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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].). [ABSTRACT FROM AUTHOR]

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.

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., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

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.

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.

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.

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.

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.

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.

Recent work from our laboratory demonstrated that carbohydrate supplementation (CHOS) during exercise improved prolonged time-trial (TT) performance of sea-level residents (SLR) living at 4300 m while they were in daily negative energy balance (- 1250 kcal x day (-1); [ ]). The purposes of the current study were to determine during initial exposure to 4300 m:1) whether CHOS also improves TT performance of moderate altitude residents (MAR) who are in energy balance and 2) if acclimatization to moderate elevations benefits TT performance. Fifteen Air Force Academy (AFA) active duty members (age: 30 +/- 1 yrs; mean +/- SE), who had been living at approximately 2000 m for 21 +/- 3 months performed a maximal-effort 720-kJ cycle TT at the AFA and at Pikes Peak (PP), CO, (4300 m) on days 1 (PP1) and 3 (PP3). Daily energy intake and expenditure were maintained similarly at the AFA and PP. At the start of the TTs at PP, and then every 15 min thereafter, 9 subjects drank a 10 % CHO solution (0.175 g x kg (-1) body weight) and 6 subjects drank a placebo (PLA) solution. All subjects were allowed to freely adjust the power output of the cycle ergometer and drank water AD LIBITUM. Performance time did not differ between groups on PP1 (CHOS vs. PLA; 101 +/- 8 vs. 116 +/- 10 min) or PP3 (95 +/- 8 vs. 107 +/- 12 min). For both groups, cycle times on PP1 and PP3 were longer compared to the AFA (p<0.01) and were improved from PP1 to PP3 (p<0.05). Exercise intensity (i.e., % peak oxygen uptake) was maintained similarly at approximately 62 % during the TTs at the AFA and PP. Blood glucose was 1.5 to 2.0 mmol x L (-1) higher for CHOS vs. PLA (p<0.01). It was concluded that CHOS provided no TT performance benefit for MAR at 4300 m when energy balance was maintained. However, the decrements in TT performance and exercise intensity were attenuated at 4300 m in MAR compared to those of SLR as a result of acclimatization attained while living for nearly 2 years at approximately 2000 m.

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., ((c) 2006 APA, all rights reserved.)

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.

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.

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.

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.

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.

Carbohydrate supplementation (CHOS) typically improves prolonged time-trial (TT) performance at sea level (SL). This study determined whether CHOS also improves TT performance at high altitude (ALT; 4,300 M) despite increased hypoxemia and while in negative energy balance (approximately 1,250 kcal/day). Two groups of fasting, fitness-matched men performed a 720-kJ cycle TT at SL and while living at ALT on days 3 (ALT3) and 10 (ALT10). Eight men drank a 10% carbohydrate solution (0.175 g/kg body wt) and eight drank a placebo (PLA; double blind) at the start of and every 15 min of the TT. Blood glucose during each TT was higher (P < 0.05) for CHOS than for PLA. At SL, TT duration (approximately 59 min) and watts (approximately 218 or approximately 61% of peak watts; %SL Wpeak) were similar for both groups. At ALT, the TT was longer for both groups (P < 0.01) but was shorter for CHOS than for PLA on ALT3 (means +/- SE: 80 +/- 7 vs. 105 +/- 9 min; P < 0.01) and ALT10 (77 +/- 7 vs. 90 +/- 5 min; P < 0.01). At ALT, %SL Wpeak was reduced (P < 0.01) with the reduction on ALT3 being larger for PLA (to 33 +/- 3%) than for CHOS (to 43 +/- 2%; P < 0.05). On ALT3, O2 saturation fell similarly from 84 +/- 2% at rest to 73 +/- 1% during the TT for both groups (P < 0.05), and on ALT10 O2 saturation fell more (P < 0.02) for CHOS (91 +/- 1 to 76 +/- 2%) than for PLA (90 +/- 1 to 81 +/- 1%). %SL Wpeak and O2 saturation were inversely related during the TT for both groups at ALT (r > or = -0.76; P < or = 0.03). It was concluded that, despite hypoxemia exacerbated by exercise, CHOS greatly improved TT performance at ALT in which there was a negative energy balance.

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.

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.

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.

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.

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.

Background: An objective method that accurately quantifies the severity of Acute Mountain Sickness (AMS) symptoms is needed to enable more reliable evaluation of altitude acclimatization and testing of potentially beneficial interventions., Hypothesis: Changes in human articulation, as quantified by timed variations in acoustic waveforms of specific spoken words (voice onset time; VOT), are correlated with the severity of AMS., Methods: Fifteen volunteers were exposed to a simulated altitude of 4300 m (446 mm Hg) in a hypobaric chamber for 48 h. Speech motor control was determined from digitally recorded and analyzed timing patterns of 30 different monosyllabic words characterized as voiced and unvoiced, and as labial, alveolar, or velar. The Environmental Symptoms Questionnaire (ESQ) was used to assess AMS., Results: Significant AMS symptoms occurred after 4 h, peaked at 16 h, and returned toward baseline after 48 h. Labial VOTs were shorter after 4 and 39 h of exposure; velar VOTs were altered only after 4 h; and there were no changes in alveolar VOTs. The duration of vowel sounds was increased after 4 h of exposure and returned to normal thereafter. Only 1 of 15 subjects did not increase vowel time after 4 h of exposure. The 39-h labial (p = 0.009) and velar (p = 0.037) voiced-unvoiced timed separations consonants and the symptoms of AMS were significantly correlated., Conclusions: Two objective measures of speech production were affected by exposure to 4300 m altitude and correlated with AMS severity. Alterations in speech production may represent an objective measure of AMS and central vulnerability to hypoxia.

Background: Physical performance of sea-level (SL) residents acutely exposed to altitude (ALT) is diminished and may improve somewhat with ALT acclimatization., Hypothesis: A large reduction in lean body mass (LBM), due to severe energy intake deficit during the first 21 d of ALT (4300 m) acclimatization, will adversely affect performance., Methods: At ALT, 10 men received a deficit (DEF) of 1500 kcal x d(-1) below body weight (BW) maintenance requirements and 7 men received adequate (ADQ) kcal x d(-1) to maintain BW. Performance was assessed by: 1) maximal oxygen uptake (VO2max); 2) time to complete 50 cycles of a lift and carry task (L+C); 3) number of one-arm elbow flexions (10% BW at 22 flexions x min(-1); and 4) adductor pollicis (AP) muscle strength and endurance time (repeated 5-s static contractions at 50% of maximal force followed by 5-s rest, to exhaustion). Performance and body composition (using BW and circumference measures) were determined at SL and at ALT on days 2 through 21., Results: At SL, there were no between-group differences (p > 0.05) for any of the performance measures. From SL to day 21 at ALT, BW and LBM declined by 6.6 +/- 3 kg and 4.6 kg, respectively, for the DEF group (both p < 0.01), but did not change (both p > 0.05) for the ADQ group. Performance changes from day 2 or 3 to day 20 or 21 at ALT were as follows (values are means +/- SD): VO2max (ml x min(-1)): DEF = +97 +/- 237, ADQ = +159 +/- 156; L + C (s): DEF = -62 +/- 35*, ADQ = -35 +/- 20* (*p < 0.05; improved from day 3); arm flex (reps): DEF = -2 +/- 7, ADQ = +2 +/- 8; AP endurance (min): DEF = +1.4 +/- 2, ADQ = + 1.9 +/- 2; AP strength (kg): DEF = -0.7 +/- 4, ADQ = -1.2 +/- 2. There were no differences in performance between groups., Conclusions: A significant BW and LBM loss due to underfeeding during the first 21 d of ALT acclimatization does not impair physical performance at ALT.

Because the ovarian steroid hormones, progesterone and estrogen, have higher blood levels in the luteal (L) than in the follicular (F) phase of the menstrual cycle, and because of their known effects on ventilation and hematopoiesis, we hypothesized that less hypoxemia and less erythropoiesis would occur in the L than the F phase of the cycle after arrival at altitude. We examined erythropoiesis with menstrual cycle phase in 16 women (age 22.6 +/- 0.6 yr). At sea level, 11 of 16 women were studied during both menstrual cycle phases, and, where comparison within women was available, cycle phase did not alter erythropoietin (n = 5), reticulocyte count (n = 10), and red cell volume (n = 9). When all 16 women were taken for 11 days to 4,300-m altitude (barometric pressure = 462 mmHg), paired comparisons within women showed no differences in ovarian hormone concentrations at sea level vs. altitude on menstrual cycle day 3 or 10 for either the F (n = 11) or the L (n = 5) phase groups. Arterial oxygen saturation did not differ between the F and L groups at altitude. There were no differences by cycle phase on day 11 at 4,300 m for erythropoietin [22.9 +/- 4.7 (L) vs. 18.8 +/- 3.4 mU/ml (F)], percent reticulocytes [1.9 +/- 0.1 (L) vs. 2.1 +/- 0.3% (F)], hemoglobin [13.5 +/- 0.3 (L) vs. 13.7 +/- 0.3 g/100 ml (F)], percent hematocrit [40.6 +/- 1.4 (L) vs. 40.7 +/- 1.0% (F)], red cell volume [31.1 +/- 3.6 (L) vs. 33.0 +/- 1.6 ml/kg (F)], and blood ferritin [8.9 +/- 1.7 (L) vs. 10.2 +/- 0.9 microg/l (F)]. Blood level of erythropoietin was related (r = 0.77) to arterial oxygen saturation but not to the levels of progesterone or estradiol. We conclude that erythropoiesis was not altered by menstrual cycle phase during the first days at 4,300-m altitude.

Background: Increased blood level of norepinephrine, a primary alpha-adrenergic agonist, is associated with high-altitude exposure, and may help regulate key physiological functions (e.g., blood pressure). We hypothesized that blocking alpha1-adrenergic receptors would impair circulatory compensation for an orthostatic challenge to a greater extent at altitude than at sea level., Methods: Sixteen healthy women (23 +/- 2 yr) were randomly assigned to receive either 2 mg prazosin (n = 8) or placebo (n = 8) t.i.d. (double-blind design) for 12 d at sea level and during the first 12 d of altitude residence (4300 m). Passive 60 degrees upright tilt was performed at sea level (10 d of treatment), and after 3 and 10 d at altitude. Mean arterial BP (MABP, via auscultation) and heart rate (HR, via ECG) were measured every min during 10 min each of supine rest and tilt., Results: For the prazosin group compared with the placebo group: 1.) Supine and tilt MABP were consistently lower (p < 0.05) at sea level; 2.) MABP did not differ (p > 0.05) for either day at altitude; 3.) HR was similar for both positions at sea level and altitude; and 4.) MABP was consistently less only at sea level and HR was consistently greater only at altitude (both p < 0.05) in response to tilt., Conclusions: alpha1-adrenergic blockade altered MABP and HR responses to tilt at sea level and altitude, but circulatory responses to orthostasis were well maintained in both environments. At altitude, BP during tilt was sufficiently maintained by a compensatory increase in heart rate, likely mediated by parasympathetic withdrawal.

We hypothesized that blockade of alpha(1)-adrenergic receptors would prevent the rise in peripheral vascular resistance that normally occurs during acclimatization. Sixteen eumenorrheic women were studied at sea level (SL) and at 4,300 m (days 3 and 10). Volunteers were randomly assigned to take the selective alpha(1)-blocker prazosin or placebo. Venous compliance, forearm vascular resistance, and blood flow were measured using plethysmography. Venous compliance fell by day 3 in all subjects (1.39 +/- 0.30 vs. 1.62 +/- 0.43 ml. Delta 30 mmHg(-1) x 100 ml tissue(-1) x min(-1) at SL, means +/- SD). Altitude interacted with prazosin treatment (P < 0.0001) such that compliance returned to SL values by day 10 in the prazosin-treated group (1.68 +/- 0.19) but not in the placebo-treated group (1.20 +/- 0.10, P < 0.05). By day 3 at 4,300 m, all women had significant falls in resistance (35.2 +/- 13.2 vs. 54.5 +/- 16.1 mmHg x ml(-1) x min(-1) at SL) and rises in blood flow (2.5 +/- 1.0 vs. 1.6 +/- 0.5 ml. 100 ml tissue(-1) x min(-1) at SL). By day 10, resistance and flow returned toward SL, but this return was less in the prazosin-treated group (resistance: 39.8 +/- 4.6 mmHg x ml(-1) x min(-1) with prazosin vs. 58.5 +/- 9.8 mmHg x ml(-1) x min(-1) with placebo; flow: 1.9 +/- 0.7 ml. 100 ml tissue(-1) x min(-1) with prazosin vs. 2.3 +/- 0.3 ml x 100 ml tissue(-1) x min(-1) with placebo, P < 0.05). Lower resistance related to higher circulating epinephrine in both groups (r = -0.50, P < 0.0001). Higher circulating norepinephrine related to lower venous compliance in the placebo-treated group (r = -0.42, P < 0.05). We conclude that alpha(1)-adrenergic stimulation modulates peripheral vascular changes during acclimatization.

Women living at low altitudes or acclimatized to high altitudes have greater effective ventilation in the luteal (L) compared with follicular (F) menstrual cycle phase and compared with men. We hypothesized that ventilatory acclimatization to high altitude would occur more quickly and to a greater degree in 1) women in their L compared with women in their F menstrual cycle phase, and 2) in women compared with men. Studies were conducted on 22 eumenorrheic, unacclimatized, sea-level (SL) residents. Indexes of ventilatory acclimatization [resting ventilatory parameters, hypoxic ventilatory response, hypercapnic ventilatory response (HCVR)] were measured in 14 women in the F phase and in 8 other women in the L phase of their menstrual cycle, both at SL and again during a 12-day residence at 4,300 m. At SL only, ventilatory studies were also completed in both menstrual cycle phases in 12 subjects (i.e., within-subject comparison). In these subjects, SL alveolar ventilation (expressed as end-tidal PCO(2)) was greater in the L vs. F phase. Yet the comparison between L- and F-phase groups found similar levels of resting end-tidal PCO(2), hypoxic ventilatory response parameter A, HCVR slope, and HCVR parameter B, both at SL and 4,300 m. Moreover, these indexes of ventilatory acclimatization were not significantly different from those previously measured in men. Thus female lowlanders rapidly ascending to 4,300 m in either the L or F menstrual cycle phase have similar levels of alveolar ventilation and a time course for ventilatory acclimatization that is nearly identical to that reported in male lowlanders.

After short-term exposure to high altitude (HA), men appear to be less sensitive to insulin than at sea level (SL). We hypothesized that the same would be true in women, that reduced insulin sensitivity would be directly related to the rise in plasma epinephrine concentrations at altitude, and that the addition of alpha-adrenergic blockade would potentiate the reduction. To test the hypotheses, 12 women consumed a high-carbohydrate meal at SL and after 16 h at simulated 4,300-m elevation (HA). Subjects were studied twice at each elevation: once with prazosin (Prz), an alpha(1)-adrenergic antagonist, and once with placebo (Pla). Mathematical models were used to assess insulin resistance based on fasting [homeostasis model assessment of insulin resistance (HOMA-IR)] and postprandial [composite model insulin sensitivity index (C-ISI)] glucose and insulin concentrations. Relative to SL-Pla (HOMA-IR: 1.86 +/- 0.35), insulin resistance was greater in HA-Pla (3.00 +/- 0.45; P < 0.05), SL-Prz (3.46 +/- 0.51; P < 0.01), and HA-Prz (2.82 +/- 0.43; P < 0.05). Insulin sensitivity was reduced in HA-Pla (C-ISI: 4.41 +/- 1.03; P < 0.01), SL-Prz (5.73 +/- 1.01; P < 0.05), and HA-Prz (4.18 +/- 0.99; P < 0.01) relative to SL-Pla (8.02 +/- 0.92). Plasma epinephrine was significantly elevated in HA-Pla (0.57 +/- 0.08 ng/ml; P < 0.01), SL-Prz (0.42 +/- 0.07; P < 0.05), and HA-Prz (0.82 +/- 0.07; P < 0.01) relative to SL-Pla (0.28 +/- 0.04), but correlations with HOMA-IR, HOMA-beta-cell function, and C-ISI were weak. In women, short-term exposure to simulated HA reduced insulin sensitivity compared with SL. The change does not appear to be directly mediated by a concurrent rise in plasma epinephrine concentrations.

Recently, we reported that, at similar voluntary force development during static submaximal intermittent contractions of the adductor pollicis muscle, fatigue developed more slowly in women than in men under conditions of normobaric normoxia (NN) (Acta Physiol Scand 167: 233-239, 1999). We postulated that the slower fatigue of women was due, in part, to a greater capacity for muscle oxidative phosphorylation. The present study examined whether a gender difference in adductor pollicis muscle performance also exists during acute exposure to hypobaric hypoxia (HH; 4,300-m altitude). Healthy young men (n = 12) and women (n = 21) performed repeated static contractions at 50% of maximal voluntary contraction (MVC) force of rested muscle for 5 s followed by 5 s of rest until exhaustion. MVC force was measured before and at the end of each minute of exercise and at exhaustion. Exhaustion was defined as an MVC force decline to 50% of that of rested muscle. For each gender, MVC force of rested muscle in HH was not significantly different from that in NN. MVC force tended to decline at a faster rate in HH than in NN for men but not for women. In both environments, MVC force declined faster (P < 0.01) for men than for women. For men, endurance time to exhaustion was shorter (P < 0.01) in HH than in NN [6.08 +/- 0.7 vs. 8.00 +/- 0.7 (SE) min]. However, for women, endurance time to exhaustion was similar (not significant) in HH (12.86 +/- 1.2 min) and NN (13.95 +/- 1.0 min). In both environments, endurance time to exhaustion was longer for women than for men (P < 0.01). Gender differences in the impact of HH on adductor pollicis muscle endurance persisted in a smaller number of men and women matched (n = 4 pairs) for MVC force of rested muscle and thus on submaximal absolute force and, by inference, ATP demand in both environments. In contrast to gender differences in the impact of HH on small-muscle (adductor pollicis) exercise performance, peak O(2) uptake during large-muscle exercise was lower in HH than in NN by a similar (P > 0.05) percentage for men and women (-27.6 +/- 2 and -25.1 +/- 2%, respectively). Our findings are consistent with the postulate of a higher adductor pollicis muscle oxidative capacity in women than in men and imply that isolated performance of muscle with a higher oxidative capacity may be less impaired when the muscle is exposed to HH.

We applied a novel MR imaging technique to investigate the effect of acute mountain sickness on cerebral tissue water. Nine volunteers were exposed to hypobaric hypoxia corresponding to 4572 m altitude for 32 h. Such an exposure may cause acute mountain sickness. We imaged the brains of the volunteers before and at 32 h of hypobaric exposure with two different MRI techniques with subsequent data processing. (1) Brain volumes were calculated from 3D MRI data sets by applying a computerized brain segmentation algorithm. For this specific purpose a novel adaptive 3D segmentation program was used with an automatic correction algorithm for RF field inhomogeneity. (2) T(2) decay rates were analyzed in the white matter. The results demonstrated that a significant brain swelling of 36.2 +/- 19.6 ml (2.77 +/- 1.47%, n = 9, P < 0.001) developed after the 32-h hypobaric hypoxia exposure with a maximal observed volume increase of 5.8% (71.3 ml). These volume changes were significant only for the gray matter structures in contrast to the unremarkable changes seen in the white matter. The same study repeated 3 weeks later in 6 of 9 original subjects demonstrated that the brains recovered and returned approximately to the initially determined sea-level brain volume while hypobaric hypoxia exposure once again led to a significant new brain swelling (24.1 +/- 12.1 ml, 1.92 +/- 0.96%, n = 6, P < 0.005). On the contrary, the T(2) mapping technique did not reveal any significant effect of hypobaria on white matter. We present here a technique which is able to detect reversible brain volume changes as they may occur in patients with diffuse brain edema or increased cerebral blood volume, and which may represent a useful noninvasive tool for future evaluations of antiedematous drugs., (Copyright 2001 Academic Press.)

We have previously documented the importance of the sympathetic nervous system in acclimatizing to high altitude in men. The purpose of this investigation was to determine the extent to which alpha-adrenergic blockade affects the sympathoadrenal responses to exercise during acute high-altitude exposure in women. Twelve eumenorrheic women (24.7 +/- 1.3 yr, 70.6 +/- 2.6 kg) were studied at sea level and on day 2 of high-altitude exposure (4,300-m hypobaric chamber) in either their follicular or luteal phase. Subjects performed two graded-exercise tests at sea level (on separate days) on a bicycle ergometer after 3 days of taking either a placebo or an alpha-blocker (3 mg/day prazosin). Subjects also performed two similar exercise tests while at altitude. Effectiveness of blockade was determined by phenylephrine challenge. At sea level, plasma norepinephrine levels during exercise were 48% greater when subjects were alpha-blocked compared with their placebo trial. This difference was only 25% when subjects were studied at altitude. Plasma norepinephrine values were significantly elevated at altitude compared with sea level but to a greater extent for the placebo ( upward arrow 59%) vs. blocked ( upward arrow 35%) trial. A more dramatic effect of both altitude ( upward arrow 104% placebo vs. 95% blocked) and blockade ( upward arrow 50% sea level vs. 44% altitude) was observed for plasma epinephrine levels during exercise. No phase differences were observed across any condition studied. It was concluded that alpha-adrenergic blockade 1) resulted in a compensatory sympathoadrenal response during exercise at sea level and altitude, and 2) this effect was more pronounced for plasma epinephrine.

Background: Studies were conducted to determine the effect of altitude exposure on intraocular pressure (IOP) and any relationship with the severity of acute mountain sickness (AMS)., Hypotheses: a) IOP is decreased during exposure to 4300 m altitude; b) there is a positive correlation between IOP and AMS; and c) there is a correlation between changes in urinary catecholamines and IOP., Methods: IOP (noncontact tonometry) was measured in 11 resting males during acute simulated altitude (446 mmHg, < 2 h, hypobaric chamber), during altitude acclimatization (15 d at 4300 m), and in 6 of the 11 volunteers during re-exposure in the chamber after 8 d at sea level (Study A). In a second study (Study B) of 12 females, IOP (contact tonometry) and 24-h urinary catecholamines were measured during a 50-h chamber exposure (446 mmHg). AMS severity was assessed using the Environmental Symptoms Questionnaire (ESQ-C)., Results: IOP decreased 25% after 2 d at altitude and returned toward sea level values by 15 d (Study A). IOP was reduced 13% after 5 h of exposure followed by return toward sea level values (Study B). Significant correlation was found between the sea level IOP and ESQ-C (Study A); significant correlation was found between the reduction in IOP and the ESQ-C and urinary epinephrine concentrations (Study B)., Conclusions: Altitude exposure resulted in a reduction in IOP that occurred within hours and recovered during acclimatization. This reduction may be related to increases in epinephrine concentration. Measurement of IOP before and during altitude exposure may provide an objective method of assessing an individual's response to hypoxic stress.

The purpose of this investigation was to determine the sympathoadrenal response to exercise in women after acclimatization to high altitude. Sixteen eumenorrheic women (age, 23.6 +/- 1.2 years; weight, 56.2 +/- 4.3 kg) were studied at sea level and after 10 days of high-altitude exposure (4,300 m) in either the follicular (n = 11) or luteal (n = 5) phase. Subjects performed two 45-minute submaximal steady-state exercise tests (50% and 65% peak O2 consumption [VO2 peak]) at sea level on a bicycle ergometer. Exercise tests were also performed on day 10 of altitude exposure (50% VO2 peak at sea level). As compared with rest, plasma epinephrine levels increased 36% in response to exercise at 50% VO2 peak at sea level, with no differences found between cycle phases. This increase was significantly greater (increase 44%) during exercise at 65% VO2 peak. At altitude, the epinephrine response was identical to that found for 65% VO2 peak exercise at sea level (increase 44%), with no differences found between phase assignments. The plasma norepinephrine response differed from that for epinephrine such that the increase with exercise at altitude (increase 61%) was significantly greater compared with 65% Vo2 peak exercise at sea level (increase 49%). Again, no phase differences were observed. It is concluded that the sympathoadrenal response to exercise (1) did not differ between cycle phases across any condition and (2) was similar to that found previously in men, and (3) the relative exercise intensity is the primary factor responsible for the epinephrine response to exercise, whereas altitude had an additive effect on the norepinephrine response to exercise.

Background: The increased metabolic energy requirement imposed by a chemical defense uniform (CDU) and the lower maximal aerobic capacity associated with increased altitude should produce greater demands on the cardiopulmonary system during the performance of a given work task at increasing altitudes. We hypothesized that: a) relative to sea level, the decrements in physical work performance caused by ascending to high terrestrial altitudes would be greater in a CDU compared with a standard fatigue uniform (U.S. Army, BDU); b) the aversive subjective reactions to the CDU would be accentuated with increasing altitude; and c) that staging at moderate altitude, to induce acclimatization, would restore work performance at higher altitudes to sea level norms., Methods: The physiological and subjective responses of 8 male soldiers to work (10-min lift-and-carry task and rifle marksmanship) were measured. Subjects wore the BDU and a CDU ensemble (U.S. Army, BDO) at sea level, intermediate (2743 m) and high (4,300 m) altitudes following rapid and staged (3 d at 1,830 m) ascents to the higher altitudes., Results: Lift/carry task performance tended to be lower (p = 0.076) in the CDU vs. the BDU at altitude. The cardiopulmonary responses to the lift/carry task increased at altitude and were greater in the CDU. The subjects' perception of their ability to perform the lift/carry task at altitude was adversely impacted more in the CDU than the BDU. Rapid ascent to intermediate altitude degraded marksmanship in both uniforms. Following staged ascent, lift/carry task and marksmanship performance was restored to sea level norms., Conclusions: Personnel wearing CDU or equivalent protective clothing at intermediate to high terrestrial elevations should anticipate proportionally larger CDU-induced decrements of work performance and lower tolerance to working in a CDU than experienced near sea level. Staging at moderate altitude is an effective strategy for restoring work performance to sea level norms at higher altitudes.

During constant intensity treadmill or cycle exercise, progressive muscle fatigue is not readily quantified and endurance time is poorly reproducible. However, integration of dynamic knee extension (DKE) exercise with serial measurement of maximal voluntary contraction (MVC) force of knee extensor muscles permits close tracking of leg fatigue. We studied reproducibility of four performance indices: MVC force of rested muscle (MVC(rest)) rate of MVC force fall, time to exhaustion, and percentage of MVC(rest) (%MVC(rest)) at exhaustion in 11 healthy women (22+/-1 yrs) during identical constant work rate 1-leg DKE (1 Hz) on 2 separate days at sea level (30 m). Means+/-SD for the two test days, and the correlations (r), standard estimate errors and coefficients of variation (CV%) between days were, respectively: a) MVC(rest)(N), 524+/-99 vs 517+/-111, 0.91, 43.0, 4.9%; b) MVC force fall (N x min(-1)), -10.77+/-9.3 vs -11.79+/-12.1, 0.94, 3.6, 26.5 %; c) Time to exhaustion (min), 22.6+/-12 vs 23.9+/-14, 0.98, 2.7, 7.5 %; and d) %MVC(rest) at exhaustion, 65+/-13 vs 62+/-14, 0.85, 7.8, 5.6%. There were no statistically significant mean differences between the two test days for any of the performance measures. To demonstrate the potential benefits of evaluating multiple effects of an experimental intervention, nine of the women were again tested within 24hr of arriving at 4,300 m altitude using the identical force, velocity, power output, and energy requirement during constant work rate dynamic leg exercise. Low variability of each performance index enhanced the ability to describe the effects of acute altitude exposure on voluntary muscle function.

Exercise training studies conducted at different altitudes (1250-5700 m) of varying durations (30 min to 19 wk) are critically reviewed to determine the efficacy of using altitude as a training stimulus to enhance sea level and altitude exercise performance. Four strategies are discussed: a) exercise training while residing at the same altitude; b) exercise training at altitude but residing at sea level; c) exercise training at low altitude but residing at a higher altitude; and d) exercise training under sea level and altitude conditions but only after altitude acclimatization has occurred. Residing at altitude causes a multitude of potentially beneficial physiological, ventilatory, hematological and metabolic changes that theoretically should induce a potentiating effect on endurance exercise performance. While it is accepted that endurance performance is greatly enhanced at altitude, there is less support for the view that altitude training while residing at altitude improves subsequent sea level endurance performance. There is some evidence, though also not universally accepted, that training at altitude but residing at sea level may benefit sea level endurance performance. Most recently, the combination of "living high" (e.g., at 2500 m) to obtain beneficial physiological changes associated with altitude acclimatization and "training low" (e.g., at 1250 m) to allow maintenance of high-intensity training is accumulating scientific and popular support as the most advantageous strategy to improve subsequent sea level exercise performance in well-trained, competitive runners.

To test the hypotheses that prolonged exposure to moderately high altitude increases the energy requirement of adequately fed women and that the sole cause of the increase is an elevation in basal metabolic rate (BMR), we studied 16 healthy women [21.7 +/- 0.5 (SD) yr; 167.4 +/- 1.1 cm; 62.2 +/- 1.0 kg]. Studies were conducted over 12 days at sea level (SL) and at 4,300 m [high altitude (HA)]. To test that menstrual cycle phase has an effect on energetics at HA, we monitored menstrual cycle in all women, and most women (n = 11) were studied in the same phase at SL and HA. Daily energy intake at HA was increased to respond to increases in BMR and to maintain body weight and body composition. Mean BMR for the group rose 6.9% above SL by day 3 at HA and fell to SL values by day 6. Total energy requirement remained elevated 6% at HA [ approximately 670 kJ/day (160 kcal/day) above that at SL], but the small and transient increase in BMR could not explain all of this increase, giving rise to an apparent "energy requirement excess." The transient nature of the rise in BMR may have been due to the fitness level of the subjects. The response to altitude was not affected by menstrual cycle phase. The energy requirement excess is at present unexplained.

To evaluate the hypothesis that exposure to high altitude would reduce blood glucose and total carbohydrate utilization relative to sea level (SL), 16 young women were studied over four 12-day periods: at 50% of peak O(2) consumption in different menstrual cycle phases (SL-50), at 65% of peak O(2) consumption at SL (SL-65), and at 4,300 m (HA). After 10 days in each condition, blood glucose rate of disappearance (R(d)) and respiratory exchange ratio were measured at rest and during 45 min of exercise. Glucose R(d) during exercise at HA (4.71 +/- 0.30 mg. kg(-1). min(-1)) was not different from SL exercise at the same absolute intensity (SL-50 = 5.03 mg. kg(-1). min(-1)) but was lower at the same relative intensity (SL-65 = 6.22 mg. kg(-1). min(-1), P < 0.01). There were no differences, however, when glucose R(d) was corrected for energy expended (kcal/min) during exercise. Respiratory exchange ratios followed the same pattern, except carbohydrate oxidation remained lower (-23.2%, P < 0.01) at HA than at SL when corrected for energy expended. In women, unlike in men, carbohydrate utilization decreased at HA. Relative abundance of estrogen and progesterone in women may partially explain the sex differences in fuel utilization at HA, but subtle differences between menstrual cycle phases at SL had no physiologically relevant effects.

In previous gender comparisons of muscle performance, men and women rarely have been closely matched, absolute force has not been equalized, and rates of fatigue and early recovery have not been determined. We compared adductor pollicis muscle performance at a similar absolute force development in healthy men and women (both n=9) matched for adductor pollicis maximal voluntary contraction (MVC) force (132 +/- 5 N for women and 136 +/- 4 N for men, mean +/- SE, P > 0.05). Subjects repeated static contractions at a target force of approximately 50% of MVC force of rested muscle (68 +/- 3 N or 51.9 +/- 1.0% MVC for women and 72 +/- 2 N or 53.0 +/- 2.0% MVC for men, P > 0.05) for 5 s followed by 5 s rest until exhaustion, i. e. inability to maintain the target force for 5 s. MVC force was measured following each minute of exercise, at exhaustion, and after each minute for 3 min of passive recovery. For women compared with men: MVC force fell less after 1 min of exercise (to 93 +/- 1% vs. 80 +/- 3% of MVC force of rested muscle, respectively, P < 0.05); MVC force (N min-1) fell approximately 2-fold slower (P < 0.05); and endurance time to exhaustion was nearly two times longer (14.7 +/- 1. 6 min vs. 7.9 +/- 0.7 min, P < 0.05). After declining to a similar level of MVC force of rested muscle at exhaustion (56 +/- 1% for women and 56 +/- 3% for men), MVC force rose faster in women than in men (to 71 +/- 2% vs. 65 +/- 3% of MVC force of rested muscle, respectively; P < 0.05) during the first minute of recovery. The findings are consistent with the hypothesis that slower adductor pollicis muscle fatigue in women is linked with differences between men and women both in impairment of force generating capacity, per se, and in rates of recovery between contractions.

We hypothesized that progesterone-mediated ventilatory stimulation during the midluteal phase of the menstrual cycle would increase exercise minute ventilation (VE; l/min) at sea level (SL) and with acute altitude (AA) exposure but would only increase arterial O2 saturation (SaO2, %) with AA exposure. We further hypothesized that an increased exercise SaO2 with AA exposure would enhance O2 transport and improve both peak O2 uptake (VO2 peak; ml x kg-1 x min-1) and submaximal exercise time to exhaustion (Exh; min) in the midluteal phase. Eight female lowlanders [33 +/- 3 (mean +/- SD) yr, 58 +/- 6 kg] completed a VO2 peak and Exh test at 70% of their altitude-specific VO2 peak at SL and with AA exposure to 4,300 m in a hypobaric chamber (446 mmHg) in their early follicular and midluteal phases. Progesterone levels increased (P < 0.05) approximately 20-fold from the early follicular to midluteal phase at SL and AA. Peak VE (101 +/- 17) and submaximal VE (55 +/- 9) were not affected by cycle phase or altitude. Submaximal SaO2 did not differ between cycle phases at SL, but it was 3% higher during the midluteal phase with AA exposure. Neither VO2 peak nor Exh time was affected by cycle phase at SL or AA. We conclude that, despite significantly increased progesterone levels in the midluteal phase, exercise VE is not increased at SL or AA. Moreover, neither maximal nor submaximal exercise performance is affected by menstrual cycle phase at SL or AA.

We hypothesized that, in women, the blood glucose response to a meal (BGR) would be lower after exposure to 4,300 m compared with sea level (SL) and that BGR would be reduced in the presence of estrogen plus progesterone (E+P) relative to estrogen alone (E). Sixteen women were studied in both the E and E+P conditions at SL and in either the E or E+P condition at 4,300 m. On day 9 in each condition, blood was sampled before, and every 30 min for 2 h after, the subjects ate a high-carbohydrate meal. At 4,300 m, BGR peaked at a lower value (5.73 +/- 0.94 mM) than at SL (6.44 +/- 1.45 mM) and returned to baseline more slowly (P < 0.05). Plasma insulin values were the same but C peptide was slightly higher at 4,300 m (P < 0. 05). At SL, BGR returned to baseline more slowly in E+P condition (5. 13 +/- 0.89 and 5.21 +/- 0.91 mM at 60 and 90 min, respectively) relative to E condition (4.51 +/- 0.52 and 4.69 +/- 0.88 mM, respectively) (P < 0.05). Insulin and C peptide were not different between E and E+P conditions. The data indicate that BGR is lower in women at high altitude compared with the SL, possibly due to greater suppression of hepatic glucose production or stimulation of peripheral glucose uptake by insulin. BGR was lower in E condition relative to E+P condition at SL and possibly at 4,300 m, but the relative concentrations of ovarian hormones do not appear to alter the magnitude of the change in BGR when women are exposed to high altitude.

Background: Exercise performance data of numerous altitude research studies and competitive sporting events of the last four decades are reviewed., Methods: The primary focus is on the wide interindividual variation associated with maximal and submaximal exercise performance that occurs at different altitudes and for different periods of time at altitude., Results: Fitness level, pre-exposure resident altitude, gender, and duration of altitude exposure are qualitatively assessed to determine their contribution to the overall variability. Of these, pre-altitude exposure fitness level difference contributes the most variability and gender difference contributes the least. It is also determined that beginning at an altitude of 580 m, maximal aerobic power (VO2max reduced and does not improve with extended exposure as long as the individual's level of fitness level is not altered significantly by increases in activity, exercise training or by altitude-induced physical deterioration. Submaximal exercise performance is also impaired at altitude., Conclusion: By assessing the performance of elite athletes, who are performing at an "all-out" effort in precisely timed events for which they are trained, it is determined that: a) the magnitude of submaximal exercise impairment is proportional to both the elevation and exercise duration at a given altitude; and b) submaximal exercise performance at altitude can improve with continued exposure without an increase in VO2max. Muscle strength, maximal muscle power, and anaerobic performance at altitude are not affected as long as muscle mass is maintained. In addition, performance is not impaired in athletic activities that have a minimal aerobic component and can be performed at high velocity (e.g., sprints).

Study Objective: To determine whether urinary leukotriene E4 (uLTE4) levels increase upon exposure to high altitude, and also to ascertain the relationship between uLTE4 levels and symptoms of acute mountain sickness (AMS)., Design: Prospective, unblinded, single-factor (altitude) experimental study., Settings: US Army research laboratory facilities at sea level ([SL] 50 m), 1,830 m, and 4,300 m., Participants: Eight healthy male subjects ranging in age from 19 to 24 years., Measurements: uLTE4 levels and symptoms of AMS were measured at just above SL (50 m), 3 1/2 days after being transported from SL to moderate altitude (MA) (1,830 m), and 1 1/2 days after ascent from 1,830 to 4,300 m (high altitude [HA]). Symptoms of AMS were assessed using standard indexes derived from the Environmental Symptoms Questionnaire weighted toward cerebral (AMS-C) and respiratory (AMS-R) manifestations. Oxygen saturation was measured noninvasively by pulse oximetry at SL and HA., Results: The mean (+/-SEM) uLTE4 levels (pg/mg creatinine) were 67.9 (+/-13.2) at SL; 82.3 (+/-5.5) at MA; and 134.8 (+/-19.4) at HA (p < 0.05 comparing HA with SL and MA)., Conclusions: We conclude that uLTE4 levels increase shortly after exposure to HA even after staging for 4 days at MA. Although this study does not clearly demonstrate a relationship between uLTE4 levels and symptoms of AMS, it supports the hypothesis that leukotrienes may be involved in the pathophysiologic state of AMS.

We studied sea-level residents during 13 days of altitude acclimatization to determine 1) altitude acclimatization effects on erythrocyte volume and plasma volume, 2) if exogenous erythrocyte volume expansion alters subsequent erythrocyte volume and plasma volume adaptations, 3) if an increased blood oxygen content alters erythropoietin responses during altitude acclimatization, and 4) mechanisms responsible for plasma loss at altitude. Sixteen healthy men had a series of hematologic measurements made at sea level, on the first and ninth days of altitude (4,300 m) residence, and after returning to sea level. Twenty-four hours before the ascent to altitude, one group received a 700-ml infusion of autologous erythrocytes (42% hematocrit), whereas the other group received only a saline infusion. Erythrocyte infusion increased erythrocyte volume by approximately 10%, whereas saline infusion had no effect; in addition, initially at altitude, blood oxygen content was 8% higher in erythrocyte-infused than in saline-infused subjects. The new findings regarding altitude acclimatization are summarized as follows: 1) erythrocyte volume does not change during the first 13 days and is not affected by prior exogenous expansion, 2) a modest increase in blood oxygen content does not modify erythropoietin responses, 3) plasma losses are related to vascular protein losses, and 4) exogenous erythrocyte volume expansion coincides with transient increases in plasma loss, vascular protein loss, and mean arterial pressure elevation. These findings better define human blood volume responses during altitude acclimatization.

This study investigated whether autologous erythrocyte infusion would ameliorate the decrement in maximal O2 uptake (VO2max) experienced by lowlanders when they ascend to high altitude. VO2max was measured in 16 men (treadmill running) at sea level (SL) and on the 1st (HA1) and 9th (HA9) days of high-altitude (4,300 m) residence. After VO2max was measured at SL, subjects were divided into two matched groups (n = 8). Twenty-four hours before ascent to high altitude, the experimental group received a 700-ml infusion of autologous erythrocytes and saline (42% hematocrit), whereas the control group received only saline. The VO2max of erythrocyte-infused [54 +/- 1 (SE) ml.kg-1.min-1] and control subjects (52 +/- 2 ml.kg-1.min-1) did not differ at SL before infusion. The decrement in VO2max on HA1 did not differ between groups, averaging 26% overall, despite higher (P < 0.01) arterial hematocrit, hemoglobin concentration, and arterial O2 content in the erythrocyte-infused subjects. By HA9, there were no longer any differences in hematocrit, hemoglobin concentration, or arterial O2 content between groups. No change in VO2max occurred between HA1 and HA9 for either group. Thus, despite increasing arterial O2-carrying capacity, autologous erythrocyte infusion did not ameliorate the decrement in VO2max at 4,300-m altitude.

Background: Acclimatization to high altitude appears to prevent acute mountain sickness (AMS), as evidenced by a decline in AMS symptoms as acclimatization progresses., Hypothesis: We hypothesized that partial retention of acclimatization would attenuate the incidence and/or severity of AMS upon reinduction to altitude., Methods: To test this hypothesis 6 male lowlanders returned to sea level after the acclimatizing of the 16 d at 4300 m (HA). After 8 d at sea level (PA), they were reexposed to 4300 m in a hypobaric chamber for 30 h (RA). AMS symptom severity was determined by the AMS-cerebral (AMS-C) scores calculated from the daily administration of the Environmental Symptoms Questionnaire during HA and RA., Results: The mean AMS-C scores were reduced from 0.6 on HA day 1 (HA1) to 0.1 during RA (p < 0.05). Four subjects were "sick" (AMS-C > 0.7) during HA1, while only one was "sick" during RA. The % oxyhemoglobin, hemoglobin concentration and hematocrit were higher during RA compared to HA1., Conclusions: These results suggest that the retention of acclimatization after 8 d at low altitude is sufficient to attenuate AMS upon reinduction to high altitude.

Large muscle exercise performance is impaired during acute exposure to normobaric or hypobaric hypoxia, but the effects of hypoxic conditions on fatigue of isolated smaller muscle groups per se are poorly defined. We studied how acute and chronic altitude (ALT) exposure and post-ALT return to sea level (SL) affects voluntary strength and fatigue of the adductor pollicis muscle. Eight healthy men (mean age 28 yr) were studied on five separate occasions: at SL, on days 1 (acute) and 13 (chronic) at ALT (4,300 m), and on days 1 (post 1) and 3 or 4 (post 2) at SL after 20 days of residence at ALT. On each day, maximal voluntary contractions (MVCs) of the adductor pollicis were obtained before and at the end of each minute of submaximal intermittent contractions of the adductor pollicis (50% of MVC of rested muscle, 5 s of contraction/5 s of rest) until exhaustion, defined as the inability to exert or maintain 50% of rested MVC. MVC of rested muscle did not differ among days. Time to exhaustion was shorter at acute ALT [5.1 +/- 0.5 (SE) min] than at SL (7.4 +/- 0.8 min, P < 0.05) and tended to be shorter than at chronic ALT (6.6 +/- 0.7 min, P > 0.05). Compared with acute and chronic ALT, time to exhaustion was prolonged during post 1 (9.0 +/- 1.2 min, P < 0.05) but not post 2 (6.1 +/- 0.5 min, P > 0.05). We conclude that 1) MVC of rested adductor pollicis muscle is not impaired during or after ALT exposure, 2) compared with SL conditions, acute but not chronic ALT exposure leads to a more rapid decline in adductor pollicis MVC associated with submaximal contractions, and 3) time to exhaustion is prolonged for > or = 1 day after return from ALT.