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Biomedical subjects

A Cymerman

Publications and source records attributed to A Cymerman.

At least 73 records · Page 4Linked to original sources

Cardiocirculatory responses to upright tilt at sea level and high altitude.

A collaborative study was conducted to measure the cardiocirculatory responses to upright tilt in eight young men at sea level (SL); after 1h at 4300m simulated altitude (SA) and at 18h, 66h and 114h during residence at 4300m (HA). Heart rate (HR), stroke volume (SV), cardiac output (CO), calf blood flow (CBF), blood pressure (BP) and total peripheral resistance (TPR) were obtained during supine rest and after 13 min of 60 degrees head-up tilt using an impedance monitor and an electrosphygmomanometer. SL to HA changes in blood volume (BV) were calculated from hematocrit and hemoglobin values. Supine HR, TPR and BP were increased while SV, CO and CBP were reduced SL to HA (P less than .05). HR and BP in the upright position were increased SL to HA (P less than .05). The responses to tilt (delta supine to upright) were unaltered SL vs SA. With prolonged exposure, SV, CO, TPR and CBP responses to tilt were reduced (P less than .05). The reduced responses to tilt at HA were associated with a 10% decline in BV (P less than .01). It was concluded that the reduction in SV during tilt at SL and SA was compensated for by increases in HR and TPR in order to maintain BP. After 18h HA, BP in the upright position was maintained only by an increase in HR.

Adult↗

Alterations in human upper extremity motor function during acute exposure to simulated altitude.

We tested the hypothesis that mild motor dysfunction was associated with Acute Mountain Sickness (AMS) by measuring arm movement characteristics in 14 subjects at sea level and at the end of a 30-h simulated altitude exposure (4,600 m). A computerized upper extremity movement analyzer (UEMA) was used to quantitate arm movements between a "start" position and randomly-generated targets on a large digitizing tablet by measuring selected speed parameters and error indices. The UEMA results were compared with the results of the Environmental Symptoms Questionnaire (ESQ) and with neurologic examinations. When compared with sea-level values, the mean values for all the speed-related parameters measured at the end of the 30-h exposure significantly declined by 20% to 32%. The error indices were not different. The declines in the speed-related parameters were significantly correlated with the severity of AMS symptoms as measured by the ESQ (R = 0.82). The neurologic abnormalities were limited to changes in mental status items. These results demonstrate that subclinical alterations in upper extremity speed are associated with mild, reversible AMS and provide evidence that hypoxia may produce supraspinal inhibition of motor pathways.

Adult↗

A latex mask for collection of expired gases from goats.

A latex respiratory mask was developed to collect expired gas from goats in studies of ventilatory adaptation to high altitude. The snouts of 15 animals were dimensioned by taking girth measurements. The procedure requires a rough positive mold of wood which is repeatedly submerged into latex, then slowly rotated upon removal until skim-like layers form a mask. A supporting harness is attached to the mask by use of three flat straps connected by Dot fasteners. A period of several hours per day for up to 2 weeks may be necessary to allow the animal to become accustomed to wearing the mask.

Adaptation, Physiological↗

The electrocardiogram at rest and exercise during a simulated ascent of Mt. Everest (Operation Everest II).

To evaluate the effect of extreme altitude on cardiac function in normal young men, electrocardiograms were recorded at rest and during maximal exercise at several simulated altitudes up to the equivalent of the summit of Mt. Everest (240 torr or 8,848 m). The subjects spent 40 days in a hypobaric chamber as the pressure was gradually reduced to simulate an ascent. Changes in the resting electrocardiogram were evident at 483 torr (3,660 m) and were more marked at 282 torr (7,620 m) and 240 torr (8,848 m). They consisted of an increase in resting heart rate from 63 +/- 5 to a maximum of 89 +/- 8 beats/min; increase in P-wave amplitude in inferior leads; right-axis shift in the frontal plane; increased S/R ratio in the left precordial leads; and increased T negativity in V1 and V2. No significant arrhythmias or conduction defects were observed. Most changes reverted to normal within 12 hours of return to sea level, with the exception of the frontal-plane axis and T-wave alterations. Maximal cycle ergometer exercise at 282 torr (7,620 m) and 240 torr (8,848 m) resulted in a heart rate of 138 +/- 7 and 119 +/- 6 beats/min at the 2 altitudes, respectively. No ST depression or T-wave changes suggestive of ischemia occurred despite a mean arterial oxygen saturation of 49% and a mean pH of 8 during peak exercise. Occasional ventricular premature beats were observed during exercise in 2 subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

An automated method of quantifying retinal vascular responses during exposure to novel environmental conditions.

The width of retinal arteries and veins was measured by digital image analysis using an automated vessel-tracking software program. Mean coefficients of variations in vessel width of less than 3% were easily achieved from digitized 35-mm retinal photographs taken with a table-top or hand-held fundus camera. Retinal images were analyzed from seven subjects exposed to sea level or altitudes equivalent to 10,000 (3048 m), 17,500 (5334 m), and 25,000 (7620 m) ft and nine subjects exposed to sea level and 14,110 ft (4300 m). At each altitude, retinal veins dilated more than did arteries (5 +/- 1 versus 0 +/- 1% at 10,000 ft and 28 +/- 9% versus 9 +/- 2% at 25,000 ft; veins versus arteries, respectively). However, widths of retinal arteries and veins were reduced in nine subjects tested after 15 minutes, 24 hours, and 48 hours of 10 degrees head-down tilt; and values varied inversely with intraocular pressures (IOP). Hand-held retinal fundus photography and digital image analysis were found to provide a sensitive and objective method for detecting and quantifying retinal vascular responses in humans exposed to novel environments.

Adolescent↗

Operation Everest II: neuromuscular performance under conditions of extreme simulated altitude.

The force output of the ankle dorsiflexors was studied during a 40-day simulated ascent of Mt. Everest in a hypobaric chamber; both electrically activated and maximal voluntary contractions (MVCs) were employed. The purpose of this study was to establish whether, under conditions of progressive chronic hypoxia, there was a decrease in muscle force output and/or increased fatigability. We also attempted to identify the main site of any failure, i.e., central nervous system, neuromuscular junction, or muscle fiber. Muscle twitch torque (Pt), tetanic torque (Po), MVC torque, and evoked muscle compound action potential (M wave) were monitored during 205-s exercise periods in five subjects at three simulated altitudes (760, 335, and 282 Torr). All three types of torque measurement were well preserved at the three altitudes. In some subjects, the responses to stimuli interpolated during repeated MVCs provided evidence of "central" fatigue at altitude. In addition, the rate of fatigue during 20-Hz electrical stimulation was greater (P less than 0.01) at altitude and there was increased fatigability of the twitch (P less than 0.025); however, the M wave amplitude was maintained. We conclude that central motor drive becomes more precarious at altitude and is associated with increased muscle fatigue at low excitation frequencies; the latter is the result, in part, of chronic hypoxia and occurs in the muscle fiber interior because no impairment in neuromuscular transmission could be demonstrated.

Adult↗

Decreased ventilation and hypoxic ventilatory responsiveness are not reversed by naloxone in Lhasa residents with chronic mountain sickness.

Persons with chronic mountain sickness (CMS) hypoventilate and are more hypoxemic than normal individuals, but the cause of the hypoventilation is unclear. Studies of 14 patients with CMS and 11 healthy age-matched control subjects residing in Lhasa, Tibet, China (3,658 m) were conducted to test the hypothesis that hypoventilation, blunted hypoxic ventilatory responsiveness (HVR), and hypoxic ventilatory depression of CMS were due to increased endogenous opioid production. Patients with CMS compared with control subjects exhibited hypoventilation (end-tidal carbon dioxide pressure [PETCO2] = 36.6 +/- 1.0 versus 31.5 +/- 0.5 mm Hg, p less than 0.05), lower tidal volume (VT = 0.54 +/- 0.02 versus 0.61 +/- 0.02 ml BTPS, p less than 0.05), blunted HVR (shape parameter A = 17 +/- 8 versus 114 +/- 22 mm Hg/L BTPS/min, p less than 0.05), and a depressant effect of ambient hypoxia on ventilation (delta PETCO2 with acute hyperoxia = -3.5 +/- 0.5 versus -1.0 +/- 0.6 mm Hg, p less than 0.05). Reduced forced expiratory volume in 1 s to vital capacity ratios (FEV1/VC) and a higher proportion of cigarette smokers in the group of patients with CMS compared with control subjects suggested that at least some patients with CMS had mild airway obstructive lung disease. Naloxone infusion (0.14 mg/kg) to six patients with CMS did not change resting VT, PETCO2, HVR, or SaO2.(ABSTRACT TRUNCATED AT 250 WORDS)

Altitude Sickness↗

Symptomatology during hypoxic exposure to flame-retardant chamber atmospheres.

Hypoxia was studied in 12 men during 63-h exposures to 17 and 13% O2, with the subjects serving as their own controls by repeating the measurements in 21% O2. All test atmospheres were contaminated with 0.9% CO2 to simulate the condition of living aboard submarines. The mean SaO2's were 97-98% in all conditions of 21% O2, 96% in 17% O2 (n.s.), and 92% in 13% O2 (P less than 0.05). The blood concentrations of 2,3-diphosphoglycerate were elevated in 13 and 17% O2 (P less than 0.05). Seventeen percent O2 did not cause significant symptoms of environmental stress; however, 13% O2 caused symptoms of acute mountain sickness in 5 of 12 men. In the last 7 h of exposure to 17% O2, reduction of the barometric pressure to 576 Torr reduced the ambient PO2 to 98 Torr (similar to the PO2 of 13% O2 at normobaric pressure). This induced symptoms of acute mountain sickness in 3 of 11 men. All symptomatology and physiologic changes were reversed during recovery in 21% O2. Monitoring devices indicated the presence of volatile organic contaminants at a mean concentration of 6.1 ppm in the chamber atmosphere. Combustion tests in the occupied chamber showed that flame propagation was retarded by lowering the O2 concentration from 21 to 13-17%. We conclude that men can live comfortably in a normobaric, flame-retardant atmosphere consisting of 17% O2-0.9% CO2-6.1 ppm volatile organic compounds-balance N2.

2,3-Diphosphoglycerate↗

Operation Everest II: ventilatory adaptation during gradual decompression to extreme altitude.

To assess the ventilatory adaptation during gradual ascent to extreme altitude, we studied seven healthy males as part of the 40 d simulated ascent of Mt. Everest in a hypobaric chamber. We measured resting ventilation (VE, l.min-1), arterial oxygen saturation (SaO2%), the ventilatory response to oxygen breathing, isocapnic hypoxic ventilatory response (HVR), and hypercapnic ventilatory response (HCVR) at sea level prior to the ascent (760 torr), 14,000 feet (428 torr), 24,000 feet (305 torr), and within 24 h of descent (765 torr). VE increased from 9.3 +/- 1.1 l.min-1 at 760 torr to 23.4 +/- 1.3 l.min-1 at 305 torr and remained elevated at 14.7 +/- 0.7 l.min-1 after descent. Oxygen breathing decreased VE by 9.6 +/- 1.3 l.min-1 at 305 torr. Isocapnic HVR (expressed as a positive slope of VE/SaO2, l.min-1.%SaO2(-1) increased from 0.18 +/- 0.07 at 760 torr to 0.34 +/- 0.11 and 0.38 +/- 0.5 at 428 torr and 305 torr (P less than 0.05) respectively. HVR was elevated further upon return to sea level (0.8 +/- 0.09, P less than 0.05). HCVR (S = VE/PETCO2, l.min-1.torr-1) increased from sea level (S = 4.4 +/- 0.09) to 305 torr (S = 18.7 +/- 3.5, P less than 0.01) and remained elevated upon return to sea level (S = 10.7 +/- 4.6, P less than 0.001). This study is the first to investigate the ventilatory response to such extreme altitude and so soon after descent and shows that hypoxic and hypercapnic responses increase during prolonged progressive hypoxic exposure and remain significantly elevated from pre-ascent levels immediately upon descent.

Acclimatization↗

The use of tympanometry to detect aerotitis media in hypobaric chamber operations.

Diagnosis and quantification of aerotitis media were performed using a modified commercially-available tympanometer under hypobaric conditions. Subjects were 22 males and 9 females, 22-43 years of age, who were tested in each ear with the tympanometer prior to and after exposure, sequentially at the barometric pressure plateaus of 706, 656, 609, 586, 564, and 522 mm Hg, and following an induced ear block during a 1-min descent from 522 to 586 mm Hg. Each subject was examined once either alone or in pairs during a 90-min exposure. Aerotitis media was detected using tympanometry at simulated altitude as evidenced by the difference between measurements made during induced ear blocks and those made prior to inducement, as well as following relief of the pressure differential with the Valsalva maneuver. There were no significant differences between pre- and post-induced aerotitis media values at 586 mm Hg, or between pre- and post-hypobaria. Our study suggests that tympanometry can be a valuable tool in managing aerotitis media in the aeromedical environment.

Acoustic Impedance Tests↗

Mental performance during submaximal exercise in 13 and 17% oxygen.

Submarine crews live in atmospheres containing variable levels of O2 and CO2. Under these conditions, significant reduction of the O2 may impair mental function during physical exertion. Therefore, psychomotor performance was measured in exercising men during Hours 26 and 57 of exposure to 21, 17, and 13% O2 in a hypobaric chamber (each gas contained 0.9% CO2, balance N1). Sea-level pressure was used except when reduced to 576 Torr at Hour 57 in 17% O2 (hypobaric-17% O2). At Hour 26 the subjects exercised at 35 and 65% of predicted VO2max They were hypoxic during exercise in 17 and 13% O2, as indicated by reduced SaO2 values (P less than 0.05). The psychomotor test (timed arithmetic) was affected by the exposure condition (P less than 0.05) but not by the work rate. At Hour 57, subjects repeated the arithmetic task at rest and at 65% of predicted VO2max. SaO2 was reduced in hypobaric-17 and 13% O2 (P less than 0.05). The math scores were affected by the work rate (P less than 0.05) but not by the exposure condition. From post-hoc analyses we conclude that 17% O2 does not impair the timed arithmetic task during submaximal exercise at normobaric pressures.

Adult↗

Operation Everest II: muscle energetics during maximal exhaustive exercise.

To investigate the metabolic basis for the reduction in peak blood lactate concentration that occurs with maximal exercise after acclimatization to altitude, eight male subjects [maximal O2 uptake of 51.2 +/- 3.0 (SE) ml.kg-1.min-1] were acclimated to progressive hypobaria over a 40-day period. Before decompression (SL-1), at 380 and 282 Torr, and on return to sea level (SL-2) the subjects performed progressive cycle exercise to exhaustion. Analysis of muscle samples obtained from the vastus lateralis before exercise and at exhaustion indicated a pronounced reduction (P less than 0.05) in muscle lactate concentration (mmol/kg dry wt) at 282 Torr (39.2 +/- 11) compared with SL-1 (113 +/- 9.7), 380 Torr (94.6 +/- 18), and SL-2 (92.7 +/- 22). For the other glycolytic intermediates studied (glucose 1-phosphate, glucose 6-phosphate, fructose 6-phosphate, fructose 1,6-bisphosphate, and pyruvate) only the increase in glucose 1-phosphate, glucose 6-phosphate, and fructose 6-phosphate were blunted (P less than 0.05) at 282 Torr. The reduction in muscle glycogen concentration during exercise was similar (P less than 0.05) for all environmental conditions. Although exercise resulted in reductions (P less than 0.05) in ATP and creatine phosphate averaging 30 and 51%, respectively, the magnitude of the change was not dependent on the degree of hypobaria. Inosine monophosphate was elevated (P less than 0.05) approximately 11-fold with exercise at both SL-1 and SL-2. These findings support the hypothesis that the lower lactate concentration observed at 282 Torr after exhaustive exercise is due to a reduction in anaerobic glycolysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗

Operation Everest II: plasma lipid and hormonal responses during a simulated ascent of Mt. Everest.

To examine the effect of hypobaric hypoxia on plasma lipid profiles, fasting blood samples were collected from six men (21-31 yr) at 760 Torr and periodically during a 40-day exposure to decreasing barometric pressure culminating in a final ambient pressure of 282 Torr. Preascent plasma total cholesterol concentration ([TC]) was decreased by 25% after the 40-day exposure (P less than 0.01). High-density lipoprotein concentrations ([HDL-C]) decreased 32% (P less than 0.001) with no alteration in the TC-to-HDL-C weight ratio. Plasma triglyceride concentration increased twofold during this period (P less than 0.01). There were no significant differences in fasting plasma free fatty acid concentrations or free fatty acid-to-albumin molar ratio throughout the study. Fasting plasma insulin levels were increased approximately twofold with no significant changes in glucagon concentration or the insulin-to-glucagon molar ratio. Plasma norepinephrine concentrations were increased threefold on reaching 282 Torr (P less than 0.01), with no significant changes in plasma epinephrine concentrations. Mean energy intake (kcal/day) decreased 42%, whereas mean body weights decreased by 8.9 +/- 0.8% (P less than 0.01) with exposure. Increased concentrations of insulin may lead to increased hepatic production of triglyceride-rich lipoproteins, thus eliciting metabolic changes independent of weight loss and dietary intake.

Adult↗

Operation Everest II: maximal oxygen uptake at extreme altitude.

Chronic exposure to high altitude reduces maximal O2 uptake (VO2max). At extreme altitudes approaching the summit of Mt. Everest [inspiratory PO2(PIO2) = 43 Torr], mean VO2max have been determined to be 15.3 ml.kg-1.min-1 in two subjects who breathed 14% O2 at 6,300 m on Mt. Everest (West et al., J. Appl. Physiol. 54: 1188-1194, 1983). To provide a more complete description of performance near the limits of human tolerance to chronic hypoxia, we measured VO2max in volunteers in an altitude chamber before, during, and after a 40-day decompression to a barometric pressure (PB) of 240 Torr (PIO2 = 43 Torr). In five of eight subjects studied at sea level and PB of 464, 347, 289, and 240 Torr, VO2max was reduced from 4.13 to 1.17 l/min (49.1-15.3 ml.kg-1.min-1) in agreement with the prior study. Although the range decreased, the rank order among the subjects was preserved. Arterial O2 saturation at maximum effort decreased (46% by ear oximetry), but minute ventilation, respiratory frequency, and tidal volume did not. The highest minute ventilation (201 l/min BTPS) was observed at PB of 464 Torr. Arterial PCO2 in three subjects at PB of 240 Torr, at rest, and with maximum effort, averaged 10.3 and 9.6 Torr, respectively. Sustained hyperventilation was crucial to exercise performance during chronic, severe hypoxemia. VO2max was lower after altitude exposure compared with initial sea level values, indicating that exposure had not improved sea level exercise capacity.

Adult↗

Operation Everest II: adaptations in human skeletal muscle.

Adaptations in skeletal muscle in response to progressive hypobaria were investigated in eight male subjects [maximal O2 uptake = 51.2 +/- 3.0 (SE) ml.kg-1.min-1] over 40 days of progressive decompression to the stimulated altitude of the summit of Mt. Everest. Samples of the vastus lateralis muscle extracted before decompression (SL-1), at 380 and 282 Torr, and on return to sea level (SL-2) indicated that maximal activities of enzymes representative of the citric acid cycle, beta-oxidation, glycogenolysis, glycolysis, glucose phosphorylation, and high-energy phosphate transfer were unchanged (P greater than 0.05) at 380 and 282 Torr over initial SL-1 values. After exposure to 282 Torr, however, representing an additional period of approximately 7 days, reductions (P less than 0.05) were noted in succinic dehydrogenase (21%), citrate synthetase (37%), and hexokinase (53%) between SL-2 and 380 Torr. No changes were found in the other enzymes. Capillarization as measured by the number of capillaries per cross-sectional area (CC/FA) was increased (P less than 0.05) in both type I (0.94 +/- 0.8 vs. 1.16 +/- 0.05) and type II (0.84 +/- 0.07 vs. 1.05 +/- 0.08) fibers between SL-1 and SL-2. This increase was mediated by a reduction in fiber area. No changes were found in fiber-type distribution (type I vs. type II). These findings do not support the hypothesis, at least in humans, that, at the level of the muscle cell, extreme hypobaric hypoxia elicits adaptations directed toward maximizing oxidative function.

Acclimatization↗

Increased exercise SaO2 independent of ventilatory acclimatization at 4,300 m.

Arterial O2 saturation (Sao2) decreases in hypoxia in the transition from rest to moderate exercise, but it is unknown whether other several weeks at high altitude SaO2 in submaximal exercise follows the same time course and pattern as that of ventilatory acclimatization in resting subjects. Ventilatory acclimatization is essentially complete after approximately 1 wk at 4,300 m, such that improvement in submaximal exercise SaO2 would then require other mechanisms. On days 2, 8, and 22 on Pikes Peak (4,300 m), 6 male subjects performed prolonged steady-state cycle exercise at 79% maximal O2 uptake (VO2 max). Resting SaO2 rose from day 1 (78.4 +/- 1.6%) to day 8 (87.5 +/- 1.4%) and then did not increase further by day 20 (86.4 +/- 0.6%). During exercise, SaO2 values (mean of 5-, 15-, and 30-min measurements) were 72.7% (day 2), 78.6% (day 8), and 82.3% (day 22), meaning that all of the increase in resting SaO2 occurred from day 1 to day 8, but exercise SaO2 increased from day 2 to day 8 (5.9%) and then increased further from day 8 to day 22 (3.7%). On day 22, the exercise SaO2 was higher than on day 8 despite an unchanged ventilation and O2 consumption. The increased exercise SaO2 was accompanied by decreased CO2 production. The mechanisms responsible for the increased exercise SaO2 require further investigation.

Acclimatization↗

Decreased exercise muscle lactate release after high altitude acclimatization.

Blood lactate concentration during exercise decreases after acclimatization to high altitude, but it is not clear whether there is decreased lactate release from the exercising muscle or if other mechanisms are involved. We measured iliac venous and femoral arterial lactate concentrations and iliac venous blood flow during cycle exercise before and after acclimatization to 4,300 m. During hypoxia, at a given O2 consumption the venous and arterial lactate concentrations, the venous and arterial concentration differences, and the net lactate release were lower after acclimatization than during acute altitude exposure. While breathing O2-enriched air after acclimatization at a given O2 consumption the venous and arterial lactate concentrations and the venous and arterial concentration differences were significantly lower, and the net lactate release tended to be lower than while breathing ambient air at sea level before acclimatization. We conclude that the lower lactate concentration in venous and arterial blood during exercise after altitude acclimatization reflected less net release of lactate by the exercising muscles, and that this likely resulted from the acclimatization process itself rather than the hypoxia per se.

Acclimatization↗

Operation Everest II: comparison of four instruments for measuring blood O2 saturation.

The bias and precision of four different methods for determining O2 saturation (SO2) were evaluated during a study of hypobaric hypoxia conducted with seven male subjects exposed progressively over a 40-day period to simulated altitudes from sea level (760 Torr) to 8,840 m (240 Torr). SO2 of arterial and mixed venous blood samples were measured with the Instrumentation Laboratory 282 CO-oximeter (CO-OX), the Radiometer ABL-300 (ABL), and the Lex-O2-Con-K (LEX). Noninvasive measurements of arterial SO2 were made with a Hewlett-Packard 47201A ear oximeter (EAR-OX). The CO-OX method was used as a secondary standard for comparison with the other methods because it has been validated against the classical Van Slyke method over a wide physiological range (Maas et al., Clin. Chim. Acta 29: 303-309, 1970). The LEX results most closely approximated but consistently underestimated those of the CO-OX: LEX = 0.93 CO-OX -0.86, standard error of the estimate (SEE) = 5.17, r = 0.98, n = 670. The ABL method appeared to combine two linear trends: for SO2 greater than 75%, ABL = 0.84 CO-OX +14.4, SEE = 1.77, r = 0.97, n = 369; less than 75%, ABL = 0.98 CO-OX +5.9, SEE = 4.44, r = 0.97, n = 486. The EAR-OX results were found to approximate those of the CO-OX at SO2 values only greater than 65%: EAR-OX = 1.07 CO-OX -6.12, SEE = 7.71, r = 0.98, n = 326.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗