing subjects were experimentally exposed to external breathing resistance. Two of them were, unbeknownst to themselves, severely incapacitated. In the first incident the subject had been exercising for 25 min (end-tidal PCO2 60-65 mmHg, 7.3-8.0 kPa) when the breathing resistance was rapidly increased from low to very high (requiring pressure swings of 80 cmH2O, 8 kPa, peak to peak). He functioned normally (end-tidal PCO2 72 mmHg, 9.6 kPa) for about 100 s but 20 s later he was confused and irrational. After being extracted from the water (end-tidal PCO2 above 90 mmHg, 12 kPa), he lost consciousness for about 60 s. In the second incident the subject was exercising and breathing against a high resistance (pressure swings of 50-55 cmH2O, 5.0-5.6 kPa). His end-tidal PCO2 was high (65-68 mmHg, 8.7-9.3 kPa) throughout the exercise period, and after 24 min he reported mild dyspnea. A few seconds later he became confused. In other experiments both subjects voluntarily terminated experiments when the breathing resistance became overwhelming. These 2 subjects generally had high end-tidal PCO2 levels, but 1 other subject with end-tidal PCO2 levels in the same range never experienced any problems. These incidents indicate that severe hypercapnia does not necessarily correlate with dyspnea and that severe disturbances in mental function due to hypercapnia can develop suddenly when high breathing resistance is encountered in diving.