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This paper will review the function of the lung at high altitude in humans. As the first interface between the environment and the body, the lung serves a vital role in the transfer of oxygen from the air to the blood. I will describe the limits of response and adaptation of the lung to this hypoxic stress, both at rest and during exercise when oxygen and carbon dioxide flux from the tissues is greater. First, ventilation will be described in terms of the hypoxic stimulus that causes an increase in breathing (ventilatory drives) and the metabolic cost from the respiratory muscles incurred by this increase. Individuals at high altitude also have a substantial sense of dyspnea which, in and of itself, may limit exercise tolerance. The final function of the lung is to exchange oxygen and carbon dioxide, which it does at the alveolar-capillary interface. Here, important limitations are encountered because the driving pressure for oxygen from the air to the blood is lower and the more rapid transit time of blood across the pulmonary capillary allows less time for equilibration of oxygen with the blood. Both these phenomena lead to a limitation of diffusion of oxygen across the alveolar-capillary membrane and, thus, more accentuated hypoxemia. In spite of these restrictions, humans still do remarkably well in times of great stress from the hypoxic environment.

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This study examined the effects of exhaustive exercise on cognitive functioning among 21 monozygotic twin pairs discordant for chronic fatigue syndrome (CFS). The co-twin control design adjusts for genetic and family environmental factors not generally accounted for in more traditional research designs of neuropsychological function. Participants pedaled a cycle ergometer to exhaustion; maximum oxygen output capacity (VO2max) as well as perceived exertion were recorded. Neuropsychological tests of brief attention and concentration, speed of visual motor information processing, verbal learning and recognition memory, and word and category fluency were administered with alternate forms to participants pre- and postexercise. The preexercise neuropsychological test performance of CFS twins tended to be slightly below that of the healthy twin controls on all measures. However, twins with CFS did not demonstrate differential decrements in neuropsychological functioning after exercise relative to their healthy co-twins. Because exercise does not appear to diminish cognitive function, rehabilitative treatment approaches incorporating exercise are not contraindicated in CFS.

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STUDY OBJECTIVE: To determine the effect of an aerobic conditioning program on fitness, respiratory physiology, and resting lung function in patients with mild asthma. DESIGN: Prospective cohort study. SETTING: Outpatient rehabilitation facility. METHODS: Five patients with mild intermittent asthma and five normal control subjects completed a 10-week aerobic conditioning program. Pulmonary function studies and noninvasive cardiopulmonary exercise tests were performed before and after the conditioning program. RESULTS: After aerobic conditioning, there were significant gains in maximum oxygen consumption (VO(2)max; 22.73 mL/kg/min vs 25.29 mL/kg/min, p = 0.01, asthma; 22.94 mL/kg/min vs 27.85 mL/kg/min, p = 0.03, control) and anaerobic threshold (0.99 L/min vs 1.09 L/min, p = 0.03, asthma; 0.89 L/min vs 1.13 L/min, p = 0.01, control) in both groups. Although FEV(1) was unchanged, the maximum voluntary ventilation (MVV) improved in the asthma group (96.0 L/min vs 108.2 L/min, p = 0.08, asthma; 134.0 L/min vs 131.2 L/min, p = 0.35, control). During exercise, minute ventilation (VE) for each level of work was decreased in the asthma group after conditioning, while little change occurred in the control group (68. 48 L/min vs 51.70 L/min at initial VO(2)max, p = 0. 02, asthma; 65.82 L/min vs 63.12 L/min at initial VO(2)max, p = 0.60, control). A significant decrease in the ventilatory equivalent (VE/oxygen consumption, 40.8 vs 30.4 at VO(2)max, p = 0.02, asthma; 37.2 vs 35.8 4 at VO(2)max, p = 0.02, control) and the dyspnea index (VE/MVV) at submaximal (0.44 vs 0.38, p = 0.05, asthma; 0.32 vs 0.38, p < 0.01, control) and maximal exercise (0.72 vs 0.63, p = 0.03, asthma; 0.49 vs 0.62, p = 0.02, control) occurred in the asthma group. CONCLUSIONS: Exercise rehabilitation improves aerobic fitness in both asthmatic and nonasthmatic participants of a 10-week aerobic fitness program. Additional benefits of improved ventilatory capacity and decreased hyperpnea of exercise occurred in patients with mild asthma.

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This paper asks how the decline in maximal O(2) uptake rate (VO(2),max) with age is related to the properties of a key muscle group involved in physical activity - the quadriceps muscles. Maximal oxygen consumption on a cycle ergometer was examined in nine adult (mean age 38.8 years) and 39 elderly subjects (mean age 68.8 years) and compared with the oxidative capacity and volume of the quadriceps. VO(2),max declined with age between 25 and 80 years and the increment in oxygen consumption from unloaded cycling to VO(2),max (delta VO(2)) in the elderly was 45 % of the adult value. The cross-sectional areas of the primary muscles involved in cycling - the hamstrings, gluteus maximus and quadriceps - were all lower in the elderly group. The quadriceps volume was reduced in the elderly to 67 % of the adult value. Oxidative capacity per quadriceps volume was reduced to 53 % of the adult value. The product of oxidative capacity and muscle volume - the quadriceps oxidative capacity - was 36 % of the adult value in the elderly. Quadriceps oxidative capacity was linearly correlated with delta VO(2) among the subjects with the slope indicating that the quadriceps represented 36 % of the VO(2) increase during cycling. The decline in quadriceps oxidative capacity with age resulted from reductions in both muscle volume and oxidative capacity per volume in the elderly and appears to be an important determinant of the age-related reduction in delta VO(2) and VO(2),max found in this study.

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The sport of high-altitude climbing encompasses a number of factors of stress that supersede the usual endurance activities at lower altitudes. The effect of hypoxia on both physical and mental performance can be profound and, therefore, compound the risk. Much is yet to be known, particularly about the brain. Hopefully, a better understanding of the effect of hypoxia on neurotransmitters, the effect of hypoxemia on blood flow to all areas of the brain, and the potential subsequent anatomic changes that may take place are all yet to be discovered. Perhaps the more we know about it, the more appropriate it will be to call climbing a "no-brainer."

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The lungs are a delicate interface between the atmosphere and our bodies across which oxygen diffuses from the air we breathe to the blood which carries oxygen to the cells and mitochondria. In healthy lungs at sea level where there is a surfeit of oxygen, this process occurs easily, whereas, in lungs with disease it becomes a task which may not be fully successful and hypoxemia may ensue or worsen. At high altitude where the barometric pressure (Pb) and thus the supply of oxygen is lower, the job of getting oxygen to the blood, even in the healthy lung is more difficult, and in the diseased lung it may be impossible. This presentation will review the lungs' responses to high altitude, with emphasis on the abnormal. Both acute and chronic responses of patients with pre-existing lung disease will be reviewed. Pulmonary diseases encountered at high altitude in previously healthy people, such as high altitude pulmonary edema and chronic mountain sickness will be touched on only as they pertain to other patients. Pre-existing lung disease (with and without hypoxemia at sea level) such as obstructive lung diseases (asthma, COPD, emphysema), and restrictive lung diseases (sarcoid, asbestosis, interstitial pulmonary fibrosis) will be discussed in terms of gas exchange, lung mechanics, and treatment at high altitude. Disorders of ventilatory control; e.g., obesity-hypoventilation syndrome and sleep apnea, may present formidable problems, and guidelines for their treatment will be discussed. Infectious lung diseases; e.g., pneumonia, cystic fibrosis, and pulmonary vascular disorders such as chronic mountain sickness, primary pulmonary hypertension, and congenital absence of the pulmonary artery are important disorders that require special attention because of the accentuated hypoxic pulmonary vascular response encountered at high altitude. The purpose therefore, is to provide the medical practitioner with the insight into prevention, recognition, and treatment of pulmonary problems encountered specifically at high altitude, as well as guidance on how best to advise patients with lung disease who want to fly in airplanes and/or ascend to high altitude for work or pleasure.

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BACKGROUND: Acute mountain sickness (AMS) is a usually self-limiting syndrome encompassing headache, nausea and dizziness. AMS is seen in those that go from low to high altitudes too quickly, without allowing sufficient time to acclimatize. At present, susceptibility to AMS cannot be predicted. One feature of AMS noted in some studies is impaired gas exchange. If impaired gas exchange presages AMS then those individuals with exaggerated hypoxemia at high altitude may be more likely to develop AMS. If true, then monitoring of arterial oxygen saturation (SaO2%) may differentiate AMS-resistant individuals from those with impending AMS. METHODS: To test this hypothesis, we measured SaO2% and AMS symptom scores in 102 healthy asymptomatic climbers at 4200 m on Denali (Mt. McKinley) prior to their further ascent toward the summit at 6194 m, and on their return from higher altitudes to 4200 m. RESULTS: The results show that exaggerated hypoxemia in asymptomatic climbers prior to further ascent correlates with subsequent AMS (r = -0.48, p < 0.001). Criteria are presented for identification of 80-100% of those climbers who later become ill with AMS. CONCLUSION: We conclude that resting arterial hypoxemia is related to later development of clinical AMS, and can exclude the occurrence and caution those at risk for development of subsequent AMS. Likely mechanisms are hypoventilation relative to normally acclimatizing individuals and/or abnormalities of gas exchange. Thus, non-invasive oximetry provides a simple, specific indicator of inadequate acclimatization to high altitudes and impending AMS.

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BACKGROUND: Recently, TH2 lymphocyte activation has been shown to play a key role in initiating and propagating the inflammatory response in asthmatic airways. This is manifest through increased numbers of "activated" CD25-(IL-2R)-bearing T-helper cells and can be seen through the IL-5 driven recruitment of eosinophils and IL-4-mediated B-cell expression of CD23 (low affinity IgE receptor) and ultimately IgE production. OBJECTIVE: To gain a better understanding of the role of immune cells in asthma by describing the peripheral blood immune cell phenotypes in mild atopic asthma. METHODS: We enrolled 13 patients with mild atopic asthma and a group of seven nonatopic, nonasthmatic controls. Objective measures of lung function were obtained. The peripheral blood was analyzed by flow cytometry for specific cellular markers at rest and during the development of exercise induced bronchospasm. RESULTS: At rest the number of CD23-bearing B cells (169/mL versus 117/mL; P = .05) and the number of CD25-bearing T cells (355/mL versus 237/mL; P = .03) were increased in the asthma group. There was a linear relationship between these two lymphocyte subsets and the maximum voluntary ventilation at rest (r = 0.56, P = .01 and r = 0.57, P = .01). With the development of exercise-induced bronchospasm there was a significantly greater increase in CD23-positive B cells (96.7/mL versus 59.7/mL; P = .05) and CD25-positive T cells (111.8/mL versus 45.1; P = .01) in the asthma group. CONCLUSIONS: These data indicate that TH2 lymphocyte activation is manifested by increased numbers of CD23-bearing B cells and CD25-bearing T cells in the peripheral blood of patients with stable mild atopic asthma. Further, these immune cell subsets correlate with markers of resting lung function and increase in the peripheral blood early after the development of exercise-induced bronchospasm.

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The extreme thinness of the pulmonary blood-gas barrier results in high mechanical stresses in the capillary wall when the capillary pressure rises during exercise. We have previously shown that, in elite cyclists, 6-8 min of maximal exercise increase blood-gas barrier permeability and result in higher concentrations of red blood cells, total protein, and leukotriene B4 in bronchoalveolar lavage (BAL) fluid compared with results in sedentary controls. To test the hypothesis that stress failure of the barrier only occurs at the highest level of exercise, we performed BAL in six healthy athletes after 1 h of exercise at 77% of maximal O2 consumption. Controls were eight normal nonathletes who did not exercise before BAL. In contrast with our previous study, we did not find higher concentrations of red blood cells, total protein, and leukotriene B4 in the exercising athletes compared with control subjects. However, higher concentrations of surfactant apoprotein A and a higher surfactant apoprotein A-to-phospholipid ratio were observed in the athletes performing prolonged exercise, compared with both the controls and the athletes from our previous study. These results suggest that, in elite athletes, the integrity of the blood-gas barrier is altered only at extreme levels of exercise.

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OBJECTIVES: To characterize spirometry and to document the incidence of exercise-induced bronchospasm (EIB) during competition in elite track and field athletes. DESIGN: Spirometry was performed in 120 men and 69 women athletes before competition and peak expiratory flows in 50 men and 23 women athletes before and after competition. SETTING: The 1991 (Randalls Island, NY, U.S.A.) and the 1993 (Eugene, OR, U.S.A.) National Track and Field Championships (World Championship team-qualifying meet). PARTICIPANTS: American track and field athletes who met World Championship qualifying standards. MEASUREMENTS: Spirometry (Cybermedic, Inc., Boulder, CO, U.S.A.) and peak expiratory flows (Personal Best, Healthscan Products, Cedar Grove, NJ, U.S.A.)--the best of three reproducible efforts. RESULTS: Male sprinters had lower vital capacities than other track athletes, whereas both male and female field (throwing) athletes had larger vital capacities than both runners and other field athletes. Decreases of 10% peak expiratory flows were found in 10% of men and 26% of women track athletes within 15 min after competition. The incidence was higher in longer-distance events. Most participants did not have a history of asthma. CONCLUSIONS: A higher-than-expected prevalence of EIB was found in high-level track athletes. The results suggest that spirometry and/or peak flows should be measured in track athletes because small decreases in airflow may impair training or performance, a condition that is easily treated.

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We investigated whether a diet of increased carbohydrate content reduces the symptoms of acute mountain sickness (AMS) and whether concentrations of circulating cytokines rise and correlate with hypoxia and AMS. There were 19 healthy volunteers who ingested in randomized order both a high carbohydrate (68% CHO) or normal carbohydrate (45% CHO) diet for 4 d. On the 4th d, subjects were exposed to 8 h of 10% normobaric oxygen. Each subject completed the Lake Louise Consensus Questionnaire (LLCQ: a questionnaire developed to quantify the common symptoms and consequences of AMS) at the beginning and end of each hypoxic session, at which times venous blood was obtained for the following cytokines: interleukins 1 beta, 6 and 8 (IL-1 beta, IL-6, IL-8) and tumor necrosis factor alpha (TNF-alpha). AMS symptoms did not differ significantly between the diets (LLCQ scores: 68% CHO = 10.1 +/- 3.8 vs. 45% CHO = 10.3 +/- 4.1). Cytokine concentrations did not change with hypoxia on either diet, nor did individual changes correlate with AMS symptoms. We conclude that a high carbohydrate diet for 4 d does not reduce the symptoms of AMS; and plasma cytokine concentrations do not change with hypoxia and the development of AMS and, thus, are not likely mediators of this syndrome.

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The blood-gas barrier must be very thin to allow gas exchange and it is therefore subjected to high mechanical stresses when the capillary pressure rises. In some animals, such as the thoroughbred race-horse during intense exercise, the stresses are so large that the capillaries fail and bleeding occurs. We tested the hypothesis that, in elite human athletes, the high capillary pressure that occurs during severe exercise alters the structure and function of the blood-gas barrier. We performed bronchoalveolar lavage (BAL) in six healthy athletes, who had a history suggestive of lung bleeding, 1 h after a 7-min cycling race simulation and four normal sedentary control subjects who did not exercise before BAL. The athletes had higher (p < 0.05) concentrations of red blood cells (0.51 x 10(5) versus 0.01 x 10(5).ml-1), total protein (128.0 versus 94.1 micrograms/ml), albumin (65.6 versus 53.0 micrograms/ml), and leukotriene B4 (LTB4) (243 versus 0 pg/ml) in BAL fluid than control subjects. The proportion of neutrophils was similar in athletes and control subjects but the proportion of lymphocytes in BAL fluid was reduced (p < 0.05). There were no differences in levels of surfactant apoprotein A, tumor necrosis factor bioactivity, lipopolysaccharide, or interleukin-8 (IL-8) between groups. These results show that brief intense exercise in athletes with a history suggestive of lung bleeding alters blood-gas barrier function resulting in higher concentrations of red cells and protein in BAL fluid. The lack of activation of proinflammatory pathways (except LTB4) in the airspaces supports the hypothesis that the mechanism for altered blood-gas barrier function is mechanical stress.

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Ventilatory acclimatization to high altitude has been discussed in a chronologic fashion, i.e. the acute, prolonged, and chronic or lifelong phases, and the integration of exercise ventilation as it relates to each of these phases has been outlined. Unanswered questions in each of these areas have been posed as fertile grounds for future investigation.

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STUDY OBJECTIVES: Inflammation may contribute to the pathogenesis of high-altitude pulmonary edema (HAPE). This study was designed to determine whether a marker of inflammation, urinary leukotriene E4 (LTE4), is elevated in patients with HAPE. DESIGN: We conducted a case-control study to collect clinical data and urine samples from HAPE patients and healthy control subjects at moderate altitude (> or = 2727 m), and follow-up urine samples from HAPE patients following their return to low altitude (< or = 1,600 m). SETTING: Five medical clinics in Summit County, Colorado. PATIENTS: Questionnaire data were evaluated in 71 HAPE patients and 36 control subjects. Urinary LTE4 levels were determined from a random subset of 38 HAPE patients and 10 control subjects presenting at moderate altitude, and on 5 HAPE patients who had returned to low altitude. MEASUREMENTS AND RESULTS: Using an enzyme immunoassay technique, urinary LTE4 levels were found to be significantly higher in HAPE patients (123 [16 to 468] pg/mg creatinine, geometric mean [range]) than in control subjects (69 [38 to 135]), p = 0.02. Following return to low altitude, urinary LTE4 levels fell significantly from 122 (41.8 to 309) to 53.6 (27.6 to 104) pg/mg creatinine (p = 0.05). Urinary LTE4 levels were not related to age, sex, time at altitude, physical condition or habitual exercise, recent use of alcohol or nonsteroidal anti-inflammatory drugs (NSAIDs), or oxygen saturation. Clinical factors associated with HAPE included male sex, regular exercise, and recent use of NSAIDs. CONCLUSIONS: We conclude that urinary LTE4 levels are elevated in patients with HAPE, supporting the view that HAPE involves inflammatory mechanisms.

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Acute hypoxia causes increased sodium and water excretion. Animal studies suggest that this renal response is largely driven by direct peripheral arterial chemoreceptor stimulation, independent of accompanying changes in ventilation and acid-base status. Whether the diuresis and natriuresis observed in humans made acutely hypoxic are caused by peripheral chemoreceptor stimulation is not known, but, if so, we hypothesized that people with a high ventilatory response to hypoxia (high peripheral chemosensitivity) should have greater diuresis and natriuresis than those with a low ventilatory response to hypoxia. The isocapnic hypoxic ventilatory response (HVR) of 16 subjects on a fixed sodium intake was measured, as were their urinary volume and sodium and bicarbonate losses during 6 h of breathing air (in a normobaric environmental chamber) and, on the subsequent day, 12% O2. The isocapnic HVR correlated positively with hypoxic diuresis (r = 0.87) and natriuresis (r = 0.76). In contrast, the isocapnic HVR did not correlate with bicarbonate excretion, despite the expected respiratory alkalosis of acute hypoxia. The magnitude of diuresis and natriuresis with hypoxia did not correlate with changes in circulating aldosterone, renin, atrial natriuretic peptide, vasopressin, or a digoxin-like immunoreactive substance. These findings are compatible with a role of the peripheral arterial chemoreceptors in mediating the renal response to hypoxia in humans. The efferent pathway remains unknown.

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We hypothesized that oral ingestion of sodium bicarbonate (NaHCO3) would improve performance in seven competitive female cyclists VO2 = 51.6 +/- 4.8 ml.kg-1.min-1 at moderate altitude (2800 m). Two hours before exercise subjects ingested either NaHCO3 (300 mg.kg-1) or NaCl (207 mg.kg-1), both containing equimolar amounts of sodium. The exercise protocol consisted of repeated 1-min intervals at 95% VO2max (277 +/- 38 W) followed by 1 min of recovery at 60 W until exhaustion. Continuous cardiopulmonary physiologic variables and arterialized venous blood gases were measured. Maximum interval ventilation, heart rate, and VO2 did not differ between the two interventions, but pH was significantly higher before and throughout the NaHCO3 trial. pH values for NaHCO3 vs NaCl trials were 7.47 +/- 0.04 vs 7.40 +/- 0.03 prior to exercise and 7.32 +/- 0.08 vs 7.23 +/- 0.04 post-exercise (P < 0.01). The number of intervals completed with NaHCO3 (10.0 +/- 0.9) was not different from NaCl (8.4 +/- 0.9). The failure of bicarbonate to enhance performance at moderate altitude may be attributed to our controlling for the amount of sodium ingested. The intravascular volume expansion with NaHCO3 rather than the increase in blood buffer capacity may underlie the previously reported benefit of orally ingested bicarbonate in exercise performance.

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To investigate pulmonary gas exchange during exercise in athletes, 10 high aerobic capacity athletes (maximal aerobic capacity = 5.15 +/- 0.52 l/min) underwent testing on a cycle ergometer at rest, 150 W, 300 W, and maximal exercise (372 +/- 22 W) while trace amounts of six inert gases were infused intravenously. Arterial blood samples, mixed expired gas samples, and metabolic data were obtained. Indexes of ventilation-perfusion (VA/Q) mismatch were calculated by the multiple inert gas elimination technique. The alveolar-arterial difference for O2 (AaDO2) was predicted from the inert gas model on the basis of the calculated VA/Q mismatch. VA/Q heterogeneity increased significantly with exercise and was predicted to increase the AaDO2 by > 17 Torr during heavy and maximal exercise. The observed AaDO2 increased significantly more than that predicted by the inert gas technique during maximal exercise (10 +/- 10 Torr). These data suggest that this population develops diffusion limitation during maximal exercise, but VA/Q mismatch is the most important contributor (> 60%) to the wide AaDO2 observed.

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