Percent carboxyhemoglobin in resting humans exposed repeatedly to 1,500 and 7,500 ppm CO.

Eleven nonsmoking male resting subjects were exposed to two transient CO profiles to examine whether the resultant carboxyhemoglobin (HbCO) differs with CO concentration for a fixed total CO dose and to determine the predictive capability of the theoretical model of Coburn et al. (J. Clin. Invest. 44: 1899-1910, 1965) using measured alveolar ventilation. One profile consisted of five sequential exposures to 1,500 ppm CO for 5 min each and spaced 3 min apart. The other consisted of five sequential exposures to 7,500 ppm CO for 1 min each and spaced 7 min apart. The subjects, therefore, were exposed to the same overall nominal dose of 37,500 ppm.min. During the experiment, the subject's ventilatory functions and respiratory gases were recorded continuously, and the resultant HbCO% was measured in venous blood samples by gas chromatography. Mean increase (+/- SD) in HbCO% per exposure was 2.08 +/- 0.27% for the 1,500 ppm CO exposures and 2.05 +/- 0.29% for the 7,500 ppm CO exposures with no significant difference between the two. When the measured values of the subject's alveolar ventilation were applied to the theoretical model of Coburn et al., the predicted rate of HbCO% formation was found to agree with the experimental results.

Factors affecting blood pressure during heavy weight lifting and static contractions.

Brachial arterial pressure was directly recorded in 31 healthy male volunteers through protocols examining the effects of the Valsalva maneuver, muscle size and strength, contraction force, contraction type (concentric, isometric, eccentric), changes in joint angle, and muscle fatigue on the blood pressure response to resistance exercise. Weight lifting at the same relative intensity produced similar increases in blood pressure, regardless of individual differences in muscle size or strength. Concentric, isometric, or eccentric exercise at the same relative intensity caused similar increases despite differences in force production. In weight lifting, the greatest increase in blood pressure occurred at the joint angle corresponding to the weakest point in the strength curve and the least at the angle corresponding to the strongest point. Isometric contractions of the same relative intensity at different joint angles produced identical blood pressures despite differences in absolute force production. When subjects attempted to maintain a maximum isometric contraction for 45 s, the blood pressure increase remained the same despite a marked diminution in force. Thus the magnitude of the blood pressure response depends on the degree of effort or central command and not actual force production. A brief Valsalva maneuver, which exaggerates the increase in blood pressure, is unavoidable when desired force production exceeds approximately 80% maximum voluntary contraction.

Rate of formation of carboxyhemoglobin in exercising humans exposed to carbon monoxide.

The purpose of this study was to test the CFK equation for its prediction of the rate of formation of carboxyhemoglobin (HbCO) in exercising humans by use of measured values of the respiratory variables and to characterize the rate of appearance of HbCO with frequent blood sampling. Ten nonsmoking male subjects were exposed to carbon monoxide (CO) on two separate occasions distinguished by the level of activity. Steady-state exercise was conducted on a cycle ergometer at either a low (approximately 45 W) or moderate (approximately 90 W) power output. Each experiment began with an exposure of 3,000 ppm CO for 3 min during a rest period followed by three intermittent exposures ranging from 3,000 ppm CO for 1 min at low exercise to 667 ppm CO for 3 min at moderate exercise. Increases in HbCO were normalized against predicted values to account for individual differences in the variables that govern CO uptake. No difference in the normalized uptake of CO was found between the low- and moderate-exercise trials. However, the CFK equation underpredicted the increase in HbCO for the exposures at rest and the first exposure at exercise, whereas it overpredicted for the latter two exposures at exercise. The net increase in HbCO after all exposures (approximately 10% HbCO) deviated by less than 1% HbCO between the measured and predicted values. The rate of appearance of HbCO fits a sigmoidal shape with considerable overshoot at the end of exposure. This can be explained by delays in the delivery of CO to the blood sampling point (dorsal hand vein) and by a relatively small blood circulation time compared with other regions of the body. A simple circulation model is used to demonstrate the overshoot phenomenon.

Determination of a pressure breathing schedule for improving +Gz tolerance.

A base of empirical data for developing optimal pressure breathing during +Gz (PBG) schedules is lacking. Relaxed +Gz-intensity tolerance with PBG was measured during gradual +Gz-onset rate centrifuge profiles using standard lightbar criteria. Constant PBG levels ranging from 18-73 mm Hg were randomly assigned. G-suit pressure followed the standard or an increased inflation schedule. Nine subjects wore a jerkin, CSU-15/P G-suit, and TLSS helmet and mask. With mean mask cavity pressures of 0, 18, 38, 60, and 73 mm Hg, corresponding +Gz-tolerances (mean +/- S.E.M.) were: 5.3 +/- 0.2, 5.8 +/- 0.1, 6.6 +/- 0.2, 7.3 +/- 0.3, and 7.5 +/- 0.3 Gz (linear correlation, r = 0.994). Increased G-suit pressure did not change the +Gz-tolerance improvement with PBG. The inverse of individual subject regression slopes ranged from 22.6 to 58.1 mm Hg/+Gz. Considering additional factors and adequate +Gz protection for all subjects while relaxed, the proposed schedule would apply 42 mm Hg PBG/+Gz beginning at +3.3 Gz with a maximum pressure of at least 73 mm Hg.

Respiratory muscle fatigue during simulated air combat maneuvering (SACM).

HYPOTHESIS: This study tested the hypothesis that respiratory muscle fatigue occurs during a simulated air combat maneuver (SACM) centrifuge profile. METHODS: Six subjects (four males, two females) were exposed to a SACM consisting of alternating +4 Gz to +7 Gz plateaus until volitional fatigue. Electrical activities of the diaphragm, scalene, intercostal and external oblique muscles were monitored along with esophageal pressure and ventilation. RESULTS: SACM times averaged 358 +/- 115 s. The mean frequency of the electromyographic signal of the diaphragm and scalenes during inspiration, and the intercostals during the static expiratory portion of the anti-G straining maneuver (AGSM), decreased significantly (p < 0.05) over the course of the SACM by about 9%, 10% and 4%, respectively, indicating muscle fatigue. Esophageal pressure (PES) during the straining portion of the AGSM decreased significantly from 72 +/- 20 to 66 +/- 21 mmHg (mean +/- SD). Ventilation increased significantly both at +4 Gz and +7 Gz (32 +/- 16 L.min-1 to 56 +/- 19 L.min-1 at +4 Gz and 27 +/- 5 to 35 +/- 9 L.min-1 at +7 Gz) over time. PES during a maximal AGSM at +1.4 Gz (baseline) was decreased post- vs. pre-SACM (p = 0.0575). PES exerted during a maximal static inspiratory maneuver at residual lung volume was not changed after the SACM. Inspiratory work increased significantly during the SACM. The elastance of the respiratory system did not change during the SACM, but it was significantly increased when tested after the SACM. CONCLUSION: Increased inspiratory work, decreased pressure generation during a maximal AGSM and EMG frequency shifts suggest respiratory muscle fatigue coincides with the termination of SACM.

Effect of simulated air combat maneuvering on muscle glycogen and lactate.

Muscle glycogen and muscle and blood lactate were evaluated before and after a +4.0/7.0 Gz simulated air combat maneuvering (SACM) protocol in the human centrifuge. The subjects were eight healthy males, ages 25-43 years. Muscle glycogen and lactate were determined from biopsies of m. vastus lateralis in six subjects and whole blood lactate was analyzed in finger-tip blood samples from eight subjects. G-tolerance time was 256 +/- 33 s (Mean +/- S.E.M.). The decrease in glycogen concentration averaged 81 +/- 36 mmol.kg-1 dry wt (p = 0.07). The rate of glycogen utilization was low, averaging 0.4 +/- 0.1 mmol.kg-1.s-1. Muscle lactate increased significantly from 28 +/- 2 mmol.kg-1 dry wt pre-SACM to 51 +/- 4 mmol.kg-1 post-SACM. Post-SACM blood lactate was 4.2 +/- 0.3 mmol.L-1. Neither final blood nor muscle lactate values nor the difference between pre- and post-SACM muscle lactate concentrations were related to G-tolerance time. It was concluded that glycogen availability in m. vastus lateralis is not a limiting factor during exposure to headward acceleration of this type and duration. The lactate values, while high, cannot fully explain the muscular fatigue occurring during centrifuge exposures of the type used here. Therefore, the suggestion by others that anaerobic energy metabolism in skeletal muscles is the crucial factor limiting the ability to resist fatigue during exposure SACM is not supported and is likely an oversimplification of a much more complex problem.

Maximum intra-thoracic pressure with anti-G straining maneuvers and positive pressure breathing during +Gz.

Positive pressure breathing during +Gz (PBG) and anti-G straining maneuvers (AGSM) each improve +Gz tolerance by increasing blood pressure through increases in intra-thoracic pressure, but the maximal intra-thoracic pressure from their combined effect is not known. Six subjects performed the following: 1) maximal AGSM at +1 Gz; 2) assisted PBG (constant 60 mm Hg) at +Gz; 3) submaximal AGSM at +Gz (enough to maintain peripheral vision); 4) maximal AGSM at +Gz; and 5) combined PBG and maximal AGSM at +Gz. They wore TLSS mask/helmet ensemble, CSU-15/P G-suit, and TLSS-style jerkin. Intra-thoracic pressure was measured with a catheter-tip pressure transducer in the esophagus (Pes). The change in gastric pressure was also measured (delta Pga). For both Pes and delta Pga, there were no significant differences among experimental conditions (1), (4) and (5), as above. Group mean Pes and delta Pga in these three conditions were 139 and 197 mm Hg, respectively. The similar results between maximal AGSM, and maximal AGSM and PBG are explained by limited support from the thoracic counter-pressure garment, and the characteristics of the respiratory system.

Oxyhemoglobin saturation following rapid decompression to 18,288 m preceded by diluted oxygen breathing.

This investigation studied oxyhemoglobin saturation (SaO2) and cardiovascular indices after rapid decompression (RD). Before RD, fractional inspired O2 concentration (FIO2) simulated the range of product gas from molecular sieve O2 generating systems (MSOGS). Four subjects breathed 1.0-0.80 FIO2 at 6,858 m. After decompression to 18,288 m, the subject received 1.0 FIO2 at a positive pressure of 70 mm Hg for 3 min. There were no incidents of severe hypoxia. The mean SaO2 was 98.0% before RD. After RD, SaO2 was maintained at the pre-RD level for 8 s, decreased rapidly over the next 10 s, and over the rest of the 1st min decreased more gradually to reach approximately 82%. Varying FIO2 before RD had no effect on the alteration in SaO2, heart rate, stroke index, and blood pressure after RD. The MSOGS O2 product range offers adequate protection against hypoxia during RD to 18,288 m.

Electromyographic indices of muscle fatigue during simulated air combat maneuvering.

Pilots exposed to high levels of headward (+Gz) acceleration must perform voluntary muscle contractions in order to maintain head-level arterial pressure. To study the possibility that muscular fatigue can limit human +Gz duration tolerance, electromyographic (EMG) activity and EMG indices of muscular fatigue were measured during a simulated air combat maneuvering (SACM) centrifuge profile. Eight experienced male volunteers were exposed to a +4-7 Gz centrifuge profile until volitional fatigue. Electrical activity (EMG) was recorded from 7 muscles: biceps brachii (BB), latissimus dorsi (LD), pectoralis major (PM), rectus abdominis (RA), vastus lateralis (VL), biceps femoris (BF) and gastrocnemius (GN). EMG and force during isometric contractions of the same muscles were also recorded at 1 G. Root mean square (RMS) and mean power frequency (MPF) were calculated for each second of EMG data. G-tolerance time averaged 256 +/- 33 s (mean +/- SD). RMS activity was expressed relative to activity during a maximal muscle contraction. The mean values (%) for each muscle during the 7 Gz plateaux were: RA, 30.8; BB, 26.4; LD, 44.0; PM, 48.5; VL, 43.4; BF, 31.4; GN, 39.3. The estimated level of contraction relative to a MVC (%) was: RA, 36.6; BB, 30.5; LD, 43.9 and PM, 61.4. There was no significant difference between contraction levels for any of the muscles studied. RMS activity did not increase over time and MPF decreased significantly only in BF and LD, however, these decreases were small. EMG activity and estimated contraction intensities were considered to be low to moderate. These results suggest that it is unlikely that fatigue in the muscles studied would limit G-tolerance time.

Is there central fatigue during simulated air combat maneuvering?

This study tested the hypothesis that repeated exposure to high levels of +Gz acceleration, in conjunction with repeated execution of an Anti-G Straining Maneuver (AGSM), causes central fatigue, presumably by impairing central nervous system (CNS) function. We speculated that central fatigue would impair the ability to recruit sufficient musculature at the intensity required to perform an adequate anti-G straining maneuver. Central fatigue was evaluated by measuring maximal force generation and surface electromyographic activity of leg extensor muscles before, during, and immediately upon termination of an SACM, and comparing these values to those obtained when the muscles were electrically stimulated during maximal voluntary contractions (MVCs). We assumed that any observed increase in force generation during the MVCs, caused by the stimulation, would indicate central fatigue. G-tolerance time was 230 +/- 172 s. Hypoxia was induced by the SACM as the arterial oxygen saturation decreased significantly from 97% to 90%. In spite of this hypoxia, there was no significant change in MVC force when the pre- and post-SACM values were compared. Electrical stimulation during the MVC's did not cause an increase in force generation. The average forces generated during the +7 Gz phase of the SACM were only about 35% of MVC force. This force value did not change significantly during the SACM. The results indicate that the inability to continue to perform the AGSM during an SACM is not likely due to central fatigue or to fatigue of the large skeletal muscle groups we have examined.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of variations in the anti-G straining maneuver on blood pressure at +Gz acceleration.

The increase in blood pressure provided by the standard AGSM is caused by both the contraction of the muscles of the lower body and by an increased intrathoracic pressure due to a respiratory straining (Valsalva) maneuver. This study examined the relative effectiveness and fatigability of the two components at +1 Gz and during +Gz acceleration in a human centrifuge. Brachial arterial pressure was recorded from a pressure-tip transducer in six subjects performing isometric leg presses only and on a separate occasion while performing respiratory straining only. Measurements were made over a range of intensities for the leg press contractions and Valsalva maneuvers and were conducted at +1 Gz and during slow and rapid onset runs up to +5 Gz in a human centrifuge. Blood pressure was also recorded during pulsing or intermittent contractions of the legs. We found it difficult to completely separate the blood pressure response to the leg press component from that of the respiratory straining alone component, since a moderate respiratory straining maneuver usually accompanied forceful contractions of the legs. We conclude, however, that a major portion of the elevation in blood pressure caused by the AGSM can be attributed to contraction of the muscles of the lower body and that this component is less fatiguing than the respiratory straining component. At +1 Gz a pulsing isometric contraction of the legs was no more effective in elevating blood pressure than a constant isometric contraction over the same duration.

Implementation of a computer-controlled life support system in the acceleration research environment.

Electronic control of the G-valve and pressure breathing regulator is being implemented in some advanced life support systems used in aircrew protection. This technological improvement, however, has not reached its full potential in the research environment. A computer-controlled life support system interface providing programmable schedules for G-suit inflation and positive pressure breathing during +Gz (PBG) was developed. Output pressures from a G-valve and pressure breathing regulator (Carleton Technologies) were controlled by a Macintosh computer running LabVIEW software. Required pressures were determined as functions of single or multiple control inputs (i.e. +Gz level, a pressure signal, time, etc.). Subject safety was ensured via hardware limitations and status checks incorporated into the software. Experiments conducted at +1 Gz and at various +Gz levels evaluated the computer software-life support hardware interface. Open-loop algorithms allowed independent control of multiple regulators using simple (single input) and complex (multiple input with adaptive loop) control structures. The system provided accurate and reproducible G-suit and mask pressures. Time of inflation, peak pressure attained, and deflation rate were effectively controlled at all +Gz levels. The ability to alter the pressure schedules independent of +Gz or time allowed comprehensive control over all parameters necessary to conduct acceleration research involving advanced life support systems.

Effect of induced erythrocythemia on aerobic work capacity.

The aerobic work capacity of 11 highly trained runners was studied employing a double-blind design 1) before phlebotomy (C1), 2) following restoration of normocythemia (C2), 3) after a sham reinfusion of 50 ml of saline (sham), 4) following autologous reinfusion of approximately 900 ml of freeze-preserved blood (reinfusion), and 5) upon reestablishment of control hematologic levels after erythrocythemia (C3). There were no hematologic differences among C1, C2, sham, and C3, but following reinfusion, hemoglobin was significantly elevated (15.7-16.7 g . 100 ml-1). Maximum O2 consumption (VO2max) and running time to exhaustion were significantly increased 24 h postreinfusion (5.11-5.37 l . min-1 and 7.20-9.65 min, respectively) and 7 days postreinfusion. When sham preceded reinfusion, VO2 max and time to exhaustion were the same as control. However, 16 wk postreinfusion, despite the return to normal hematologic values, VO2max remained significantly above control levels at sham and C3. These findings indicate that there is a distinct increase in VO2max following induced erythrocythemia and suggest that oxygen transport limits maximal aerobic capacity.

VA/Q inhomogeneity and AaDO2 in man during exercise: effect of SF6 breathing.

Pulmonary gas exchange was studied in five normal subjects both at rest and during moderate steady-state exercise on a bicycle ergometer while breathing a) room air and b) a mixture of 20.9% O2-balance sulfur hexafluoride (SF6). The alveolar-arterial oxygen pressure differences (AaDO2) widened significantly from rest to exercise. Breathing the O2-SF6 mixture reduced the AaDo2 significantly from 10.9 to 4.2 Torr at rest and from 15.5 to 10.1 Torr during exercise (P less than or equal to 0.01). There were no concurrent changes in metabolism, cardiac output, or heart rate during the SF6 breathing. Possible changes in the anatomic shunt fraction, alveolar-end-capillary equilibration, or the distribution of blood flow cannot account for these observations. We conclude that the AaDO2 increase during exercise reflects an inhomogeneity of ventilation-perfusion ratios (VA/Q) most probably arising within regions of the lung (intraregional inhomogeneity) rather than between regions (interregional inhomogeneity).