Effect of 8 days of exercise-heat acclimation on aerobic exercise performance of men in hypobaric hypoxia.

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 (V̇o2peak) 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.

Aerobic Exercise Performance During Load Carriage and Acute Altitude Exposure.

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.

Effectiveness of preacclimatization strategies for high-altitude exposure.

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).

Performance during simple and complex military psychomotor tasks at various altitudes.

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.

Acute mountain sickness and sleep disturbances differentially influence cognition and mood during rapid ascent to 3000 and 4050 m.

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.

Effect of repeated normobaric hypoxia exposures during sleep on acute mountain sickness, exercise performance, and sleep during exposure to terrestrial altitude.

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.

Impact of 2 days of staging at 2500-4300 m on sleep quality and quantity following subsequent exposure to 4300 m.

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 (sSpO2 , %) 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 SpO2 was assessed after AMS measurements. The mean of all variables for both staging days (STG) and Pikes Peak days (PP) was calculated. The sSpO2 and daytime SpO2 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 sSpO2 , 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.

Acetazolamide does not alter endurance exercise performance at 3,500-m altitude.

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 (VO2peak): 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 VO2peak, 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.

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

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

New metric of hypoxic dose predicts altitude acclimatization status following various ascent profiles.

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.

Two-Day Residence at 2500 m to 4300 m Does Not Affect Subsequent Exercise Performance at 4300 m.

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.

Separate and combined influences of heat and hypobaric hypoxia on self-paced aerobic exercise performance.

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 (V̇o2peak), 41.5 ± 4.4 mL·kg-1·min-1, mean ± SD] completed 30 min of steady-state cycling exercise (50% SL V̇o2peak), 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.

Seven intermittent exposures to altitude improves exercise performance at 4300 m.

PURPOSE: The purpose of this study was to determine whether seven intermittent altitude exposures (IAE), in combination with either rest or exercise training, improves time-trial exercise performance and induces physiologic adaptations consistent with chronic altitude adaptation at 4300 m. METHODS: Ten adult lowlanders (26 +/- 2 yr; 78 +/- 4 kg; means +/- SE) completed cycle endurance testing during an acute exposure to a 4300-m-altitude equivalent (446 mm Hg) once before (pre-IAE) and once after (post-IAE) 7 d of IAE (4h x d(-1), 5 d x wk(-1), 4300 m). Cycle endurance testing consisted of two consecutive 15-min constant-work rate exercise bouts followed immediately by a time-trial exercise performance test. During each IAE, five subjects performed exercise training, and the other group of five subjects rested. RESULTS: Both groups demonstrated similar improvements in time-trial cycle exercise performance and physiologic adaptations during constant-work rate exercise from pre-IAE to post-IAE. Thus, data from all subjects were combined. Seven days of IAE resulted in a 16% improvement (P < 0.05) in time-trial cycle exercise performance (min) from pre-IAE (35 +/- 3) to post-IAE (29 +/- 2). During the two constant-work rate exercise bouts, there was an increase (P < 0.05) in exercise arterial O2 saturation (%) from pre-IAE (77 +/- 2; 75 +/- 1) to post-IAE (80 +/- 2; 79 +/- 1), a decrease (P < 0.05) in exercise heart rate (bpm) from pre-IAE (136 +/- 6; 162 +/- 5) to post-IAE (116 +/- 6; 153 +/- 5), and a decrease (P < 0.05) in exercise ratings of perceived exertion from pre-IAE (10 +/- 1; 14+/- 1) to post-IAE (8 +/- 1; 11 +/- 1). CONCLUSIONS: Our findings indicate that 7 d of IAE, in combination with either rest or exercise training, improves time-trial cycle exercise performance and induces physiologic adaptations during constant-work rate exercise consistent with chronic altitude adaptation at 4300 m.

Intermittent hypoxic exposure does not improve sleep at 4300 m.

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.

Acute Mountain Sickness is Reduced Following 2 Days of Staging During Subsequent Ascent to 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.

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

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

Is normobaric hypoxia an effective treatment for sustaining previously acquired altitude acclimatization?

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.

Voluntary muscle function after creatine supplementation in acute hypobaric hypoxia.

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.

Changes in ventilatory threshold at high altitude: effect of antioxidants.

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.

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

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