Efficacy of residence at moderate versus low altitude on reducing acute mountain sickness in men following rapid ascent to 4300 m.

To determine if residence at moderate (~2000 m) compared to low (<50 m) altitude reduces acute mountain sickness (AMS) in men during subsequent rapid ascent to a higher altitude. Nine moderate-altitude residents (MAR) and 18 sea-level residents (SLR) completed the Environmental Symptoms Questionnaire (ESQ) at their respective baseline residence and again at 12, 24, 48, and 72 h at 4300 m to assess the severity and prevalence of AMS. AMS cerebral factor score (AMS-C) was calculated from the ESQ at each time point. AMS was judged to be present if AMS-C was ≥0.7. Resting end-tidal CO2 (PETco2) and arterial oxygen saturation (Sao2) were assessed prior to and at 24, 48, and 72 h at 4300 m. Resting venous blood samples were collected prior to and at 72 h at 4300 m to estimate plasma volume (PV) changes. MAR compared to SLR: 1) AMS severity at 4300 was lower (p<0.05) at 12 h (0.50±0.69 vs. 1.48±1.28), 24 h (0.15±0.19 vs. 1.39±1.19), 48 h (0.10±0.18 vs. 1.37±1.49) and 72 h (0.08±0.12 vs. 0.69±0.70); 2) AMS prevalence at 4300 was lower (p<0.05) at 12 h (22% vs. 72%), 24 h (0% vs. 56%), 48 h (0% vs. 56%), and 72 h (0% vs. 45%); 3) resting Sao2 (%) was lower (p<0.05) at baseline (95±1 vs. 99±1) but higher (p<0.05) at 4300 at 24 h (86±2 vs. 81±5), 48 h (88±3 vs. 83±6), and 72 h (88±2 vs. 83±5); and 4) PV (%) did not differ at 72 h at 4300 m in the MAR (4.5±6.7) but was reduced for the SLR (-8.1±10.4). These results suggest that ventilatory and hematological acclimatization acquired while living at moderate altitude, as indicated by a higher resting Sao2 and no reduction in PV during exposure to a higher altitude, is associated with greatly reduced AMS after rapid ascent to high altitude.

Sun and sky: Does human vision assume a mixture of point and diffuse illumination when interpreting shape-from-shading?

People readily perceive smooth luminance variations as being due to the shading produced by undulations of a 3-D surface (shape-from-shading). In doing so, the visual system must simultaneously estimate the shape of the surface and the nature of the illumination. Remarkably, shape-from-shading operates even when both these properties are unknown and neither can be estimated directly from the image. In such circumstances humans are thought to adopt a default illumination model. A widely held view is that the default illuminant is a point source located above the observer's head. However, some have argued instead that the default illuminant is a diffuse source. We now present evidence that humans may adopt a flexible illumination model that includes both diffuse and point source elements. Our model estimates a direction for the point source and then weights the contribution of this source according to a bias function. For most people the preferred illuminant direction is overhead with a strong diffuse component.

What is second-order vision for? Discriminating illumination versus material changes.

The human visual system is sensitive to second-order modulations of the local contrast (CM) or amplitude (AM) of a carrier signal. Second-order cues are detected independently of first-order luminance signals; however, it is not clear why vision should benefit from second-order sensitivity. Analysis of the first- and second-order contents of natural images suggests that these cues tend to occur together, but their phase relationship varies. We have shown that in-phase combinations of LM and AM are perceived as a shaded corrugated surface whereas the anti-phase combination can be seen as corrugated when presented alone or as a flat material change when presented in a plaid containing the in-phase cue. We now extend these findings using new stimulus types and a novel haptic matching task. We also introduce a computational model based on initially separate first- and second-order channels that are combined within orientation and subsequently across orientation to produce a shading signal. Contrast gain control allows the LM + AM cue to suppress responses to the LM - AM when presented in a plaid. Thus, the model sees LM - AM as flat in these circumstances. We conclude that second-order vision plays a key role in disambiguating the origin of luminance changes within an image.

The impact of moderate-altitude staging on pulmonary arterial hemodynamics after ascent to high altitude.

Staged ascent (SA), temporary residence at moderate altitude en route to high altitude, reduces the incidence and severity of noncardiopulmonary altitude illness such as acute mountain sickness. To date, the impact of SA on pulmonary arterial pressure (PAP) is unknown. We tested the hypothesis that SA would attenuate the PAP increase that occurs during rapid, direct ascent (DA). Transthoracic echocardiography was used to estimate mean PAP in 10 healthy males at sea level (SL, P(B) approximately 760 torr), after DA to simulated high altitude (hypobaric chamber, P(B) approximately 460 torr), and at 2 times points (90 min and 4 days) during exposure to terrestrial high altitude (P(B) approximately 460 torr) after SA (7 days, moderate altitude, P(B) approximately 548 torr). Alveolar oxygen pressure (Pao(2)) and arterial oxygenation saturation (Sao(2)) were measured at each time point. Compared to mean PAP at SL (mean +/- SD, 14 +/- 3 mmHg), mean PAP increased after DA to 37 +/- 8 mmHg (Delta = 24 +/- 10 mmHg, p < 0.001) and was negatively correlated with both Pao(2) (r(2) = 0.57, p = 0.011) and Sao(2) (r(2) = 0.64, p = 0.005). In comparison, estimated mean PAP after SA increased to only 25 +/- 4 mmHg (Delta = 11 +/- 6 mmHg, p < 0.001), remained unchanged after 4 days of high altitude residence (24 +/- 5 mmHg, p = not significant, or NS), and did not correlate with either parameter of oxygenation. SA significantly attenuated the PAP increase associated with continuous direct ascent to high altitude and appeared to uncouple PAP from both alveolar hypoxia and arterial hypoxemia.

Exercise performance of sea-level residents at 4300 m after 6 days at 2200 m.

UNLABELLED: Partial acclimatization resulting from staging at moderate altitude reduces acute mountain sickness during rapid exposure to higher altitudes (e.g., 4300 m). Whether staging also benefits endurance performance has not yet been scientifically evaluated. PURPOSE: Determine the effectiveness of staging at 2200 m on time trial (TT) performance of unacclimatized sea-level residents (SLR) during rapid exposure to 4300 m. There were 10 healthy men (mean +/- SE: 21 +/- 1 yrs) who performed 720 kJ cycle TT at SL and following -2 h of exposure to 4300 m (459 Torr) before (ALT-1) and after (ALT-2) living for 6 d at 2200 m (601 Torr). METHODS: Hemoglobin concentration ([Hb]), hematocrit (Hct), arterial oxygen saturation (SaO2), ratings of perceived exertion (RPE), and heart rate (HR) were measured before and during exercise. RESULTS: Compared to SL (73 +/- 6 min), TT performance was impaired (P < 0.01) by 38.1 +/- 6 min at ALT-1, but only by 18.7 +/- 3 min at ALT-2. The 44 +/- 8% TT improvement at 4300 m was directly correlated with increases in exercise SaO2 (R = 0.88, P < 0.03), but not to changes in [Hb] or Hct. In addition, RPE was lower (13 +/- 1 vs.16 +/- 1, P < 0.01) and HR remained at approximately 148 +/- 5 bpm despite performing the TT at a higher power output during ALT-2 than ALT-1 (120 +/- 7 vs.100 +/- 10 W, P < 0.01). CONCLUSION: Partial acclimatization resulting from staging attenuated the impairment in TT performance of SLR rapidly exposed to 4300 m. The close association between improved TT performance and changes in exercise SaO2, compared to a lack of association with changes in [Hb] or Hct, suggest ventilatory acclimatization may have been the major factor contributing to the performance improvement.

Effect of six days of staging on physiologic adjustments and acute mountain sickness during ascent to 4300 meters.

This study determined the effectiveness of 6 days (d) of staging at 2200 m on physiologic adjustments and acute mountain sickness (AMS) during rapid, high-risk ascent to 4300 m. Eleven sea-level (SL) resident men (means +/- SD; 21 +/- 3 yr; 78 +/- 13 kg) completed resting measures of end-tidal CO(2) (Petco(2)), arterial oxygen saturation (Sao(2)), heart rate (HR), and mean arterial pressure (MAP) at SL and within 1 h of exposure to 4300 m in a hypobaric chamber prior to 6 d of staging at 2200 m (preSTG) and on the summit of Pikes Peak following 6 d of staging at 2200 m (postSTG). Immediately following resting ventilation measures, all performed submaximal exercise ( approximately 55% of altitude-specific maximal oxygen uptake) for approximately 2 h on a bicycle ergometer to induce higher levels of AMS. AMS-C, calculated from the Environmental Symptoms Questionnaire, was measured following 4 h and 8 h of exposure at preSTG and postSTG, and the mean was calculated. Resting Petco(2) (mmHg) was unchanged from SL (39.8 +/- 2.6) to preSTG (39.3 +/- 3.0), but decreased (p < 0.05) from preSTG to postSTG (32.8 +/- 2.6). Resting Sao(2) (%) decreased (p < 0.05) from SL (97 +/- 2) to preSTG (80 +/- 4) and increased (p < 0.05) from preSTG to postSTG (83 +/- 3). Resting HR (bpm) and MAP (mmHg) did not change in any of the test conditions. The incidence and severity of AMS-C decreased (p < 0.05) from preSTG (91 +/- 30%; 1.05 +/- 0.56) to postSTG (45 +/- 53%; 0.59 +/- 0.43), respectively. These results suggest that modest physiologic adjustments induced by staging for 6 d at 2200 m reduced the incidence and severity of AMS during rapid, high-risk ascent to 4300 m.

Sleep at simulated 2438 m: effects on oxygenation, sleep quality, and postsleep performance.

INTRODUCTION: Crewmembers on ultra long-range commercial flights have the opportunity for rest and sleep in onboard areas in which the barometric pressure is 75.3 kPa (565 mmHg) or higher, equivalent to a terrestrial altitude of 2438 m (8000 ft) or lower. Sleep at higher altitudes is known to be disturbed, resulting in postsleep neurobehavioral performance decrements. We investigated the effects of sleep at 2438 m on oxygen saturation, heart rate, sleep quantity, sleep quality, postsleep neurobehavioral performance, and mood. METHODS: Twenty men, 30-56 yr of age, participated in a blinded cross-over investigation conducted in a hypobaric chamber to compare the effects of sleep at altitude (ALT, 2438 m) and ground level (GND, 305 m). RESULTS: SpO2 measured before sleep was significantly lower at ALT than at GND, 90.7 +/- 2.0% (average +/- SD) and 96.2 +/- 2.0%, respectively. During sleep, SpO2 decreased further to 86.1 +/- 2.0% at ALT, and 92.3% +/- 2.0% at GND. The percent of time during which SpO2 was below 90% was 44.4% (3.6-86.9%) at ALT and 0.1% (0.0-22.9%) at GND. Objective and subjective measurements of sleep quantity and quality did not differ significantly with altitude, nor did postsleep neurobehavioral performance or mood. DISCUSSION: The absence of significant changes in sleep and post-sleep neurobehavioral performance associated with pronounced oxygen desaturation during sleep was unexpected. Further study is needed to determine if the same effects occur in women and to characterize the changes in respiratory physiology that occur during sleep at 2438 m in both sexes.

Validation of a shortened electronic version of the environmental symptoms questionnaire.

The purpose of this study was to validate a shortened (11-item) electronic version of the 67-item paper and pencil Environmental Symptoms Questionnaire (ESQ-III) to assess acute mountain sickness (AMS). Thirty-three volunteers (means +/- SE; 28 +/- 1 yr; 74 +/- 2 kg) were given both the paper and pencil and electronic versions of the ESQ (IPAQ 5550, Hewlett Packard, Palo Alto, CA) to complete one after the other at residence altitude (RA) and after 24-h (PP24), 48-h (PP48), and 72-h (PP72) exposure to 4300 m on the summit of Pikes Peak (PP). The AMS-Cerebral (AMS-C) weighted factor score was calculated from responses to the same 11 items for each version of the ESQ. If AMS-C was >or=0.7, then the individual was classified as having AMS. There were no differences in the AMS-C scores between the paper and pencil and electronic versions of the ESQ at RA (0.05 +/- 0.01 vs. 0.05 +/- 0.02), PP24 (0.76 +/- 0.16 vs. 0.74 +/- 0.15), PP48 (0.61 +/- 0.15 vs. 0.53 +/- 0.14), and PP72 (0.34 +/- 0.09 vs. 0.34 +/- 0.09). There were no differences in the incidence of AMS between the paper and pencil and electronic versions of the ESQ at RA (0% vs. 0%), PP24 (33% vs. 36%), PP48 (27% vs. 27%), and PP72 (21% vs. 21%). The relationships between AMS-C calculated from the two versions of the ESQ at RA (r = 0.43; p = 0.01), PP24 (r = 0.92; p = 0.0001), PP48 (r = 0.82; p = 0.0005), and PP72 (r = 0.95; p = 0.0001) were significant. The relationships between the incidence of AMS calculated from the two version of the ESQ at RA (k = 0.90; p = 0.01), PP24 (k = 0.90; p = 0.01), PP48 (k = 0.91; p = 0.01), and PP72 (k = 0.92; p = 0.01) were significant. Our findings suggest that the shortened electronic version can be substituted for the paper and pencil version of the ESQ to assess AMS.

Effect of aircraft-cabin altitude on passenger discomfort.

BACKGROUND: Acute mountain sickness occurs in some unacclimatized persons who travel to terrestrial altitudes at which barometric pressures are the same as those in commercial aircraft during flight. Whether the effects are similar in air travelers is unknown. METHODS: We conducted a prospective, single-blind, controlled hypobaric-chamber study of adult volunteers to determine the effect of barometric pressures equivalent to terrestrial altitudes of 650, 4000, 6000, 7000, and 8000 ft (198, 1219, 1829, 2134, and 2438 m, respectively) above sea level on arterial oxygen saturation and the occurrence of acute mountain sickness and discomfort as measured by responses to the Environmental Symptoms Questionnaire IV during a 20-hour simulated flight. RESULTS: Among the 502 study participants, the mean oxygen saturation decreased with increasing altitude, with a maximum decrease of 4.4 percentage points (95% confidence interval, 3.9 to 4.9) at 8000 ft. Overall, acute mountain sickness occurred in 7.4% of the participants, but its frequency did not vary significantly among the altitudes studied. The frequency of reported discomfort increased with increasing altitude and decreasing oxygen saturation and was greater at 7000 to 8000 ft than at all the lower altitudes combined. Differences became apparent after 3 to 9 hours of exposure. Persons older than 60 years of age were less likely than younger persons and men were less likely than women to report discomfort. Four serious adverse events, 1 of which may have been related to the study exposures, and 15 adverse events, 9 of which were related to study exposures, were reported. CONCLUSIONS: Ascent from ground level to the conditions of 7000 to 8000 ft lowered oxygen saturation by approximately 4 percentage points. This level of hypoxemia was insufficient to affect the occurrence of acute mountain sickness but did contribute to the increased frequency of reports of discomfort in unacclimatized participants after 3 to 9 hours. (ClinicalTrials.gov number, NCT00326703 [ClinicalTrials.gov].).

A test of the tau-dot hypothesis of braking control in the real world.

A controlled experiment used instrumented vehicles in a real-world driving task to compare D. N. Lee's (1976) tau-dot hypothesis of braking control with an alternative based on the direct estimation and control of ideal deceleration (T. Yates, M. Harris, & P. Rock, 2004). Drivers braked to stop as closely as possible to a visual target from different starting speeds and times-to-contact. The data provided little support for the tau-dot hypothesis, and analysis suggested that braking in the real world is better explained by a direct deceleration strategy.

Local luminance amplitude modulates the interpretation of shape-from-shading in textured surfaces.

The pattern of illumination on an undulating surface can be used to infer its 3-D form (shape-from-shading). But the recovery of shape would be invalid if the luminance changes actually arose from changes in reflectance. So how does vision distinguish variation in illumination from variation in reflectance to avoid illusory depth? When a corrugated surface is painted with an albedo texture, the variation in local mean luminance (LM) due to shading is accompanied by a similar modulation in local luminance amplitude (AM). This is not so for reflectance variation, nor for roughly textured surfaces. We used depth mapping and paired comparison methods to show that modulations of local luminance amplitude play a role in the interpretation of shape-from-shading. The shape-from-shading percept was enhanced when LM and AM co-varied (in-phase) and was disrupted when they were out of phase or (to a lesser degree) when AM was absent. The perceptual differences between cue types (in-phase vs out-of-phase) were enhanced when the two cues were present at different orientations within a single image. Our results suggest that when LM and AM co-vary (in-phase) this indicates that the source of variation is illumination (caused by undulations of the surface), rather than surface reflectance. Hence, the congruence of LM and AM is a cue that supports a shape-from-shading interpretation.

Tau as a potential control variable for visually guided braking.

D. N. Lee (1976) described a braking strategy based on optical expansion in which the driver brakes so that the target's time-to-contact declines around a constant slope in the range -0.5 < or = tau < 0. The present results from a series of braking simulations confirm and extend earlier reports (E. H. Yilmaz & W. H. Warren, 1995) that performance is broadly compatible with the tau hypothesis. However, performance was not enhanced in situations that favored the estimation of tau, and unlike in earlier reports, performance deteriorated in the absence of a ground plane that provided information about speed and target distance. This finding suggests that the tau hypothesis does not provide a complete account of braking control.

Cytokine responses at high altitude: effects of exercise and antioxidants at 4300 m.

PURPOSE: This study tested the hypothesis that antioxidant supplementation would attenuate plasma cytokine (IL-6, tumor necrosis factor (TNF)-alpha), and C-reactive protein (CRP) concentrations at rest and in response to exercise at 4300-m elevation. METHODS: A total of 17 recreationally trained men were matched and assigned to an antioxidant (N = 9) or placebo (N = 8) group in a double-blinded fashion. At sea level (SL), energy expenditure was controlled and subjects were weight stable. Then, 3 wk before and throughout high altitude (HA), an antioxidant supplement (10,000 IU beta-carotene, 200 IU alpha-tocopherol acetate, 250 mg ascorbic acid, 50 microg selenium, 15 mg zinc) or placebo was given twice daily. At HA, energy expenditure increased approximately 750 kcal.d(-1) and energy intake decreased approximately 550 kcal.d, resulting in a caloric deficit of approximately 1200-1500 kcal.d(-1). At SL and HA day 1 (HA1) and day HA13, subjects exercised at 55% of VO2peak until they expended approximately 1500 kcal. Blood samples were taken at rest, end of exercise, and 2, 4, and 20 h after exercise. RESULTS: No differences were seen between groups in plasma IL-6, CRP, or TNF-alpha at rest or in response to exercise. For both groups, plasma IL-6 concentration was significantly higher at the end of exercise, 2, 4, and 20 h after exercise at HA1 compared with SL and HA13. Plasma CRP concentration was significantly elevated 20 h postexercise for both groups on HA1 compared to SL and HA13. TNF-alpha did not differ at rest or in response to exercise. CONCLUSION: Plasma IL-6 and CRP concentrations were elevated following exercise at high altitude on day 1, and antioxidant supplementation did not attenuate the rise in plasma IL-6 and CRP concentrations associated with hypoxia, exercise, and caloric deficit.

Endocrine responses to acute and chronic high-altitude exposure (4,300 meters): modulating effects of caloric restriction.

High-altitude anorexia leads to a hormonal response pattern modulated by both hypoxia and caloric restriction (CR). The purpose of this study was to compare altitude-induced neuroendocrine changes with or without energy imbalance and to explore how energy sufficiency alters the endocrine acclimatization process. Twenty-six normal-weight, young men were studied for 3 wk. One group [hypocaloric group (HYPO), n = 9] stayed at sea level and consumed 40% fewer calories than required to maintain body weight. Two other groups were deployed to 4,300 meters (Pikes Peak, CO), where one group (ADQ, n = 7) was adequately fed to maintain body weight and the other [deficient group (DEF), n = 10] had calories restricted as above. HYPO experienced a typical CR-induced reduction in many hormones such as insulin, testosterone, and leptin. At altitude, fasting glucose, insulin, and epinephrine exhibited a muted rise in DEF compared with ADQ. Free thyroxine, thyroid-stimulating hormone, and norepinephrine showed similar patterns between the two altitude groups. Morning cortisol initially rose higher in DEF than ADQ at 4,300 meters, but the difference disappeared by day 5. Testosterone increased in both altitude groups acutely but declined over time in DEF only. Adiponectin and leptin did not change significantly from sea level baseline values in either altitude group regardless of energy intake. These data suggest that hypoxia tends to increase blood hormone concentrations, but anorexia suppresses elements of the endocrine response. Such suppression results in the preservation of energy stores but may sacrifice the facilitation of oxygen delivery and the use of oxygen-efficient fuels.

Saccadic velocity and pupillary reflexes during acclimatization to altitude (4300 m).

INTRODUCTION: Oculometrics have been shown to be responsive to acute hypoxemia. We investigated whether oculometrics could be used as an objective index of a hypoxic effect on the central nervous system (CNS) during altitude acclimatization. We hypothesized that oculomotor reflexes [pupil diameter (PD), constriction amplitude (CA), constriction latency (CL), and saccadic velocity (SV)] changed in concert with a select number of accepted acclimatization variables and that these changes correlated with the severity of acute mountain sickness (AMS). METHODS: After sea-level, baseline (SLB) measurements were obtained, 18 men (19-33 yr) were transported to Pikes Peak, CO (4300 m), where they remained for 14 d. Periodic measurements (days 1-4, 6, 7, 9, 10, and 12) were made of PD, CA, CL, and SV in addition to heart rate (HR), pulse oximetry (SpO2), end-tidal PO2 and PCO2, 24-h urinary catecholamine concentrations, and AMS severity (environmental symptoms questionnaire, ESQ). RESULTS: PD and CL decreased from SLB on days 1-4 and subsequently returned toward SLB; these changes paralleled changes in ventilatory and circulatory variables. CA decreased on days 1 and 2 and remained decreased for 12 d. SV increased over days 1-6 then returned toward SLB with continued exposure, similar to changes in urinary catecholamines. With acclimatization, CL correlated with HR and SpO2; SV correlated with PCO2, HR, and SpO2. AMS severity peaked during days 2-4, returned toward SLB over the next 10 d, and correlated only with CL (p = 0.045). CONCLUSIONS: Oculometrics can be used as an indicator of CNS hypoxia and altitude acclimatization, although there was no strong correlation with AMS severity.

Three weeks of caloric restriction alters protein metabolism in normal-weight, young men.

The effects of prolonged caloric restriction (CR) on protein kinetics in lean subjects has not been investigated previously. The purpose of this study was to test the hypotheses that 21 days of CR in lean subjects would 1) result in significant losses of lean mass despite a suppression in leucine turnover and oxidation and 2) negatively impact exercise performance. Nine young, normal-weight men [23 +/- 5 y, 78.6 +/- 5.7 kg, peak oxygen consumption (Vo2 peak) 45.2 +/- 7.3 ml.kg(-1).min(-1), mean +/- SD] were underfed by 40% of the calories required to maintain body weight for 21 days and lost 3.8 +/- 0.3 kg body wt and 2.0 +/- 0.4 kg lean mass. Protein intake was kept at 1.2 g.kg(-1).day(-1). Leucine kinetics were measured using alpha-ketoisocaproic acid reciprocal pool model in the postabsorptive state during rest and 50 min of exercise (EX) at 50% of Vo2 peak). Body composition, basal metabolic rate (BMR), and exercise performance were measured throughout the intervention. At rest, leucine flux (approximately 131 micromol.kg(-1).h(-1)) and oxidation (R(ox); approximately 19 micromol.kg(-1).h(-1)) did not differ pre- and post-CR. During EX, leucine flux (129 +/- 6 vs. 121 +/- 6) and R(ox) (54 +/- 6 vs. 46 +/- 8) were lower after CR than they were pre-CR. Nitrogen balance was negative throughout the intervention ( approximately 3.0 g N/day), and BMR declined from 1,898 +/- 262 to 1,670 +/- 203 kcal/day. Aerobic performance (Vo2 peak, endurance cycling) was not impacted by CR, but arm flexion endurance decreased by 20%. In conclusion, 3 wk of caloric restriction reduced leucine flux and R(ox) during exercise in normal-weight young men. However, despite negative nitrogen balance and loss of lean mass, whole body exercise performance was well maintained in response to CR.

Residence at moderate altitude improves ventilatory response to high altitude.

BACKGROUND: This study compared the distribution of arterial oxygen saturation (SaO2) and susceptibility to Acute Mountain Sickness (AMS) in moderate altitude residents (MAR) and low altitude residents (LAR) following rapid ascent to 4056 m. METHODS: Resting PETCO2 and SaO2 were measured in 38 subjects residing for > 3 mo near Colorado Springs, CO (MAR group), at 1940 m (USAF Academy), and after approximately 1 h at 4056 m on the summit of Pikes Peak, CO, following ascent by car. SaO2 was also measured at 610-m elevation intervals during the ascent. Of the LAR (50 m) group, 39 subjects were exposed to a similar ascent profile in a hypobaric chamber. RESULTS: At 1940 m the MAR SaO2 and PETCO2 were 94 +/- 1% (X +/- SD) and 33.6 +/- 2.8 mmHg, respectively. At 3048 m and higher, MAR SaO2 decreased, reaching 86 +/- 2% (p < 0.001) at 4056 m, and PETCO2 (32.1 +/- 4.5 mmHg) decreased (p < 0.05). At 50 m the LAR SaO2 and PETCO2 were 98 +/- 1% and 38.7 +/- 2.7 mmHg, respectively. At 1940 m and higher, LAR SaO2 decreased (p < 0.001), reaching 82 +/- 5% at 4056 m, and PETCO2 (36.4 +/- 3.5 mmHg) decreased (p < 0.05). Above 2438 m, the MAR SaO2 was higher (p < 0.001) than the LAR. Only one MAR subject, but nine LAR subjects reported AMS symptoms. CONCLUSIONS: Ventilatory acclimatization developed during moderate altitude residence substantially enhances arterial oxygenation during rapid ascents to higher altitudes. Compared with prior studies, the level of ventilatory acclimatization achieved at moderate altitude is similar to residing at 4056 m for approximately 5-9 d.

Antioxidant supplementation does not attenuate oxidative stress at high altitude.

INTRODUCTION: Hypobaric hypoxia and heightened metabolic rate increase free radical production. PURPOSE: We tested the hypothesis that antioxidant supplementation would reduce oxidative stress associated with increased energy expenditure (negative energy balance) at high altitude (HA 4300 m). METHODS: For 12 d at sea level (SL), 18 active men were fed a weight-stabilizing diet. Testing included fasting blood and 24-h urine samples to assess antioxidant status [plasma alpha-tocopherol, beta-carotene, lipid hydroperoxides (LPO), and urinary 8-hydroxydeoxyguanosine (8-OHdG)] and a prolonged submaximal (55% Vo2peak) oxidative stress index test (OSI) to evaluate exercise-induced oxidative stress (plasma LPO, whole blood reduced and oxidized glutathione, glutathione peroxidase, and urinary 8-OHdG). Subjects were then matched and randomly assigned to either a placebo or antioxidant supplement group for a double-blinded trial. Supplementation (20,000 IU of beta-carotene, 400 IU alpha-tocopherol acetate, 500 mg ascorbic acid, 100 microg selenium, and 30 mg zinc, or placebo) was begun 3 wk prior to and throughout a 14-d HA intervention. At HA, subjects' daily energy intake and expenditure were adjusted to achieve a caloric deficit of approximately 1400 kcal. Fasting blood and 24-h urine samples were collected throughout HA and the OSI test was repeated on HA day 1 and day 13. RESULTS: Resting LPO concentrations increased and urinary 8-OHdG concentrations decreased over HA with no effect of supplementation. Prolonged submaximal exercise was not associated with increased concentrations of oxidative stress markers at SL or HA. CONCLUSIONS: Antioxidant supplementation did not significantly affect markers of oxidative stress associated with increased energy expenditure at HA.

Ventilation after supplemental oxygen administration at high altitude.

OBJECTIVE: The present study assessed the effects of acute hyperoxia on resting-minute ventilation (VE) during altitude acclimatization to 4300 m. METHODS: Resting-minute ventilation, end-tidal partial pressure carbon dioxide (PETCO2) and oxygen (P(ET)O2), and arterial oxygen saturation (SpO2) were measured during chronic poikilocapnic hypobaric hypoxia, supplemental oxygen breathing, and the subsequent return to hypobaric poikilocapnic hypoxia at altitude. Fifteen adult male lowlanders were studied at sea level and on the 3rd and 12th days at 4300 m. At sea level, subjects first breathed room air that was followed by 25-minute steady-state poikilocapnic hypoxia (FIO2 = 0.125). Ventilatory responses to acute poikilocapnic hypoxia (APH) were collected over the first 1-10 minutes, and responses to chronic poikilocapnic hypoxia (CPH) were collected over the last 3 minutes of the hypoxia exposure. At altitude, CPH was provided by ambient-air breathing (PIO2 = 86 mm Hg) that was interrupted by 10 minutes of oxygen breathing (FIO2 = 1.0, PIO2 = 460 mm Hg) and then a subsequent return to ambient air to measure APH ventilatory responses. RESULTS: Between day 1 and day 12, during CPH, VE and SpO2 increased (P < .05) by 46% and 6%, respectively, whereas P(ET)CO2 decreased. On day 3 and day 12, breathing oxygen did not lower VE compared with CPH. However, the VE during APH immediately after oxygen breathing at high altitude was always greater (P < .05) than during CPH and did not change with duration of residence at altitude. CONCLUSIONS: These results show that short-duration oxygen breathing increases the subsequent ventilatory response to poikilocapnic hypoxia in altitude-acclimatized lowlanders, resulting in a transient elevation of SpO2.

Influence of alpha-adrenergic blockade on the catecholamine response to exercise at 4,300 meters.

This investigation examined the influence of alpha-adrenergic blockade on plasma and urinary catecholamine responses to both exercise and high-altitude exposure. Sixteen nonsmoking, eumenorrheic women (age 23.2 +/- 1.4 years, 68.7 +/- 1.0 kg) were studied at sea level and during 12 days of high-altitude exposure (4,300 m). Subjects received either alpha-blockade (prazosin 3 mg/d) or a placebo in a double-blinded, randomized fashion. Resting plasma and 24-hour urine samples were collected periodically throughout the duration of the study. Further, subjects participated in submaximal exercise tests (50 minutes at 50% sea level maximum oxygen consumption [Vo2max]) at Sea level and on days 1 and 12 at altitude. Urinary norepinephrine (NE) excretion rates increased significantly over time at altitude, with blocked subjects having greater values compared to controls. Plasma NE levels increased significantly with chronic altitude exposure compared to sea level and acute hypoxia both at rest and during exercise. NE levels at rest were greater for blocked compared to control subjects during all conditions. Urinary and plasma epinephrine (EPI) levels increased dramatically, with acute altitude exposure returning to sea level values by day 12 of altitude exposure. EPI levels were greater for blocked compared to placebo both at rest and during exercise for all conditions studied. Changes in alpha-adrenergic activity over time at altitude were associated with select metabolic and physiologic adjustments. The presence of alpha-blockade significantly affected these responses during chronic altitude exposure. It was concluded that: (1) alpha-adrenergic blockade elicited a potentiated sympathoadrenal response to the stress of both exercise as well as high-altitude exposure, and (2) the sympathetics, via alpha-adrenergic stimulation, contribute to a number of key adaptations associated with acclimatization to high altitude.