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The impact of acute mountain sickness (AMS) and sleep disturbances on mood and cognition at two altitudes relevant to the working and tourist population is unknown. Twenty unacclimatized lowlanders were exposed to either 3000 m (n = 10; 526 mmHg) or 4050 m (n = 10; 460 mmHg) for 20 h in a hypobaric chamber. AMS prevalence and severity was assessed using the Environmental Symptoms Questionnaire (ESQ) and an AMS-C score ≥ 0.7 indicated sickness. While sleeping for one night both at sea level (SL) and high altitude (HA), a wrist motion detector was used to measure awakenings (Awak, events/h) and sleep efficiency (Eff, %). If Eff was ≥85%, individuals were considered a good sleeper (Sleep+). Mood and cognition were assessed using the Automated Neuropsychological Assessment Metric and Mood Scale (ANAM-MS). The ESQ and ANAM-MS were administered in the morning both at SL and after 20 h at HA. AMS severity (mean ± SE; 1.82 ± 0.27 vs. 0.20 ± 0.27), AMS prevalence (90% vs. 10%), depression (0.63 ± 0.23 vs. 0.00 ± 0.24) Awak (15.6 ± 1.6 vs. 10.1 ± 1.6 events/h), and DeSHr (38.5 ± 6.3 vs. 13.3 ± 6.3 events/h) were greater (p < 0.05) and Eff was lower (69.9 ± 5.3% vs. 87.0 ± 5.3%) at 4050 m compared to 3000 m, respectively. AMS presence did not impact cognition but fatigue (2.17 ± 0.37 vs. 0.58 ± 0.39), anger (0.65 ± 0.25 vs. 0.02 ± 0.26), depression (0.63 ± 0.23 vs. 0.00 ± 0.24) and sleepiness (4.8 ± 0.4 vs. 2.7 ± 0.5) were greater (p < 0.05) in the AMS+ group. The Sleep- group, compared to the Sleep+ group, had lower (p < 0.05) working memory scores (50 ± 7 vs. 78 ± 9) assessed by the Sternberg 6-letter memory task, and lower reaction time fatigue scores (157 ± 17 vs. 221 ± 22), assessed by the repeated reaction time test. Overall, AMS, depression, DeSHr, and Awak were increased (p < 0.05) at 4050 m compared to 3000 m. In addition, AMS presence impacted mood while poor sleep impacted cognition which may deteriorate teamwork and/or increase errors in judgement at HA., (© Published 2022. This article is a U.S. Government work and is in the public domain in the USA. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.)

The impact of 2 days of staging at 2500-4300 m on sleep quality and quantity following subsequent exposure to 4300 m was determined. Forty-eight unacclimatized men and women were randomly assigned to stage for 2 days at one of four altitudes (2500, 3000, 3500, or 4300 m) prior to assessment on the summit of Pikes Peak (4300 m) for 2 days. Volunteers slept for one night at sea level (SL), two nights at respective staging altitudes, and two nights at Pikes Peak. Each wore a pulse oximeter to measure sleep arterial oxygen saturation (sSpO 2 , %) and number of desaturations (DeSHr, events/hr) and a wrist motion detector to estimate sleep awakenings (Awak, awakes/hr) and sleep efficiency (Eff, %). Acute mountain sickness (AMS) was assessed using the Environmental Symptoms Questionnaire and daytime SpO 2 was assessed after AMS measurements. The mean of all variables for both staging days (STG) and Pikes Peak days (PP) was calculated. The sSpO 2 and daytime SpO 2 decreased (p < 0.05) from SL during STG in all groups in a dose-dependent manner. During STG, DeSHr were higher (p < 0.05), Eff was lower (p < 0.05), and AMS symptoms were higher (p < 0.05) in the 3500 and 4300 m groups compared to the 2500 and 3000 m groups while Awak did not differ (p > 0.05) between groups. At PP, the sSpO 2 , DeSHr, Awak, and Eff were similar among all groups but the 2500 m group had greater AMS symptoms (p < 0.05) than the other groups. Two days of staging at 2500-4300 m induced a similar degree of sleep acclimatization during subsequent ascent to 4300 m but the 2500 m group was not protected against AMS at 4300 m., (Published 2021. This article is a U.S. Government work and is in the public domain in the USA. Physiological Reports published by Wiley Periodicals LLC on behalf of The Physiological Society and the American Physiological Society.)

Exercise-heat acclimation (EHA) induces adaptations that improve tolerance to heat exposure. Whether adaptations from EHA can also alter responses to hypobaric hypoxia (HH) conditions remains unclear. This study assessed whether EHA can alter time-trial performance and/or incidence of acute mountain sickness (AMS) during HH exposure. Thirteen sea-level (SL) resident men [SL peak oxygen consumption (V̇o 2peak ) 3.19 ± 0.43 L/min] completed steady-state exercise, followed by a 15-min cycle time trial and assessment of AMS before (HH1; 3,500 m) and after (HH2) an 8-day EHA protocol [120 min; 5 km/h; 2% incline; 40°C and 40% relative humidity (RH)]. EHA induced lower heart rate (HR) and core temperature and plasma volume expansion. Time-trial performance was not different between HH1 and HH2 after 2 h (106.3 ± 23.8 vs. 101.4 ± 23.0 kJ, P = 0.71) or 24 h (107.3 ± 23.4 vs. 106.3 ± 20.8 kJ, P > 0.9). From HH1 to HH2, HR and oxygen saturation, at the end of steady-state exercise and time-trial tests at 2 h and 24 h, were not different ( P > 0.05). Three of 13 volunteers developed AMS during HH1 but not during HH2, whereas a fourth volunteer only developed AMS during HH2. Heat shock protein 70 was not different from HH1 to HH2 at SL [1.9 ± 0.7 vs. 1.8 ± 0.6 normalized integrated intensities (NII), P = 0.97] or after 23 h (1.8 ± 0.4 vs. 1.7 ± 0.5 NII, P = 0.78) at HH. Our results indicate that this EHA protocol had little to no effect-neither beneficial nor detrimental-on exercise performance in HH. EHA may reduce AMS in those who initially developed AMS; however, studies at higher elevations, having higher incidence rates, are needed to confirm our findings.

Coffman, KE, Luippold, AJ, Salgado, RM, Heavens, KR, Caruso, EM, Fulco, CS, and Kenefick, RW. Aerobic exercise performance during load carriage and acute altitude exposure. J Strength Cond Res 34(4): 946-951, 2020-This study quantified the impact of combined load carriage and acute altitude exposure on 5-km running time-trial (TT) performance and self-selected pacing strategy. Furthermore, this study developed a velocity prediction tool (nomogram) for similar aerobic exercise tasks performed under various combinations of altitude and load stress. Nine volunteers (6M/3F, age: 24 ± 7 years, height: 171 ± 6 cm, body mass: 72 ± 7 kg, and V[Combining Dot Above]O2peak: 50.5 ± 5.2 ml·min·kg) completed a randomized, repeated-measures design protocol. Volunteers performed 3 familiarization (FAM) trials at sea level (SL; 250 m) with no-load carriage. Experimental testing included 3 self-paced, blinded 5-km running TT on a treadmill while carrying a 30% body mass external load at SL, moderate altitude (MA; 2000 m), and high altitude (HA; 3000 m). At SL, load carriage resulted in a 36% decrement in 5-km exercise performance in comparison with FAM trials (43 ± 7 vs. 32 ± 3 minutes; p < 0.001). Time required to complete the 5-km distance while carrying an external load was increased by 11% when performed at HA vs. SL (48 ± 7 vs. 43 ± 7 minutes; p = 0.001). TT pace was not different among experimental conditions (load carriage at SL, MA, and HA) until after 1 km of the running distance had been completed. Heart rate was not different among experimental conditions throughout the entire TT (170 ± 17 b·min). These data quantify the anticipated reduction in aerobic exercise performance under various combinations of acute altitude exposure and load carriage conditions. The self-paced running TT approach used presently allowed for development of an altitude-load nomogram for use in recreational, occupational, or military settings.

Acetazolamide (AZ) is a medication commonly used to prevent acute mountain sickness (AMS) during rapid ascent to high altitude. However, it is unclear whether AZ use impairs exercise performance; previous literature regarding this topic is equivocal. The purpose of this study was to evaluate the impact of AZ on time-trial (TT) performance during a 30-h exposure to hypobaric hypoxia equivalent to 3,500-m altitude. Ten men [sea-level peak oxygen consumption (VO 2 peak): 50.8 ± 6.5 mL·kg -1 ·min -1 ; body fat %: 20.6 ± 5.2%] completed 2 30-h exposures at 3,500 m. In a crossover study design, subjects were given 500 mg/day of either AZ or a placebo. Exercise testing was completed 2 h and 24 h after ascent and consisted of 15-min steady-state treadmill walking at 40%-45% sea-level VO 2 peak, followed by a 2-mile self-paced treadmill TT. AMS was assessed after ~12 h and 22 h at 3,500 m. The incidence of AMS decreased from 40% with placebo to 0% with AZ. Oxygen saturation was higher ( P < 0.05) in AZ versus placebo trials at the end of the TT after 2 h (85 ± 3% vs. 79 ± 3%) and 24 h (86 ± 3% vs. 81 ± 4%). There was no difference in time to complete 2 miles between AZ and PL after 2 h (20.7 ± 3.2 vs. 22.7 ± 5.0 min, P > 0.05) or 24 h (21.5 ± 3.4 vs. 21.1 ± 2.9 min, P > 0.05) of exposure to altitude. Our results suggest that AZ (500 mg/day) does not negatively impact endurance exercise performance at 3,500 m. NEW & NOTEWORTHY To our knowledge, this is the first study to examine the impact of acetazolamide (500 mg/day) versus placebo on self-paced, peak-effort exercise performance using a short-duration exercise test in a hypobaric hypoxic environment with a repeated-measures design. In the present study, acetazolamide did not impact exercise performance after 2-h or 24-h exposure to 3,500-m simulated altitude.

Medical personnel need practical guidelines on how to construct high altitude ascents to induce altitude acclimatization and avoid acute mountain sickness (AMS) following the first night of sleep at high altitude. Using multiple logistic regression and a comprehensive database, we developed a quantitative prediction model using ascent profile as the independent variable and altitude acclimatization status as the dependent variable from 188 volunteers (147 men, 41 women) who underwent various ascent profiles to 4 km. The accumulated altitude exposure (AAE), a new metric of hypoxic dose, was defined as the ascent profile and was calculated by multiplying the altitude elevation (km) by the number of days (d) at that altitude prior to ascent to 4 km. Altitude acclimatization status was defined as the likely presence or absence of AMS after ~24 h of exposure at 4 km. AMS was assessed using the Cerebral Factor Score (AMS-C) from the Environmental Symptoms Questionnaire and deemed present if AMS-C was ≥0.7. Other predictor variables included in the model were age and body mass index (BMI). Sex, race, and smoking status were considered in model development but eliminated due to inadequate numbers in each of the ascent profiles. The AAE (km·d) significantly (P < 0.0001) predicted AMS in the model. For every 1 km·d increase in AAE, the odds of getting sick decreased by 41.3%. Equivalently, for every 1 km·d decrease in AAE, the odds of getting sick increased by 70.4%. Age and BMI were not significant predictors. The model demonstrated excellent discrimination (AUC = 0.83 (95% CI = 0.79-0.91) and calibration (Hosmer-Lemeshow = 0.11). The model provides a priori estimates of altitude acclimatization status resulting from the use of various rapid, staged, and graded ascent profiles., (© 2019 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.)

Heat and hypobaric hypoxia independently compromise exercise performance; however, their combined impact on exercise performance has yet to be quantified. This study examined the effects of heat, hypobaric hypoxia, and the combination of these environments on self-paced cycling time trial (TT) performance. Twelve subjects [2 female, 10 male; sea level (SL) peak oxygen consumption (V̇o 2peak ), 41.5 ± 4.4 mL·kg -1 ·min -1 , mean ± SD] completed 30 min of steady-state cycling exercise (50% SL V̇o 2peak ), followed by a 15-min self-paced TT in four environmental conditions: SL thermoneutral [SLTN; 250 m, 20°C, 30-50% relative humidity (rh)], SL hot (SLH; 250 m, 35°C, 30% rh), hypobaric hypoxia thermoneutral (HTN; 3,000 m, 20°C, 30-50% rh), and hypobaric hypoxia hot (HH; 3,000 m, 35°C, 30% rh). Performance was assessed by the total work (kJ) completed. TT performance was lower ( P < 0.05) in SLH, HTN, and HH relative to SLTN (-15.4 ± 9.7, -24.1 ± 16.2, and -33.1 ± 13.4 kJ, respectively). Additionally, the total work completed in HTN and HH was lower ( P < 0.05) than that in SLH. In SLH, HTN, and HH, work rate was reduced versus SLTN ( P < 0.05) within the first 3 min of exercise and was consistent for the remainder of the bout. No differences ( P > 0.05) existed for heart rate or Ratings of Perceived Exertion at the end of exercise among conditions. The decrease in self-paced TT performance in the heat and/or hypobaric hypoxia conditions compared with SLTN conditions resulted from a nearly immediate reduction in work rate that may have been regulated by environmentally induced changes in physiological strain and perception of effort in response to TT exercise. NEW & NOTEWORTHY This is the first known study to examine the combined effects of heat and hypobaric hypoxia on short-duration self-paced cycling time trial performance. Regardless of environmental condition, subjects utilized an even work rate for the entire duration of the time trial. The presence of both environmental stressors led to a greater performance impairment than heat or hypobaric hypoxia alone, and the performance decrement stemmed from an early reduction of work rate.

Purpose: To determine the efficacy residing for 2 d at various altitudes while sedentary (S) or active (A; ~90 min hiking 2 d) on exercise performance at 4300 m., Methods: Sea-level (SL) resident men (n = 45) and women (n = 21) (mean ± SD; 23 ± 5 yr; 173 ± 9 cm; 73 ± 12 kg; V˙O2peak = 49 ± 7 mL·kg·min) were randomly assigned to a residence group and, S or A within each group: 2500 m (n = 11S, 8A), 3000 m (n = 6S, 12A), 3500 m (n = 6S, 8A), or 4300 m (n = 7S, 8A). Exercise assessments occurred at SL and 4300 m after 2-d residence and consisted of 20 min of steady-state (SS) treadmill walking (45% ± 3% SL V˙O2peak) and a 5-mile, self-paced running time trial (TT). Arterial oxygen saturation (SpO2) and HR were recorded throughout exercise. Resting SpO2 was recorded at SL, at 4 and 46 h of residence, and at 4300 m before exercise assessment. To determine if 2-d altitude residence improved 4300 m TT performance, results were compared with estimated performances using a validated prediction model., Results: For all groups, resting SpO2 was reduced (P < 0.01) after 4 h of residence relative to SL inversely to the elevation and did not improve after 46 h. Resting SpO2 (~83%) did not differ among groups at 4300 m. Although SL and 4300 m SS exercise SpO2 (97% ± 2% to 74% ± 4%), HR (123 ± 10 bpm to 140 ± 12 bpm) and TT duration (51 ± 9 to 73 ± 16 min) were different (P < 0.01), responses at 4300 m were similar among all groups, as was actual and predicted 4300 m TT performances (74 ± 12 min)., Conclusions: Residing for 2 d at 2500 to 4300 m, with or without daily activity, did not improve resting SpO2, SS exercise responses, or TT performance at 4300 m.

Objective: To determine whether 2 days of staging at 2500-3500 m, combined with either high or low physical activity, reduces acute mountain sickness (AMS) during subsequent ascent to 4300 m., Methods: Three independent groups of unacclimatized men and women were staged for 2 days at either 2500 m (n = 18), 3000 m (n = 16), or 3500 m (n = 15) before ascending and living for 2 days at 4300 m and compared with a control group that directly ascended to 4300 m (n = 12). All individuals departed to the staging altitudes or 4300 m after spending one night at 2000 m during which they breathed supplemental oxygen to simulate sea level conditions. Half in each group participated in ∼3 hours of daily physical activity while half were sedentary. Women accounted for ∼25% of each group. AMS incidence was assessed using the Environmental Symptoms Questionnaire. AMS was classified as mild (≥0.7 and <1.5), moderate (≥1.5 and <2.6), and severe (≥2.6)., Results: While staging, the incidence of AMS was lower (p < 0.001) in the 2500 m (0%), 3000 m (13%), and 3500 m (40%) staged groups than the direct ascent control group (83%). After ascent to 4300 m, the incidence of AMS was lower in the 3000 m (43%) and 3500 m (40%) groups than the 2500 m group (67%) and direct ascent control (83%). Neither activity level nor sex influenced the incidence of AMS during further ascent to 4300 m., Conclusions: Two days of staging at either 3000 or 3500 m, with or without physical activity, reduced AMS during subsequent ascent to 4300 m but staging at 3000 m may be recommended because of less incidence of AMS.

Although it has been shown that muscle sympathetic nerve activity increases during high altitude exposure, mechanisms of sympathoexcitation and blood pressure control after return from altitude are not well described. We hypothesized that: (1) living for 12days at 4300m (Pikes Peak, Colorado) would result in increased muscle sympathetic nerve activity 24h after return to sea level; (2) post-Pikes Peak sympathetic neural and hemodynamic responses to orthostasis would be decreased due to a potential 'ceiling effect' on sympathetic activity; and (3) the magnitude of individual increases in sympathetic nerve activity post-Pikes Peak would be inversely related to baseline sympathetic nerve activity before traveling to altitude. Muscle sympathetic nerve activity, heart rate and blood pressure were measured in 9 healthy individuals (24±8years) in supine, 30° and 45° head-up tilt positions. Measurements were conducted twice at sea level, once before (pre-Pikes Peak) a 12day residence at 4300m, and once within 24h of return (post-Pikes Peak). Supine muscle sympathetic nerve activity was higher (post: 27±5 vs pre: 17±6bursts/min) upon return from altitude (p<0.05). Individual values for pre-Pikes Peak sympathetic activity were inversely related to post-altitude sympathoexcitation (r=-0.69, p<0.05). There were no differences in neural or cardiovascular responses to tilt between pre and post- Pikes Peak (p>0.05). We conclude that 12days' residence at 4300m causes a sustained sympathoexcitation which does not impair the ability of muscle sympathetic nerves to respond appropriately to orthostasis., (Published by Elsevier B.V.)

This study examined whether normobaric hypoxia (NH) treatment is more efficacious for sustaining high-altitude (HA) acclimatization-induced improvements in ventilatory and hematologic responses, acute mountain sickness (AMS), and cognitive function during reintroduction to altitude (RA) than no treatment at all. Seventeen sea-level (SL) residents (age = 23 ± 6 yr; means ± SE) completed in the following order: 1 ) 4 days of SL testing; 2 ) 12 days of HA acclimatization at 4,300 m; 3 ) 12 days at SL post-HA acclimatization (Post) where each received either NH ( n = 9, [Formula: see text] = 0.122) or Sham ( n = 8; [Formula: see text] = 0.207) treatment; and 4 ) 24-h reintroduction to 4,300-m altitude (RA) in a hypobaric chamber (460 Torr). End-tidal carbon dioxide pressure ([Formula: see text]), hematocrit (Hct), and AMS cerebral factor score were assessed at SL, on HA2 and HA11, and after 20 h of RA. Cognitive function was assessed using the SynWin multitask performance test at SL, on HA1 and HA11, and after 4 h of RA. There was no difference between NH and Sham treatment, so data were combined. [Formula: see text] (mmHg) decreased from SL (37.2 ± 0.5) to HA2 (32.2 ± 0.6), decreased further by HA11 (27.1 ± 0.4), and then increased from HA11 during RA (29.3 ± 0.6). Hct (%) increased from SL (42.3 ± 1.1) to HA2 (45.9 ± 1.0), increased again from HA2 to HA11 (48.5 ± 0.8), and then decreased from HA11 during RA (46.4 ± 1.2). AMS prevalence (%) increased from SL (0 ± 0) to HA2 (76 ± 11) and then decreased at HA11 (0 ± 0) and remained depressed during RA (17 ± 10). SynWin scores decreased from SL (1,615 ± 62) to HA1 (1,306 ± 94), improved from HA1 to HA11 (1,770 ± 82), and remained increased during RA (1,707 ± 75). These results demonstrate that HA acclimatization-induced improvements in ventilatory and hematologic responses, AMS, and cognitive function are partially retained during RA after 12 days at SL whether or not NH treatment is utilized. NEW & NOTEWORTHY This study demonstrates that normobaric hypoxia treatment over a 12-day period at sea level was not more effective for sustaining high-altitude (HA) acclimatization during reintroduction to HA than no treatment at all. The noteworthy aspect is that athletes, mountaineers, and military personnel do not have to go to extraordinary means to retain HA acclimatization to an easily accessible and relevant altitude if reexposure occurs within a 2-wk time period.

Purpose: The objective of this study is to develop a quantitative model that can be used before ascent to altitude (ALT) to predict how much longer a sustained physical task would take for unacclimatized individuals in the early hours of exposure., Methods: Using multiple linear regression, we analyzed time-trial (TT) performance on 95 unacclimatized men (n = 83) and women (n = 12) at sea level (SL) and at an ALT ranging from 2500 to 4300 m. The TT was initiated within 4 h of ascent to ALT. The independent variables known before ascent were as follows: ALT, age, height, weight, sex, SL peak oxygen uptake, SL task duration time, and body mass index (BMI) classification (normal weight vs overweight). The dependent variable was the percent increase in TT duration from SL to ALT., Results: The most significant factor in the model was ALT (P = 0.0001), followed by BMI classification (P = 0.0009) and the interaction between BMI classification and ALT (P = 0.003). The model is as follows: percent increase in TT duration = [100 + e(-1.517+1.323 (ALT)+3.124 (BMI class)-0.769 (ALT) (BMI class)]. The percent increase in TT duration in overweight individuals was 129% greater than for normal-weight individuals at 3000 m. However, as ALT increased beyond 3000 m, the disparity between groups decreased until 4050 m where the percent increase in TT duration became greater for normal-weight individuals., Conclusions: This model provides the first quantitative estimates of the percent increase in sustained physical task duration during initial exposure to a wide range of elevations. Because only two easily obtainable factors are required as inputs for the model (ALT and BMI classification), this model can be used by many unacclimatized individuals to better plan their activities at ALT.

Background: The purpose of this study was to determine whether cycling time trial (TT) performance differs between hypobaric hypoxia (HH) and normobaric hypoxia (NH) at the same ambient PO2 (93 mmHg, 4,300-m altitude equivalent)., Methods: Two groups of healthy fit men were matched on physical performance and demographic characteristics and completed a 720-kJ time trial on a cycle ergometer at sea level (SL) and following approximately 2 h of resting exposure to either HH (n = 6, 20 ± 2 years, 75.2 ± 11.8 kg, mean ± SD) or NH (n = 6, 21 ± 3 years, 77.4 ± 8.8 kg). Volunteers were free to manually increase or decrease the work rate on the cycle ergometer. Heart rate (HR), arterial oxygen saturation (SaO2), and rating of perceived exertion (RPE) were collected every 5 min during the TT, and the mean was calculated., Results: Both groups exhibited similar TT performance (min) at SL (73.9 ± 7.6 vs. 73.2 ± 8.2), but TT performance was longer (P < 0.05) in HH (121.0 ± 12.1) compared to NH (99.5 ± 18.1). The percent decrement in TT performance from SL to HH (65.1 ± 23.6%) was greater (P < 0.05) than that from SL to NH (35.5 ± 13.7%). The mean exercise SaO2, HR, and RPE during the TT were not different in HH compared to NH., Conclusion: Cycling time trial performance is impaired to a greater degree in HH versus NH at the same ambient PO2 equivalent to 4,300 m despite similar cardiorespiratory responses.

Background: The purposes were to determine the following: 1) the threshold between 2500-4300 m at which simple and complex military task performance is degraded; 2) whether the degree of degradation, if any, is related to changes in altitude illness, fatigue, or sleepiness at a given altitude; and 3) whether the level of hypoxemia, independent of altitude, affects simple and complex military task performance., Methods: There were 57 lowlanders (mean +/- SD; 22 +/- 3 yr; 79 +/- 12 kg) who were exposed to either 2500 m (N = 17), 3000 m (N = 12), 3500 m (N = 11), or 4300 m (N = 17). Disassembly and reassembly of a weapon (DsAs, simple), rifle marksmanship (RM, complex), acute mountain sickness (AMS), fatigue, sleepiness, and arterial oxygen saturation (SaO2) were measured at sea level (SL), and after 8 h (HA8) and 30 h (HA30) of exposure to each altitude., Results: DsAs did not change from SL to HA8 or HA30 at any altitude. RM speed (target/min) decreased from SL (20 +/- 1.5) to HA8 (17 +/- 1.5) and HA30 (17 +/- 3) only at 4300 m. AMS, fatigue, and sleepiness were increased and SaO2 was decreased at 2500 m and above. Increased sleepiness was the only variable associated with decreased RM speed at 4300 m (r = -0.67; P = 0.004). Greater hypoxemia, independent of altitude, was associated with greater decrements in RM speed (r = 0.27; P = 0.04)., Conclusions: Simple psychomotor performance was not affected by exposures between 2500-4300 m; however, complex psychomotor performance (i.e., RM speed) was degraded at 4300 m most likely due to increased sleepiness. Greater levels of hypoxemia were associated with greater decrements in RM speed.

Purpose: Despite decades of research, no predictive models of acute mountain sickness (AMS) exist, which identify the time course of AMS severity and prevalence following rapid ascent to various altitudes., Methods: Using general linear and logistic mixed models and a comprehensive database, we analyzed 1292 AMS cerebral factor scores in 308 unacclimatized men and women who spent between 4 and 48 h at altitudes ranging from 1659 to 4501 m under experimentally controlled conditions (low and high activity). Covariates included in the analysis were altitude, time at altitude, activity level, age, body mass index, race, sex, and smoking status., Results: AMS severity increased (P < 0.05) nearly twofold (i.e., 179%) for every 1000-m increase in altitude at 20 h of exposure, peaked between 18 and 22 h of exposure, and returned to initial levels by 48 h of exposure regardless of sex or activity level. Peak AMS severity scores were 38% higher (P < 0.05) in men compared with women at 20 h of exposure. High active men and women (>50% of maximal oxygen uptake for >45 min at altitude) demonstrated a 72% increase (P < 0.05) in the odds (odds ratio, 1.72; confidence interval, 1.03-3.08) of AMS compared with low active men and women. There was also a tendency (P = 0.10) for men to demonstrate greater odds of AMS (odds ratio, 1.65; confidence interval, 0.84-3.25) compared with women. Age, body mass index, race, and smoking status were not significantly associated with AMS., Conclusions: These models provide the first quantitative estimates of AMS risk over a wide range of altitudes and time points and suggest that in addition to altitude and time at altitude, high activity increases the risk of developing AMS. In addition, men demonstrated increased severity but not prevalence of AMS.

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.

Acute mountain sickness (AMS) and large decrements in endurance exercise performance occur when unacclimatized individuals rapidly ascend to high altitudes. Six altitude and hypoxia preacclimatization strategies were evaluated to determine their effectiveness for minimizing AMS and improving performance during altitude exposures. Strategies using hypobaric chambers or true altitude were much more effective overall than those using normobaric hypoxia (breathing, <20.9% oxygen).

There is an expectation that repeated daily exposures to normobaric hypoxia (NH) will induce ventilatory acclimatization and lessen acute mountain sickness (AMS) and the exercise performance decrement during subsequent hypobaric hypoxia (HH) exposure. However, this notion has not been tested objectively. Healthy, unacclimatized sea-level (SL) residents slept for 7.5 h each night for 7 consecutive nights in hypoxia rooms under NH [n = 14, 24 ± 5 (SD) yr] or "sham" (n = 9, 25 ± 6 yr) conditions. The ambient percent O(2) for the NH group was progressively reduced by 0.3% [150 m equivalent (equiv)] each night from 16.2% (2,200 m equiv) on night 1 to 14.4% (3,100 m equiv) on night 7, while that for the ventilatory- and exercise-matched sham group remained at 20.9%. Beginning at 25 h after sham or NH treatment, all subjects ascended and lived for 5 days at HH (4,300 m). End-tidal Pco(2), O(2) saturation (Sa(O(2))), AMS, and heart rate were measured repeatedly during daytime rest, sleep, or exercise (11.3-km treadmill time trial). From pre- to posttreatment at SL, resting end-tidal Pco(2) decreased (P < 0.01) for the NH (from 39 ± 3 to 35 ± 3 mmHg), but not for the sham (from 39 ± 2 to 38 ± 3 mmHg), group. Throughout HH, only sleep Sa(O(2)) was higher (80 ± 1 vs. 76 ± 1%, P < 0.05) and only AMS upon awakening was lower (0.34 ± 0.12 vs. 0.83 ± 0.14, P < 0.02) in the NH than the sham group; no other between-group rest, sleep, or exercise differences were observed at HH. These results indicate that the ventilatory acclimatization induced by NH sleep was primarily expressed during HH sleep. Under HH conditions, the higher sleep Sa(O(2)) may have contributed to a lessening of AMS upon awakening but had no impact on AMS or exercise performance for the remainder of each day.

Hypoxia often causes body water deficits (hypohydration, HYPO); however, the effects of HYPO on aerobic exercise performance and prevalence of acute mountain sickness (AMS) at high altitude (ALT) have not been reported. We hypothesized that 1) HYPO and ALT would each degrade aerobic performance relative to sea level (SL)-euhydrated (EUH) conditions, and combining HYPO and ALT would further degrade performance more than one stressor alone; and 2) HYPO would increase the prevalence and severity of AMS symptoms. Seven lowlander men (25 ± 7 yr old; 82 ± 11 kg; mean ± SD) completed four separate experimental trials. Trials were 1) SL-EUH, 2) SL-HYPO, 3) ALT-EUH, and 4) ALT-HYPO. In HYPO, subjects were dehydrated by 4% of body mass. Subjects maintained hydration status overnight and the following morning entered a hypobaric chamber (at SL or 3,048 m, 27°C) where they completed 30 min of submaximal exercise immediately followed by a 30-min performance time trial (TT). AMS was measured with the Environmental Symptoms Questionnaire-Cerebral Score (AMS-C) and the Lake Louise Scoring System (LLS). The percent change in TT performance, relative to SL-EUH, was -19 ± 12% (334 ± 64 to 278 ± 87 kJ), -11 ± 10% (334 ± 64 to 293 ± 33 kJ), and -34 ± 22% (334 ± 64 to 227 ± 95 kJ), for SL-HYPO, ALT-EUH, and ALT-HYPO, respectively. AMS symptom prevalence was 2/7 subjects at ALT-EUH for AMS-C and LLS and 5/7 and 4/7 at ALT-HYPO for AMS-C and LLS, respectively. The AMS-C symptom severity score (AMS-C score) tended to increase from ALT-EUH to ALT-HYPO but was not significant (P = 0.07). In conclusion, hypohydration at 3,048 m 1) degrades aerobic performance in an additive manner with that induced by ALT; and 2) did not appear to increase the prevalence/severity of AMS symptoms.

For many low-altitude (<1500 m) residents, their travel itineraries may cause them to ascend rapidly to high (>2400 m) altitudes without having the time to develop an adequate degree of altitude acclimatization. Prior to departing on these trips, low-altitude residents can induce some degree of altitude acclimatization by ascending to moderate (>1500 m) or high altitudes during either continuous or intermittent altitude preexposures. Generally, the degree of altitude acclimatization developed is proportional to the altitude attained and the duration of exposure. The available evidence suggests that continuous residence at 2200 m or higher for 1 to 2 days or daily 1.5- to 4-h exposures to >4000 m induce ventilatory acclimatization. Six days at 2200 m substantially decreases acute mountain sickness (AMS) and improves work performance after rapid ascent to 4300 m. There is evidence that 5 or more days above 3000 m within the last 2 months will significantly decrease AMS during a subsequent rapid ascent to 4500 m. Exercise training during the altitude preexposures may augment improvement in physical performance. The persistence of altitude acclimatization after return to low altitude appears to be proportional to the degree of acclimatization developed. The subsequent ascent to high altitude should be scheduled as soon as possible after the last altitude preexposure.

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.

Purpose: This study examined the effect of 1 wk of normobaric intermittent hypoxic exposure (IHE) combined with exercise training on endurance performance at a 4300-m altitude (HA)., Methods: Seventeen male lowlanders were divided into an IHE (n = 11) or SHAM (n = 6) group. Each completed cycle endurance testing consisting of two 20-min steady state (SS) exercise bouts (at 40% and 60% V O2peak) followed by a 10-min break and then a 720-kJ cycle time trial at HA before IHE or SHAM treatment (Pre-T). IHE treatment consisted of a 2-h rest at a PO2 of 90 mm Hg followed by two 25-min bouts of exercise at approximately 80% of peak HR at a PO2 of 110 mm Hg for 1 wk in a hypoxia room. SHAM treatment was identical except that the PO2 was 148 mm Hg for both rest and exercise. After IHE or SHAM treatment (Post-T), all completed a second cycle endurance test at HA. HR, arterial oxygen saturation (SaO2), and RPE were obtained from the 10th to the 15th minute during the two SS exercise bouts and every 5 min during the time trial., Results: Seven volunteers in the IHE group could not finish the 720-kJ time trial either at Pre-T or at Post-T. Time trial analysis was limited, therefore, to the time to reach 360 kJ (halfway point) for all volunteers. From Pre-T to Post-T, there was no improvement in time trial performance (min +/- SE) in the IHE (62.0 +/- 4.8 to 63.7 +/- 5.2) or SHAM (60.9 +/- 6.3 to 54.2 +/- 6.8) group. There was no change from Pre-T to Post-T in HR, SaO2, and RPE during the two SS exercise bouts or time trial in either group., Conclusions: One week of IHE combined with exercise training does not improve endurance performance at a 4300-m altitude in male lowlanders.

The purpose of this study was to determine in sea-level residents if 6 to 7 consecutive days of normobaric intermittent hypoxic exposure (IHE) (hypoxia room: 2-h ambient PO2=90 mmHg sedentary and 1-h ambient PO2=110 mmHg exercising at 80+/-5% of maximum heart rate) improved sleep quality (awakenings per hour) and quantity at altitude (4300 m). We hypothesized that IHE would improve sleep arterial oxygen saturation (SaO2) levels and decrease desaturation events, thereby contributing to improvements in sleep quality and quantity during subsequent exposure to high altitude. Ten sea-level residents (mean+/-SE: 22+/-1 yr, 179+/-2 cm, 79+/-3 kg) were assigned to an IHE group and six to a SHAM group (20+/-0.5 yr, 180+/-3 cm, 77+/-4 kg). Sleep quantity, SaO2, and heart rate (HR) were monitored at sea level and during high altitude (i.e., 4300 m in a hypobaric chamber) before pretest (PRE-T) and 60 h after posttest (POST-T) for the last IHE or SHAM treatment. Over the 6 to 7 days of IHE, resting SaO2 increased from 75+/-1% to 81+/-3% in the IHE group, while the SHAM group remained at 98+/-1%. From PRE-T to POST-T at 4300-m exposure, both the IHE and SHAM groups had significantly higher sleep SaO2, fewer desaturation events per hour, and an increase in the percentage of time asleep while sleeping (sleep percent). The IHE group, but not the SHAM group, had significantly lower sleep HR and a trend to more awakenings during the POST-T 4300-m exposure. These results indicate that although IHE treatment induced significant ventilatory acclimatization, relative to the SHAM group, IHE did not further improve sleep SaO2 quality and quantity following rapid ascent to 4300 m. Rather, it is likely that the acquired ventilatory acclimatization was lost in the 60 h between the last IHE session and the POST-T altitude exposure.

We sought to describe cerebrovascular responses to incremental exercise and test the hypothesis that changes in cerebral oxygenation influence maximal performance. Eleven men cycled in three conditions: 1) sea level (SL); 2) acute hypoxia [AH; hypobaric chamber, inspired Po(2) (Pi(O(2))) 86 Torr]; and 3) chronic hypoxia [CH; 4,300 m, Pi(O(2)) 86 Torr]. At maximal work rate (W(max)), fraction of inspired oxygen (Fi(O(2))) was surreptitiously increased to 0.60, while subjects were encouraged to continue pedaling. Changes in cerebral (frontal lobe) (C(OX)) and muscle (vastus lateralis) oxygenation (M(OX)) (near infrared spectroscopy), middle cerebral artery blood flow velocity (MCA V(mean); transcranial Doppler), and end-tidal Pco(2) (Pet(CO(2))) were analyzed across %W(max) (significance at P < 0.05). At SL, Pet(CO(2)), MCA V(mean), and C(OX) fell as work rate rose from 75 to 100% W(max). During AH, Pet(CO(2)) and MCA V(mean) declined from 50 to 100% W(max), while C(OX) fell from rest. With CH, Pet(CO(2)) and C(OX) dropped throughout exercise, while MCA V(mean) fell only from 75 to 100% W(max). M(OX) fell from rest to 75% W(max) at SL and AH and throughout exercise in CH. The magnitude of fall in C(OX), but not M(OX), was different between conditions (CH > AH > SL). Fi(O(2)) 0.60 at W(max) did not prolong exercise at SL, yet allowed subjects to continue for 96 +/- 61 s in AH and 162 +/- 90 s in CH. During Fi(O(2)) 0.60, C(OX) rose and M(OX) remained constant as work rate increased. Thus cerebral hypoxia appeared to impose a limit to maximal exercise during hypobaric hypoxia (Pi(O(2)) 86 Torr), since its reversal was associated with improved performance.

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.

Recent studies have demonstrated that brief daily IAE (intermittent altitude exposure) was equally as effective as continuous altitude residence in inducing physiological adaptations consistent with altitude acclimatization. Although the positive benefits of IAE have been clearly defined, the potential negative consequences of IAE on health, specifically the immune system, remain undefined. The present study determined the effects of IAE on WBC (white blood cell) and hormonal responses during rest and exercise at 4300 m altitude. Six lowlanders (age, 23+/-2 years; body weight, 77+/-6 kg; values are means+/-S.E.M.) completed a VO(2)max (maximal O(2) uptake) and submaximal cycle ergometer test during a 30-h SL (sea level) exposure and during a 30 h exposure to 4300 m altitude-equivalent once before (PreIAE) and once after (PostIAE) a 3-week period of IAE (4 hxday(-1), 5 daysxweek(-1), 4300 m). The submaximal cycle ergometer test consisted of two consecutive 15-min work bouts at 40% and 70% of altitude-specific VO(2)max. Blood samples were obtained at rest and during both exercise work bouts for measurements of WBC count, leucocyte subset counts, cortisol, adrenaline (epinephrine) and noradrenaline (norepinephrine). WBC, neutrophil and lymphocyte counts increased significantly (P<0.05) during rest and exercise from SL to PreIAE and decreased (P<0.05) during rest and exercise from PreIAE to PostIAE. Monocyte counts decreased (P<0.05) during rest and exercise from PreIAE to PostIAE, but eosinophil and basophil counts did not change. Cortisol, adrenaline and noradrenaline did not change during rest or exercise from SL to PreIAE or PostIAE, but all increased significantly (P<0.05) from rest during the two work bouts. In conclusion, this type of IAE stimulus did not induce a hormonal stress response and did no harm in terms of activation of the immune system at altitude, as measured by WBC and leucocyte subset counts. This method of pre-acclimatization can therefore be highly recommended for inducing altitude acclimatization without the 'altitude residency' requirement.

Purpose: To determine whether creatine (Cr) supplementation improves muscle performance during exposure to acute hypobaric hypoxia., Methods: Seven healthy men (28 +/- 6 yr, mean +/- SD) performed submaximal intermittent static knee contractions interspersed with maximal voluntary contractions (MVCs) every minute to exhaustion (approximately 50% of rested MVC force) in normoxia and hypobaric hypoxia (separated by 3 d) after supplementation with Cr (20 g.d(-1) for 7 d then 5 g.d(-1) for 4-7 d) or placebo (Pla) in a double-blind, randomized crossover study. A 5-wk period without supplementation separated treatments. Each test day, subjects performed two bouts (separated by 2 min) at their preset submaximal force, 32 +/- 4% rested MVC)., Results: Rested MVC force (860 +/- 66 N) and MVC force at exhaustion (396 +/- 27 N; 47 +/- 3% rested MVC) did not differ among treatments or environments (P > 0.05). For bout 1, endurance time was shorter in hypobaria (26 +/- 3 min) than normoxia (34 +/- 2 min) (P < 0.01), but did not differ between Cr (27 +/- 3 min) and Pla (33 +/- 3 min) (P > 0.05). MVC force returned to similar levels (P >0.05) in bout 2 after recovery in all four sessions (to approximately 615 N). For bout 2, endurance time also was shorter in hypobaria (7 +/- 1 min) than normoxia (9 +/- 1 min) (P < 0.03) but did not differ between Cr and Pla (P > 0.05)., Conclusion: This study, which used an exercise model designed to impose the same target contraction force under all experimental conditions, found no effect of Cr on maximal force, muscle endurance, or recovery in normoxia or hypobaric hypoxia.

Purpose: To investigate the effects of prolonged hypoxia and antioxidant supplementation on ventilatory threshold (VT) during high-altitude (HA) exposure (4300 m)., Methods: Sixteen physically fit males (25 +/- 5 yr; 77.8 +/- 8.5 kg) performed an incremental test to maximal exertion on a cycle ergometer at sea level (SL). Subjects were then matched on VO2peak, ventilatory chemosensitivity, and body mass and assigned to either a placebo (PL) or antioxidant (AO) supplement group in a randomized, double-blind manner. PL or AO (12 mg of beta-carotene, 180 mg of alpha-tocopherol acetate, 500 mg of ascorbic acid, 100 mug of selenium, and 30 mg of zinc daily) were taken 21 d prior to and for 14 d at HA. During HA, subjects participated in an exercise program designed to achieve an energy deficit of approximately 1400 kcal.d(-1). VT was reassessed on the second and ninth days at HA (HA2, HA9)., Results: Peak power output (Wpeak) and VO2peak decreased (28%) in both groups upon acute altitude exposure (HA2) and were unchanged with acclimatization and exercise (HA9). Power output at VT (WVT) decreased from SL to HA2 by 41% in PL, but only 32% in AO (P < 0.05). WVT increased in PL only during acclimatization (P < 0.05) and matched AO at HA9. Similar results were found when VT was expressed in terms of % Wpeak and % VO2peak., Conclusions: VT decreases upon acute HA exposure but improves with acclimatization. Prior AO supplementation improves VT upon acute, but not chronic altitude exposure.

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.

Acetazolamide can be taken at sea level to prevent acute mountain sickness during subsequent altitude exposure. Acetazolamide causes metabolic acidosis at sea level and altitude, and increases SaO2 (arterial oxygen saturation) at altitude. The aim of the present study was to determine whether acetazolamide impairs muscle endurance at sea level but not simulated altitude (4300 m for <3 h). Six subjects (20+/-1 years of age; mean+/-S.E.M.) performed exhaustive constant work rate one-leg knee-extension exercise (25+/-2 W) once a week for 4 weeks, twice at sea level and twice at altitude. Each week, subjects took either acetazolamide (250 mg) or placebo orally in a double-blind fashion (three times a day) for 2 days. On day 2, all exercise bouts began approx. 2.5 h after the last dose of acetazolamide or placebo. Acetazolamide caused similar acidosis (pH) in all subjects at sea level (7.43+/-0.01 with placebo compared with 7.34+/-0.01 with acetazolamide; P<0.05) and altitude (7.48+/-0.03 with placebo compared with 7.37+/-0.01 with acetazolamide; P<0.05). However, endurance performance was impaired with acetazolamide only at sea level (48+/-4 min with placebo compared with 36+/-5 min with acetazolamide; P<0.05), but not altitude (17+/-2 min with placebo compared with 20+/-3 min with acetazolamide; P = not significant). In conclusion, lack of impairment of endurance performance by acetazolamide compared with placebo at altitude was probably due to off-setting secondary effects resulting from acidosis, e.g. ventilatory induced increase in SaO2 for acetazolamide compared with placebo (89+/-1 compared with 86+/-1% respectively; P<0.05), which resulted in an increased oxygen pressure gradient from capillary to exercising muscle.

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.

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.

Background: Acute Mountain Sickness (AMS) is a multi-system disorder that is characterized by headache, anorexia, nausea, vomiting, insomnia, lassitude, and malaise. The syndrome is common in unacclimatized low altitude residents who rapidly ascend to terrestrial elevations exceeding 2,500 m. AMS may be a manifestation of hypoxia-induced cerebral edema resulting, in part, from increased capillary permeability., Hypothesis: We hypothesized that cysteinyl leukotrienes (CysLTs) may be involved in the pathogenesis of AMS, as these compounds are known to increase endothelial permeability., Methods: To test this hypothesis, we orally administered a CysLTs type-1 receptor antagonist (montelukast) to 11 subjects prior to and during exposure to high altitude (4,300 m) in a hypobaric chamber in a randomized, placebo-controlled, crossover design. We measured the resulting prevalence and/or severity of AMS, plasma CysLTs levels and urinary CysLTE4, and associated physiological responses., Results: At 12 h exposure, AMS prevalence and symptom severity was lower (p = 0.002) during montelukast administration compared with placebo, but not different at 22 h exposure. Plasma CysLTs and urinary LTE4 levels were not significantly elevated at 22 h exposure, nor did these CysLTs levels correlate with AMS severity. Compared with placebo, montelukast administration was not associated with any significant differences in physiologic measures at sea level or high altitude., Conclusions: These results do not support a role for the CysLTs mediating the early development of AMS through the CysLT-1 receptor.

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.

Acute mountain sickness (AMS) commonly occurs at altitudes exceeding 2000-2500 m and usually resolves after acclimatization induced by a few days of chronic residence at the same altitude. Increased ventilation and diuresis may contribute to the reduction in AMS with altitude acclimatization. The aim of the present study was to examine the effects of intermittent altitude exposures (IAE), in combination with rest and exercise training, on the incidence and severity of AMS, resting ventilation and 24-h urine volume at 4300 m. Six lowlanders (age, 23 +/- 2 years; body weight, 77 +/- 6 kg; values are means +/- S.E.M.) completed an Environmental Symptoms Questionnaire (ESQ) and Lake Louise AMS Scoring System (LLS), a resting end-tidal partial pressure of CO2 ( PETCO2) test and a 24-h urine volume collection at sea level (SL) and during a 30 h exposure to 4300 m altitude-equivalent (barometric pressure=446 mmHg) once before (PreIAE) and once after (PostIAE) a 3-week period of IAE (4 h.day(-1), 5 days.week(-1), 4300 m). The previously validated factor score, AMS cerebral score, was calculated from the ESQ and the self-report score was calculated from the LLS at 24 h of altitude exposure to assess the incidence and severity of AMS. During each IAE, three subjects cycled for 45-60 min.day(-1) at 60-70% of maximal O2 uptake (VO2 max) and three subjects rested. Cycle training during each IAE did not affect any of the measured variables, so data from all six subjects were combined. The results showed that the incidence of AMS (%), determined from both the ESQ and LLS, increased (P<0.05) from SL (0 +/- 0) to PreIAE (50 +/- 22) at 24 h of altitude exposure and decreased (P<0.05) from PreIAE to PostIAE (0 +/- 0). The severity of AMS (i.e. AMS cerebral symptom and LLS self-report scores) increased (P<0.05) from SL (0.02 +/- 0.02 and 0.17 +/- 0.17 respectively) to PreIAE (0.49 +/- 0.18 and 4.17 +/- 0.94 respectively) at 24 h of altitude exposure, and decreased (P<0.05) from PreIAE to PostIAE (0.03 +/- 0.02 and 0.83 +/- 0.31 respectively). Resting PETCO2 (mmHg) decreased (i.e. increase in ventilation; P<0.05) from SL (38 +/- 1) to PreIAE (32 +/- 1) at 24 h of altitude exposure and decreased further (P<0.05) from PreIAE to PostIAE (28 +/- 1). In addition, 24-h urine volumes were similar at SL, PreIAE and PostIAE. In conclusion, our findings suggest that 3 weeks of IAE provide an effective alternative to chronic altitude residence for increasing resting ventilation and reducing the incidence and severity of AMS.

Chronic altitude residence improves muscular performance at altitude, but the effect of intermittent altitude exposures (IAE) on muscular performance at altitude has not been defined. The purpose of this study was to determine the effects of 3 wk of IAE, in combination with rest and cycle training, on muscular performance at altitude. Six lowlanders (23 +/- 2 yr, 77 +/- 6 kg; means +/- SE) completed a cycle time trial and adductor pollicis endurance test at sea level and during a 30-h acute exposure to 4,300 m altitude equivalent (barometric pressure = 446 mmHg) once before (pre-IAE) and once after (post-IAE) a 3-wk period of IAE (4 h/day, 5 days/wk, 4,300 m). During each IAE, three subjects cycled for 45-60 min/day at 60%-70% of maximal O2 uptake and three subjects rested. Cycle training during each IAE did not appear to affect muscular performance at altitude. Thus data from all six subjects were combined. Three weeks of IAE resulted in 1) a 21 +/- 6% improvement (P < 0.05) in cycle time-trial performance (min) from pre-IAE (32.8 +/- 3.7) to post-IAE (24.8 +/- 1.2), 2) a 63 +/- 26% improvement (P < 0.05) in adductor pollicis endurance (min) from pre-IAE (9.2 +/- 2.8) to post-IAE (14.8 +/- 4.2), and 3) a 10 +/- 4% increase (P < 0.05) in resting arterial O2 saturation (%) from pre-IAE (82 +/- 2) to post-IAE (90 +/- 1). These improvements in muscular performance after IAE correlated strongly with increases in resting arterial O2 saturation and were comparable to those reported previously after chronic altitude residence. IAE may therefore be used as an alternative to chronic altitude residence to facilitate improvements in muscular performance in athletes, soldiers, mountaineers, shift workers, and others that are deployed to altitude.

Introduction: Adverse reactions during hypobaric chamber operations result from changes in barometric pressure per se and to the related reductions in the partial pressure of inspired oxygen. Previous studies have indicated that an adverse reaction may occur in approximately 6% of exposures in chambers used for flight training. The purpose of this study was to determine the rate of adverse reactions in a chamber used exclusively for terrestrial altitude research studies., Methods: Data for incidence of ear block, sinus block, toothache, and other adverse reactions were analyzed using a master history file that contained information such as annual and total number of studies and human exposures, and onset and outcome of adverse reactions. Incidence for a given time period was calculated as (# of reactions x 100)/(# of exposures)., Results: In 33 yr, there have been 23,656 human exposures and 296 adverse reactions. The overall incidence was 1.25 reactions per 100 exposures (0.72 for research volunteers and 0.53 for staff). The majority (75% of all reactions) were ear blocks (0.93 reactions per 100 exposures). Staff members were more likely than research volunteers to have more than one reaction., Discussion: The incidence of 1.25 reactions per 100 exposures for our chamber is considerably lower than that reported in the literature. This is due primarily to our use of lower altitudes and slower rates of ascent and descent compared with other facilities whose emphasis is on aircraft flight training.

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.

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.

Short exposures to severe or moderate hypoxia can have detrimental effects on postural stability. We hypothesized that continuous 24-h exposure to simulated 4300-m altitude (446 mmHg) would adversely affect postural stability and that this change in postural stability would be related to the severity of acute mountain sickness (AMS). On two different studies with similar experimental designs, postural instability was measured after approximately 3 and approximately 24 h of exposure using a computer-controlled unstable platform system in a total of 19 volunteers on three consecutive, 30-sec tests: eyes open (EO), eyes closed (EC), and a dynamic test involving tracking a circular moving object. Compared to baseline sea-level results, increases in postural instability were obtained with the EO test after 2 to 3 h (30%, p = 0.002) and 23 to 24 h (21%, p = 0.036) of altitude exposure. Similar increases were obtained on the EC test: 2 to 3 h (25%, p < 0.001) and 23 to 24 h (31%, p < 0.001). Although absolute instability values were higher on the EC test, the ratio EC/EO and the relative temporal changes with altitude exposure were similar. There were no significant altitude-stability effects on the target-tracking task. Sixty-three percent of the subjects (12 of 19) exhibited significant AMS (> 0.7 ESQ-C score) at some point during the 24-h exposure. No statistically significant correlations were obtained between the ESQ-C and any of the postural instability tests. These results indicate that postural stability is adversely affected during a 24-h exposure to 4300 m; however, there does not appear to be a correlation with the incidence or severity of AMS.

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.