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Biomedical subjects

A Cymerman

Publications and source records attributed to A Cymerman.

At least 127 records · Page 7Linked to original sources
PubMed1981

Energy expenditure during load carriage at high altitude.

To determine the applicability of a prediction equation for energy expenditure during load carriage at high altitude that was previously validated at sea level, oxygen uptake (Vo2) was determined in five young men at 4,300 m while they walked with backpack loads of 0, 15, and 30 kg at treadmill grades of 0,8, and 16% at 1.12 m.s-1 for 10 min. Mean +/- SE maximal Vo2, determined on the cycle ergometer, was 42.2 +/- 2.3 at sea level and 35.6 +/- 1.7 ml.kg-1 .min-1 at altitude. There were no significant differences in daily Vo2 at any specific exercise intensity on days 1, 5, and 9 of exposure, nor were there any differences in endurance times at the two most difficult exercise intensities. Endurance times for 15- and 30-kg loads at 16% grade were 7.3 and 4.2 min, respectively. Measured energy expenditure was compared with that predicted by the formula of Pandolf et al. (J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 43: 577-581, 1977) and found to be significantly different. The differences could be attributed to measurements at metabolic rates exceeding 730 W or 2.1 1.min-1 Vo2. These data indicate that the prediction equation can be used at altitude for exercise intensities not exceeding this upper limit. The observed deviations from predicted values at the high exercise intensities could possibly be attributed to the occurrence of appreciable oxygen deficits and the inability to achieve steady-state conditions.

Adolescent↗
PubMed1980

Ventilatory acclimatization to high altitude is prevented by CO2 breathing.

The hypoxia of high altitude stimulates ventilation. If the resultant respiratory alkalosis inhibits the initial increase in ventilation, then with prevention of alkalosis, ventilation should rise immediately to a stable plateau. 4 subjects inspired CO2 (3.77%) from ambient air in a hypobaric chamber (PB = 440-455 Torr) during 100 h at high altitude. Ventilation (for given oxygen uptakes at rest and during exercise) increased promptly and remained stable. 4 control subjects exposed to high altitude without CO2 supplementation showed the expected progressive increases in ventilation with time. The hyperoxic CO2 ventilatory response curve shifted progressively to the left with time in the control subjects, but not in those given supplemental CO2. The latter group also failed to increase the ventilatory response to isocapnic hypoxia. Thus, CO2 supplementation at high altitude prevented the so-called "ventilatory acclimatization' from occurring. Prevention of respiratory alkalosis at high altitude probably permitted maintenance of [H+] at some central nervous system locus, thus allowing an uninhibited hypoxic stimulation of ventilation.

Acclimatization↗
PubMed1980

Skeletal muscle strength during exposure to hypobaric hypoxia.

To assess the effects of acute exposure to hypobaric hypoxia and acute mountain sickness (AMS) on skeletal muscle strength, 10 healthy young men were studied before, during, and after a 48-h sojourn at a simulated altitude of 4,572 m (15,000 feet). Measurements were made of isokinetic (180 degrees, 36 degrees, and 0 degrees/s) knee extensor strength; isometric strength of upper torso, knee, and trunk extensor muscles; and strength endurance of knee extensor and elbow flexor muscles during a bout of repeated isokinetic contractions. There were no significant differences between strength measurements at sea level and after 2 and 24 h of hypoxic exposure. After 48 h of exposure, means of strength measurements were increased relative to sea-level values but the difference was statistically significant in the case of only one test; namely, isometric strength of the upper torso. Strength endurance was unchanged throughout the exposure. Symptoms of AMS were absent after 2 h, most pronounced after 24 h, and although somewhat reduced, still present to a significant extent after 48 h of hypoxia. Thus, despite the occurrence of AMS, muscle strength was unimpaired during acute hypoxic exposure.

Adult↗
PubMed1979

Evidence for increased intrathoracic fluid volume in man at high altitude.

To determine if subclinical pulmonary edema occurs commonly at high altitude, 25 soldiers participated in two consecutive 72-h field exercises, the first at low altitude (200-875 m) and the second at high altitude (3,000-4,300 m). Various aspects of ventilatory function and pulmonary mechanics were measured at 0, 36, and 72 h of each exercise. Based on physical examination and chest radiographs there was no evidence of pulmonary edema at high altitude. There was, however, an immediate and sustained decrease in vital capacity and transthoracic electrical impedance as well as a clockwise rotation of the transpulmonary pressure-volume curve. In contrast, closing capacity and residual volume did not change immediately upon arrival at high altitude but did increase later during the exposure. These observations are consistent with an abrupt increase in thoracic intravascular fluid volume upon arrival at high altitude followed by a more gradual increase in extravascular fluid volume in the peribronchial spaces of dependent lung regions.

Adolescent↗
PubMed1979

Perception of effort during constant work to self-imposed exhaustion.

The purpose of this study was to describe the pattern of change in effort sense and the value of this pattern in predicting work end-point at relatively high work intensity (80% VO2 max). The patterns of change of various physiological functions were also observed. Two modes of work (walking and running) were compared to ascertain generalizability of results. 26 healthy male volunteers served as subjects. Time to exhaustion (ET) did not differ between walking and running. As work continued during both tasks, significant increases of VE, VE/VO2, VE/VCO2 and HR and a significant decrease of ETCO2 were observed; while VO2 and R remained fairly constant. VO2 and VE during the run were about 5% greater than during the walk; there were no differences in other measures. Ratings of perceived exertion (RPE) from the Borg Scale were identical for both conditions, increasing in a near linear fashion from a value of 12.9 at 25% of total work time to 18.9 at exhaustion. Ratings obtained at 25 and 50% ET were extrapolated to time of exhaustion; the point of intercept corresponded to ratings of perceived exertion for maximal work. At exhaustion, subjects rated perception of respiratory exertion for the walk as less than that for the run; perception of leg exertion was not different for the two conditions. Plasma lactate, epinephrine and norepinephrine concentrations following exercise did not differ between the two conditions. The findings for the walking experiment were essentially replicated in a second investigation involving another 28 subjects. It is concluded that, with the exception of VO2 and some ventilatory parameters, walking and running at the same relative work intensity resulted in comparable perceptual and physiological responses. Psychophysical judgments made early during work were reasonably accurate predictors of exhaustion time.

Adult↗
PubMed1978

Mechanism of the attenuated cardiac response to beta-adrenergic stimulation in chronic hypoxia.

A blunting of the chronotropic and inotropic responses of the heart to beta-adrenergic stimulation occurs following chronic exposure to hypobaric hypoxia. To pursue the mechanism(s) involved, observations were made in six intact, conscious goats at sea level and in another six goats maintained in a decompression chamber at 445 Torr (approximately 4,300m) for 10 days (Pao2 = 43 Torr). No significant group differences in cardiac frequency and various indices of myocardial performance (peak dP/dt, time-to-peak dP/dt, Vmax) were demonstrable either before or after cholinergic blockade with intravenous atropine methyl bromide, 1 mg/kg. Following hemodynamic studies, thoracotomies were performed and full-thickness biopsies were obtained from the free wall of each of the cardiac chambers. Neither monoamine oxidase activity nor norepinephrine level of any region of the heart was altered by chronic hypoxia. However, a twofold increase (P less than 0.001) in catechol O-methyltransferase activity above sea-level values was found in both the atria and ventricles of the hypoxic animals. Thus, the attenuation in cardiac responsiveness to beta-adrenoceptor stimulation in chronic hypoxia appears unrelated to the level of vagal activity, but may be attributable to enhanced enzymatic inactivation of catecholamines.

Altitude↗
PubMed1976

Measurement of cardiac output by electrical impedance at rest and during exercise.

A comparison was made between cardiac output values determined by the dye dilution and electrical impedance methods in ten subjects at rest and during graded exercise on a bicycle ergometer. The cardiac output values determined by the two methods were linearly related and significantly (P less than 0.001) correlated (r = 0.90). Movement artifact associated with exercise at maximum or near-maximum work loads caused severe distortion of the dZ/dt wave form and prevented calculation of impedance cardiac output at these levels of work. Use of the lowest value of L (distance between mean value of L in the impedance stroke volume equation (SV = p(L2/ZO2) (dZ/dt)mt), resulted in nearly identical values for the least-squares line and equalvalue line of impedance and dye cardiac outputs. Although absolute values of cardiac output determined by the two methods were not identical in all subjects the changes in cardiac output were nearly identical during the different levels of exercise. The data support the validity of the impedance method as a noninvasive, atraumatic measure of cardiac output at rest and during graded exercise.

Adult↗
PubMed1976

Sustained venoconstriction in man supplemented with CO2 at high altitude.

Venoconstriction occurs at high altitude. This study sought to determine whether hypoxia or hypocapnia is the cause of the venoconstriction. Five male subjects were exposed to 4,000-4,400 m (PB 440-465 mmHg) with supplemental 3.77 +/- 0.02% CO2 in a hypobaric chamber for 4 days. Similar alveolar O2 tensions were obtained in four control subjects exposed to 3,500-4,100 m (PB 455-492 mmHg) without CO2. A water-filled plethysmograph was used to determine forearm flow and venous compliance. Systemic blood pressure was measured with the cuff procedure. Catecholamines were measured in 24-h urine collections. Venous compliance fell at high altitude in both groups and was less (P less than 0.01) than control values. Forearm flow and resistance were unaltered at altitude in the group with CO2 supplementation while forearm flow decreased and resistance increased in the hypocapnic group at 72 h of exposure. Urinary catecholamines increased in the group with CO2 and remained unaltered in the hypocapnic group. It is concluded that hypoxia is responsible for decreasing venous compliance, and hypocapnia for increasing resistance and decreasing flow. Group differences observed in urinary catecholamines may be explained by differences in arterial pH.

Adolescent↗
PubMed1976

Human coagulation abnormalities during acute exposure to hypobaric hypoxia.

Multiple coagulation studies were carried out in eight healthy young men at sea level (SL) and after 1, 24, and 48 h at a simulated altitude of 4,400 m. Platelet aggregation, as induced by ADP, epinephrine, and collagen, was not significantly altered by high-altitude (HA) exposure. Mean 2,3-diphosphoglycerate, a physiological inhibitor of platelet aggregation, rose (P less than 0.001) after 24 h at HA and remained elevated while no changes in circulating catecholamines were observed. Platelet count, factor 3 availability, and membrane lipid peroxide formation were likewise unaltered at HA, as were prothrombin and thrombin times and protamine paracoagulation test. However, mean partial thromboplastin time was significantly shortened (P less than 0.01) after 1 and 24 h at HA, recovering to SL control by 48 h. Fibrinogen and factor VIII levels also fell (P less than 0.01 and P less than 0.02) after 1 h at HA but returned to the preexposure values by 24 h. Fibrin degradation products were transiently detectable in three subjects at HA. Thus, although normal platelet function did not appear to be modified by short-term exposure to simulated high altitude, evidence for a coagulopathy was obtained.

Acute Disease↗
PubMed1976

Maintained stroke volume but impaired arterial oxygenation in man at high altitude with supplemental CO2.

Hypobaric hypoxia causes hypocapina and alkalosis, hemoconcentration and increased hematocrit, and a decreased cardiac stroke volume. To assess the role of the hypocapnic alkalosis in causing these other changes, five men were exposed to hypobaric hypoxia at a barometric pressure (PB) of 440 torr with an alveolar O2 tension of 55 torr for 5 days with 3.77% CO2 added to the atmosphere to prevent alkalosis. They did not lose weight, and arterial CO2 tension, pH, and cardiac stroke volume were unchanged. An unchanged hematocrit implied an unchanged plasma volume. During exercise to maximum, stroke volumes equaled sea level values but arterial hypoxemia was profound, the arterial O2 tension being 39 torr. By contrast, three men at high altitude without CO2 supplementation (PB=455 torr; alveolar PO2=56 torr) had weight loss, hypocapnia, alkalosis, and decreased stroke volume. Increased hematocrits suggested decreased plasma volumes. During exercise, arterial PO2 (48 torr) was higher than in the group receiving CO2. Maximum oxygen uptakes were decreased to a similar degree in the two groups. Catecholamine excretion doubled in the group with CO2 but in the group without CO2 catechoamine excretion was unchanged. A normal pH at high altitude apparently maintained plasma volume, which, with the increased catecholamine excretion, may have prevented a decrease in stroke volume. However, the subjects with CO2 added did not have enhanced oxygen transport, because their arterial oxygenation was impaired.

Adult↗
PubMed1976

Increased 2,3-diphosphoglycerate during normocapnic hypobaric hypoxia.

The effect of 96 h of exposure to hypobaric hypoxia with and without 3.8% CO2 supplementation was studied in two groups of subjects. Five subjects (CO2) were exposed to 440-465 mm Hg barometric pressure (4000-4400 m), and 4 subjects (no-CO2) were exposed to 455-492 mm Hg (3500-1400 m) in order to produce similar levels of resting end-tidal PO2. After 24 h, 2,3-DPG levels of both groups significantly increased and remained elevated. The CO2 group had higher levels than the non-CO2 group after 48 and 72 h. Concurrent measurements of P50 showed similar changes over the same time course. Mean corpuscular hemoglobin concentrations remained normal for 48 h and then decreased in both groups, the CO2 group showing the larger decrease. We conclude that altitude exposure may produce an increase in 2,3-DPG without the presence of respiratory alkalosis previously thought necessary.

Adolescent↗
PubMed1975

Cardiovascular responsiveness to beta-adrenergic stimulation and blockade in chronic hypoxia.

Previous studies have shown that exposure to high altitude results in an initial increase in heart rate, followed by a return to sea-level values within several days; circulating catecholamines rise progressively during this time. Nine conscious dogs were studied in normoxia (N) and after 10 days' exposure to 445 torr (CH). The mean (plus or minus SE) hematocrit was higher in CH (50 plus or minus 2 vs. 42 plus or minus 1%) while Pa-o2 (53 plus or minus 1 vs. 97 plus or minus 2 torr) and PaCO2 (27 plus or minus 1 vs. 35 plus or minus 1 torr) were lower than in N. A 3.5-fold increase in plasma norepinephrine above the N value was found in CH. Arterial pH, heart rate (HR), and mean femoral arterial pressure (MAP) did not differ significantly in N and CH. Isoproterenol (ISO), 0.5 mug/kg iv, produced an average increase in HR of 92 plus or minus 9 beats/min in N, but only 66 plus or minus 8 beats/min in CH (P smaller than .02). Reduction in MAP after ISO were similar. Pretreatment with propranolol, 0.15 mg/kg iv, reduced HR equally in N and CH without affecting MAP, but diminished the HR response to ISO significantly more in CH than in N. The attenuated chronotropic response to beta-adrenoceptor stimulation following chronic hypobaric hypoxia suggests a relative cardiac refractoriness secondary to an increased level of sympathetic activity.

Adrenergic beta-Agonists↗
PubMed1975

Acute mountain sickness: increased severity in eucapnic hypoxia.

This study examined the hypothesis that prevention of hypocapnia and alkalosis would ameliorate the symptoms of acute mountain sickness (AMS). Five subjects were exposed to simulated high altitude for 4 d with 3.8% CO2 added to the chamber to maintain normocapnia. Four other subjects were exposed for 4 d to hypobaric hypoxia without CO2 supplementation, and became hypocapnic. Barometric pressure was lower in the group with added CO2 so that alveolar oxygen tensions (55-60 mm Hg) would not be different. The severity of symptoms was clearly greater in normocapnic than in hypocapnic subjects. Thus, prevention of hypocapnia did not alleviate AMS symptoms. The efficacy of CO2 addition in reducing symptoms, as reported by earlier workers, was probably the result of induced hyperventilation and partial relief of hypoxia. Indeed, in the present study with two comparably hypoxic groups, CO2 addition augmented the sysptoms, possibly by causing increased cerebral vasodiladation and spinal fluid pressure.

Acute Disease↗
PubMed1975

Adrenocortical activity and urinary cyclic AMP levels: effects of hypobaric hypoxia.

Six highly motivated and trained military test subjects were exposed to a simulated altitude of 4267 m (477 torr) for 48 hours, prededed and followed by sea level runs lasting 32 hours. During each scenario tests subjects were required to perform their respective military tasks on a continual basis with sporadic rest not exceeding several hours. Extremely high levels of plasma cortisol prior to the start of each session and persistently elevated concentrations of urinary 17-OH corticosteroids at sea level were consistently observed. (This observation probably explains the relatively minor changes in adrenocortical output noted during acute exposure to hypobaric hypoxia. Analogous results were obtained for urinary cyclic AMP, i.e. elevated baseline levels and minimal response to high altitude. The results indicate an attenuated response as well as an association between urinary measures of adrenocortical activity and cyclic AMP excretion.

17-Hydroxycorticosteroids↗