Beth A. Beidleman

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....

Beidleman, Beth A., Charles S. Fulco, Stephen R. Muza, Paul R. Rock, Janet E. Staab, Vincent A. Forte, Michael D. Brothers, and Allen Cymerman. Effect of six days of staging on physiological adjustments and acute mountain sickness during ascent to 4300 meters. High Alt. Med. Biol. 10:253–260, 2009.—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 CO₂ (Petco₂), arterial oxygen saturation (Sao₂), 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 (∼55% of altitude-specific maximal oxygen uptake) for ∼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 Petco₂ (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 Sao₂ (%) 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.

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). 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. 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. One week of IHE combined with exercise training does not improve endurance performance at a 4300-m altitude in male lowlanders.