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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.

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.

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.

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).

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.

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.

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.