Search PubMed⌕ Search

Biomedical subjects

C S Houston

Publications and source records attributed to C S Houston.

At least 73 records · Page 4Linked to original sources
PubMed1989

Cognitive performance deficits in a simulated climb of Mount Everest: Operation Everest II.

Cognitive function at simulated altitude was investigated in a repeated-measures, within-subject study of performance by seven volunteers in a hypobaric chamber, in which atmospheric pressure was systematically lowered over a period of 40 d to finally reach a pressure equivalent to 8,845 m, the approximate height of Mount Everest. The portable cognitive test battery used, Automated Performance Test System (APTS), was specifically designed for field research under adverse environmental conditions as evidenced by compact computer design; automated test administrations, data storage, and retrieval; psychometric properties of stability and reliability; and factorial richness. Significant impairments of cognitive function were seen for three of the five tests in the battery; on two tests, grammatical reasoning and pattern comparison, every subject showed a substantial decrement. The results are discussed in terms of the impact of altitude on specific aspects of cognitive function and the importance of having sensitive and reliable instruments to monitor such effects.

Adult↗
PubMed1988

Operation Everest II: oxygen transport during exercise at extreme simulated altitude.

A decrease in maximal O2 uptake has been demonstrated with increasing altitude. However, direct measurements of individual links in the O2 transport chain at extreme altitude have not been obtained previously. In this study we examined eight healthy males, aged 21-31 yr, at rest and during steady-state exercise at sea level and the following inspired O2 pressures (PIO2): 80, 63, 49, and 43 Torr, during a 40-day simulated ascent of Mt. Everest. The subjects exercised on a cycle ergometer, and heart rate was recorded by an electrocardiograph; ventilation, O2 uptake, and CO2 output were measured by open circuit. Arterial and mixed venous blood samples were collected from indwelling radial or brachial and pulmonary arterial catheters for analysis of blood gases, O2 saturation and content, and lactate. As PIO2 decreased, maximal O2 uptake decreased from 3.98 +/- 0.20 l/min at sea level to 1.17 +/- 0.08 l/min at PIO2 43 Torr. This was associated with profound hypoxemia and hypocapnia; at 60 W of exercise at PIO2 43 Torr, arterial PO2 = 28 +/- 1 Torr and PCO2 = 11 +/- 1 Torr, with a marked reduction in mixed venous PO2 [14.8 +/- 1 (SE) Torr]. Considering the major factors responsible for transfer of O2 from the atmosphere to the tissues, the most important adaptations occurred in ventilation where a fourfold increase in alveolar ventilation was observed. Diffusion from alveolus to end-capillary blood was unchanged with altitude. The mass circulatory transport of O2 to the tissue capillaries was also unaffected by altitude except at PIO2 43 Torr where cardiac output was increased for a given O2 uptake. Diffusion from the capillary to the tissue mitochondria, reflected by mixed venous PO2, was also increased with altitude. With increasing altitude, blood lactate was progressively reduced at maximal exercise, whereas at any absolute and relative submaximal work load, blood lactate was higher. These findings suggest that although glycogenolysis may be accentuated at low work loads, it may not be maximally activated at exhaustion.

2,3-Diphosphoglycerate↗
PubMed1988

Operation Everest. II: Nutrition and body composition.

Progressive body weight loss occurs during high mountain expeditions, but whether it is due to hypoxia, inadequate diet, malabsorption, or the multiple stresses of the harsh environment is unknown. To determine whether hypoxia due to decompression causes weight loss, six men, provided with a palatable ad libitum diet, were studied during progressive decompression to 240 Torr over 40 days in a hypobaric chamber where hypoxia was the major environmental variable. Caloric intake decreased 43.0% from 3,136 to 1,789 kcal/day (P less than 0.001). The percent carbohydrate in the diet decreased from 62.1 to 53.2% (P less than 0.001). Over the 40 days of the study the subjects lost 7.4 +/- 2.2 (SD) kg and 1.6% (2.5 kg) of the total body weight as fat. Computerized tomographic scans indicated that most of the weight loss was derived from fat-free weight. The data indicated that prolonged exposure to the increasing hypoxia was associated with a reduction in carbohydrate preference and body weight despite access to ample varieties and quantities of food. This study suggested that hypoxia can be sufficient cause for the weight loss and decreased food consumption reported by mountain expeditions at high altitude.

Adult↗
PubMed1988

Operation Everest II: lack of an effect of extreme altitude on visual contrast sensitivity.

Contrast sensitivity thresholds were studied over 40 d during gradual ascent to a simulated terrestrial altitude of 25,000 ft in a decompression chamber. Only ambient pressure, and thus inspired oxygen pressure, was varied, thereby eliminating many of the confounding effects of cold, dehydration, malnutrition and exhaustion, inevitably encountered on very high mountains. Contrast sensitivity thresholds measured by the Ginsburg Vistech test showed no overall impairment as altitude increased. These results are different from those of other previously reported vision studies involving shorter exposures, lower altitudes, and lower test luminances. However, our results can be explained on the basis of the higher stimulus luminances used in our contrast sensitivity testing. Compared to the luminance levels involved in previously reported testing, our higher luminance stimuli would be less likely to be affected by hypoxia.

Adult↗
PubMed1987

Enhanced left ventricular systolic performance at high altitude during Operation Everest II.

Serial rest and upright cycle exercise 2-dimensional echocardiographic studies were performed in 7 healthy young men during acclimatization to a simulated altitude of 29,000 feet (barometric pressure [PB] 240 torr) in a chamber for 40 days. In all subjects left ventricular (LV) end-diastolic, end-systolic and stroke volumes progressively decreased, with mean reductions of 21%, 40% and 14%, respectively, on ascent to 25,000 feet (PB 282 torr) at rest, and reductions of 23%, 43% and 14% during 60-W exercise. At PB 282 torr, mean arterial blood O2 partial pressures were 37 torr (rest) and 32 torr (exercise), with corresponding O2 saturations of 68% and 59%. All 3 indexes of LV systolic function examined--ejection fraction, ratio of peak systolic pressure to end-systolic volume and mean normalized systolic ejection rate at rest--were sustained in all subjects at high altitude despite reduced preload, pulmonary hypertension and severe hypoxemia. Increases in ejection fraction of 6% at rest and 10% during exercise developed at PB 282 torr and a higher mean normalized systolic ejection rate in association with elevated circulating catecholamines reflecting enhanced sympathetic activity. LV systolic function is not a limiting factor in compromising the exercise capacity of normal humans on ascent to high altitude, even to the peak of Mt. Everest.

Acclimatization↗
PubMed1987

Osteoporosis, calcium and physical activity.

Sales of calcium supplements have increased dramatically since 1983, as middle-aged women seek to prevent or treat bone loss due to osteoporosis. However, epidemiologic studies have failed to support the hypothesis that larger amounts of calcium are associated with increased bone density or a decreased incidence of fractures. The authors examine the evidence from controlled trials on the effects of calcium supplementation and physical activity on bone loss and find that weight-bearing activity, if undertaken early in life and on a regular basis, can increase the peak bone mass of early adulthood, delay the onset of bone loss and reduce the rate of loss. All of these factors will delay the onset of fractures. Carefully planned and supervised physical activity programs can also provide a safe, effective therapy for people who have osteoporosis.

Animals↗
PubMed1987

Murk Jansen's metaphyseal chondrodysplasia with long-term followup.

The fourteenth reported patient with Murk Jansen's metaphyseal chondrodysplasia is presented, with a remarkable followup from birth to the age of 15 years. Numerous invasive procedures were performed in pursuit of erroneous provisional diagnoses. Five of these patients presented in infancy with radiographic metaphyseal changes similar to rickets, but with preservation of the provisional zone of calcification. Following infancy, these patients reveal the more typical short-limbed dwarfism, with fusiform joints and bowed extremities.

Adolescent↗
PubMed1987

Oxygen transport during exercise at extreme altitude: Operation Everest II.

Eight male volunteers had rest and exercise measurement to determine the mechanisms of oxygen transport during a 40-day chamber decompression simulating high-altitude exposure equivalent to the summit of Mt Everest. Five subjects completing the study decreased their maximum oxygen uptake by 72%. During maximal or near-maximal exercise, arterial PCO2 fell as low as 8 mm Hg, defending the alveolar PO2 and confirming marked hyperventilation. Alveolar-arterial diffusion did not improve and V/Q worsened. Cardiac function was unimpaired. Circulatory oxygen transport resembled that at sea level. The decrease in mixed venous PO2 was not enough to preserve fractional oxygen utilization "on the summit." The PO2 gradients from atmosphere to alveolus, alveolus to arterial blood, arterial to venous blood, and from venous (capillary) blood to mitochondria all decreased. However, hyperventilation appeared to be the primary adaptation that defended the maximum oxygen uptake.

Adult↗
PubMed1987

Operation Everest II: elevated high-altitude pulmonary resistance unresponsive to oxygen.

High altitude increases pulmonary arterial pressure (PAP), but no measurements have been made in humans above 4,500 m. Eight male athletic volunteers were decompressed in a hypobaric chamber for 40 days to a barometric pressure (PB) of 240 Torr, equivalent to the summit of Mt. Everest. Serial hemodynamic measurements were made at PB 760 (sea level), 347 (6,100 m), and 282/240 Torr (7,620/8,840 m). Resting PAP and pulmonary vascular resistance (PVR) increased from sea level to maximal values at PB 282 Torr from 15 +/- 0.9 to 34 +/- 3.0 mmHg and from 1.2 +/- 0.1 to 4.3 +/- 0.3 mmHg.l-1 X min, respectively. During near maximal exercise PAP increased from 33 +/- 1 mmHg at sea level to 54 +/- 2 mmHg at PB 282 Torr. Right atrial and wedge pressures were not increased with altitude. Acute 100% O2 breathing lowered cardiac output and PAP but not PVR. Systemic arterial pressure and resistance did not rise with altitude but did increase with O2 breathing, indicating systemic control differed from the lung circulation. We concluded that severe chronic hypoxia caused elevated pulmonary resistance not accompanied by right heart failure nor immediately reversed by O2 breathing.

Adult↗
PubMed1987

Operation Everest II: preservation of cardiac function at extreme altitude.

Hypoxia at high altitude could depress cardiac function and decrease exercise capacity. If so, impaired cardiac function should occur with the extreme, chronic hypoxemia of the 40-day simulated climb of Mt. Everest (8,840 m, barometric pressure of 240 Torr, inspiratory O2 pressure of 43 Torr). In the five of eight subjects having resting and exercise measurements at the barometric pressures of 760 Torr (sea level), 347 Torr (6,100 m), 282 Torr (7,620 m), and 240 Torr, heart rate for a given O2 uptake was higher with more severe hypoxia. Slight (6 beats/min) slowing of the heart rate occurred only during exercise at the lowest barometric pressure when arterial blood O2 saturations were less than 50%. O2 breathing reversed hypoxemia but never increased heart rate, suggesting that hypoxic depression of rate, if present, was slight. For a given O2 uptake, cardiac output was maintained. The decrease in stroke volume appeared to reflect decreased ventricular filling (i.e., decreased right atrial and wedge pressures). O2 breathing did not increase stroke volume for a given filling pressure. We concluded that extreme, chronic hypoxemia caused little or no impairment of cardiac rate and pump functions.

Adult↗
PubMed1987

Operation Everest II: man at extreme altitude.

Rapid ascent to high altitude may cause serious problems for climbers, skiers, and aviators. In contrast, gradual ascent enables humans to function where the unacclimatized cannot. To examine changes in the O2 transport system that produce acclimatization, eight men were taken in a decompression chamber (without other stresses experienced on high mountains) to a simulated altitude of 8,840 m (29,028 ft, ambient PO2 = 43 Torr) in 40 days. Maximal O2 uptake fell to 1.2 l/min, and arterial PO2 and PCO2 were 30 and 11 Torr, respectively, with arterial pH of 7.56. Many sophisticated studies were done: Swan-Ganz catheterization and inert gas diffusion studies at three altitudes showed that normal cardiac function persisted, pulmonary vascular resistance increased and at extreme altitude was not lowered by O2, and pulmonary ventilation-perfusion mismatch increased, though variably. This appears to be an important factor limiting performance at extreme altitude. This paper presents the background, general approach, and a summary of major observations reported in detail in other papers.

Acclimatization↗
PubMed1987

Operation Everest II: Altitude decompression sickness during repeated altitude exposure.

The incidence of altitude decompression sickness (ADS) was studied in 23 altitude scientists during repeated altitude exposure to 15,000-29,000 ft (4572-8839 m) in a decompression chamber. Prior to each altitude exposure, a 30-60-mm pre-breathing period with 100% oxygen took place. Ascent was made to an altitude at a rate of 2000 ft X min-1. The altitudes studied ranged from 15,000-29,000 ft (4572-8839 m). Symptoms reported appear consistent with previous reports. Incidence of ADS at 26,000-29,000 ft (7925-8839 m) was 29.7%, during 274 chamber flights and 1264.6 h of altitude time. Incidence appeared related to frequency of exposure, severity of altitude, and physical activity. Incidence was not related to age, duration of exposure, or body index (weight/height 2). This high incidence of ADS reported in this study is similar to that reported by NASA.

Adult↗