Factors influencing G-tolerance.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to U I Balldin.
Explore the source record for details and available documents.
The USAF is developing an On Board Oxygen Generation System (OBOGS) for use in fighter aircraft. This study was conducted to determine the inert gas dilution requirements of the OBOGS necessary to prevent acceleration atelectasis. Human subjects were exposed to either 21, 50, 70, 82.5, 95 or 100% inspired oxygen, along with an increased +Gz Simulated Aerial Combat Maneuver (SACM) profile using the USAF School of Aerospace Medicine human centrifuge. The SACM profile utilized four +4.5z peaks (136 s at this +Gz) superimposed on a +3 Gz baseline, representing a total ride time of 276 s. A significant reduction in vital capacity (VC) occurred at inspired oxygen concentrations of 70% and greater. The addition of 5% argon (a natural product of OBOGS) to pure oxygen did not reduce the magnitude of acceleration atelectasis observed, nor the severity of breathing symptoms. A 30-s exposure to positive pressure breathing at 30 mm Hg during the end of the SACM reduced the level of VC reduction caused by subjects breathing 100% oxygen during +Gz.
Exposure to high gravitational forces acting along the body axis towards the feet (+Gz) causes considerable strain on several organ systems, including the kidneys. During +Gz tolerance studies without anti-G suits, significant amounts of protein and hyaline casts were found in 17 of 20 fighter pilots after centrifugation. The G load alternated between 3.5 and 5.5 G. Mean time in the centrifuge was 15 min. For comparison we examined another group of 19 fighter pilots after air combat maneuver training with anti-G suits. None showed proteinuria. The proteinuria most likely indicates a severely depressed renal blood flow during centrifugation.
Methods to increase G tolerance of pilots flying high-performance aircraft are of vital importance. Straining maneuvers to increase G tolerance involve abdominal muscles, and high intra-abdominal pressures (IAP) are recorded during G exposure. This study was carried out to examine the effects of an 11-week abdominal muscle training program on maximal IAP, G tolerance and muscle strength/endurance in 10 fighter pilots. G tolerance was measured in a human centrifuge using simulated aerial combat maneuvers (ACM). The pilots had a higher maximal IAP before training than a control group. G tolerance, maximal IAP, and maximal peak torque of knee extensors were not changed by the training. In contrast, leg muscle endurance increased (p less than 0.01) and ratings of local perceived exertion decreased (p less than 0.01). Static endurance of the knee extensors was positively correlated (p less than 0.05) with G tolerance. It is concluded that the present abdominal training program, employed in experienced fighter pilots, is not sufficient to increase IAP or G tolerance.
Explore the source record for details and available documents.
The physiological effects of diving with two types of closed-circuit oxygen breathing apparatus were investigated in 4 divers. In one apparatus the breathing bag was mounted on the dorsum and in the other on the chest, inducing -2 kPa and +1 to +2 kPa static lung load in the prone position, respectively. The back-mounted bag caused an unfavorable swimming position, with increased heart rate, breathing rate, and rating of perceived exertion (RPE) for work load. The greater internal and external work of breathing (the latter judged from the higher RPE for breathing resistance) probably contributed to a higher RPE for discomfort with the back-mounted bag. Three divers showed great reduction in vital capacity (VC) (0.8 to 1.9 liters) and developed coughing attacks after dives with this apparatus; these results were interpreted as possible indications of atelectasis formation. The 4th diver showed slight reduction in VC with both types of bag, possibly because the changes in static lung loads did not influence the airway closure in this man.
Inward leakage in a respiratory protective device may constitute a health hazard. The pressure demand system causes a slightly positive pressure in the facepiece throughout the breathing cycle, so that any insufficient seal in such a system will result in an outward leakage. One question is whether this positive pressure will influence work capacity. Five subjects worked until exhaustion on a bicycle ergometer with four different breathing equipments: two masks with positive pressure (0.5 kPa and 0.8 kPa) and two mouthpieces without positive pressure, one control and one with high resistance. No difference in endurance time was found. Heart rate, oxygen consumption, rated perceived exertion and blood lactate at breaking point did not show any significant changes. The high resistance mouthpiece, -1.1 kPa to +1.3 kPa, at breaking point, did reduce minute ventilation by 21% and end tidal PCO2 was increased by 16% without any influence on work performance.
The relationship between sustained G-tolerance and muscle fiber type composition was studied in 28 fighter pilots and 10 nonpilots. The G-tolerance, as assessed by the aerial combat maneuver (ACM) acceleration profile and modifications of it, was measured in a human centrifuge. Percutaneous muscle biopsies were obtained from m. vastus lateralis at rest. Histochemical analyses were carried out to identify and calculate the percentage of fast twitch (FT) and slow twitch (ST) fiber types. Additional analyses were performed for determination of muscle fiber size and capillary density. Mean (+/- S.D.) muscle fiber type composition in pilots and nonpilots, respectively, were 60 +/- 5 and 52 +/- 10% FT. There was no correlation of fiber type composition, fiber size, or capillary supply with G-tolerance. It is concluded that muscle fiber type composition and associated metabolic characteristics do not modify sustained G-tolerance to any significant extent.
Explore the source record for details and available documents.
The effect on vital capacity of 1 h of oxygen breathing with and without continuous positive pressure was studied in five subjects during immersion. Vital capacity (VC) was used as an index of pulmonary atelectasis. The negative-pressure breathing induced by head-out immersion will cause airway closure and thus atelectasis if the closed-off regions contain oxygen. Without positive-pressure breathing, VC was reduced by 42%, and the subjects complained of tightness in the chest and had attacks of coughing. When 1.5 kPa positive pressure was used, three subjects had no decrease in VC, and in the remaining two subjects the decrease was halved. The latter two subjects were also studied during continuous positive-pressure oxygen breathing at 2.5 kPa. The decrease in VC was only one-fifth of the decrease in the control immersion condition without positive pressure (0 kPa), and they had no subjective feelings of discomfort. The results are relevant for the design of closed-circuit oxygen breathing apparatus.
The G tolerance of pilots flying modern, high-performance fighter aircraft is crucial. Therefore, methods to increase G tolerance are of vital importance. In this study, G tolerance was studied in a human centrifuge using simulated aerial combat maneuvers (ACM)--consisting of 15-s periods of 4.5 and 7 G until exhaustion--before and after 11 weeks of muscle strength training. The ACM-time in 11 fighter pilots was increased after this training by 39%. Gains were observed in knee extensor muscle strength during slow contractions by 17% and in anaerobic power by 14%. Aerobic performance and various muscle histochemical indices, as assessed from muscle biopsy samples obtained from m. vastus lateralis, were unchanged. Neuromuscular adaptation seems to be responsible for the increased muscle strength, as well as for the improved performance of the M-1 straining maneuver. This might explain the enhanced G tolerance.
The central hemodynamics during extreme positve pressure breathing (PPB) with 4.0-9.3 kPa breathing pressures using a two-pressure flying suit was studied with the thermodilution technique. Pressures measured simultaneously in right atrium, pulmonary artery, and systemic circulation increased in proportion to, but somewhat less than, the breathing pressures. A decreased transmural right atrial and pulmonary arterial pressure was found during PPB to be most pronounced during simultaneous counterpressure to the thorax. Stroke volume (SV) as well as cardiac output (CO) decreased successively during PPB, mostly during PPB with more than 4 kPa. Simultaneous counterpressure to the thorax added further hemodynamic effects. During recovery after PPB, a marked compensatory increase in SV and CO was registered. An increased systemic blood pressure and heart frequency was found at all levels of PPB, suggesting that PPB may be of value to increase G tolerance.
Explore the source record for details and available documents.
Decompression venous gas bubbles were detected with the precordial Doppler utrasound technique in humans at simulated altitudes of 1,000-3,000 m 3 h after no-stage decompression dives to 15 or 39 m. Bubbles were detected at 3,000 m in a total of 60% of the subjects: in 90% after the 100-min shallow dives to 15 m with some bubbles present in the first minutes (mean onset 12 min), and in only 30% after the 10-min deeper dives to 39 m with later appearances of bubbles (mean onset 28 min). At both 2,000 and 1,000 m bubbles could also be detected, sometimes in the first minutes. The risk of decompression sickness must be considered high with the amount of gas bubbles found, even though only uncertain symptoms appeared in this study. Thus, a safe interval between ordinary SCUBA-diving and flying in airliners or general aviation aircraft seems to be more than 3 h.
The RSAF two-pressure flying suit system to protect the pilot at high altitude has been tested from different medical safety aspects. To secure adequate alveolar oxygen pressure, the suit admits up to 70 mm Hg (9.3 kPa) positive pressure breathing by counter-pressure against the thorax and by a 3.2 times higher pressure in the anti-G suit. After 1 h of oxygen breathing, subjects were exposed to explosive decompression from an altitude of 9,000 m to 17,500 or 20,000 m in 0.5 s in a hypobaric chamber. No symptoms of decompression sickness or of alveolar rupture with gas embolism to the central nervous system were seen. Pulmonary X-rays after the test did not reveal any signs of lung rupture with extrapulmonary gas leakage. With the precordial Doppler ultrasound technique, intracardial gas bubbles (silent bubbles) could be detected only in one subject after explosive decompression to a 20,000-m altitude in the 10 experiments.
Intracardial gas bubbles, detected with Doppler ultrasound, and symptoms of decompression sickness were registered at 9,000 m simulated altitude within 12, 18, and 24 h of exposures to 15 or 39 m simulated water depth allowing no stage decompression. With a time interval of 12 h between diving and flying, the earliest intracardial bubbles were found in some subjects already during the first minutes at altitude, and the earliest symptoms of decompression sickness some minutes afterwards. With an 18-h interval, the earliest bubbles and symptoms as well as their average time onsets appeared somewhat later. With a 24-h interval, the earliest bubbles and symptoms were detected slightly later, i.e. after 17 min and 23 min, respectively. Thus, a safe time interval between no-stage decompression dives and flying at 9,000 m cabin altitude for a maximum of 15 min appears to be 24 h. For prolonged such flights, a longer time interval seems to be necessary.
A case of altitude decompression chokes in a subject is described, which occurred unintentionally in an experimental series dealing with safe time intervals between diving and flying at 9,000 m of altitude. Before the development of the first signs of chokes, intracardial gas bubbles could be registered during 65 min and heavy showers of bubbles during 38 min with the precordial Doppler ultrasound technique. The intracardial bubbles and symptoms partly continued after recompression to surface pressure. After 10 min of hyperbaric oxygen treatment, the symptoms disappeared completely. The same subject, as well as others, did not develop chokes with similar durations of heavy showers of intracardial gas bubbles in other experiments.
The influence of negative pressure breathing on the appearance of intracardial gas bubbles at a subsequent decompression to altitude was investigated in five subjects using the precordial Doppler ultrasound technique. Every subject was tested for a suitable exposition that, after 30 min oxygen breathing at surface, caused both intracardial bubbles and decompression sickness. An identical exposition followed a week later, except that oxygen breathing at the surface now included negative pressure breathing. In all cases, negative pressure breathing caused a delay of the onset of both intracardial bubbles and bends and, in some cases, neither bubbles nor bends appeared at all. The total amount of bubbles was always less after negative pressure breathing. Thus, negative pressure breathing in connection with decompression may reduce the amount of intracardial bubbles and the risk of decompression sickness. This may be of importance in diving procedures and in the construction of diving devices.