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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.

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.

Objective: To study the relationship between changes in the cerebral blood flow (CBF) velocity with symptoms of acute mountain sickness (AMS) during simulated high altitude. Research Design and Methods: Mean middle arterial cerebral flow velocity (MCAv) was assessed by transcranial Doppler sonography in 8 healthy lowland male adults aged 20 - 24 yrs before and after 6 h and 48 h at simulated altitude corresponding to 4572 m. The same study was repeated three weeks later in the same subjects. End-tidal pCO2 (ETCO2) and arterial oxygen saturation (SaO2) were measured by standardized procedures. AMS symptoms were recorded using the modified environmental symptoms questionnaire after 6 h and 48 h exposure to calculate the mean score of cerebral (AMS-C) symptoms. Results: Mean MCAv significantly increased with high altitude (HA) by 4% at 6 h HA and 24% at 48 h HA (P 2 (mean ± SD 32 ± 4 mmHg; r = 0.47, P 2 (77% ± 8%; r = - 0.43, P 2 (r = - 0.55, P

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

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.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 and1.5), moderate (≥1.5 and2.6), and severe (≥2.6).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.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.

AB 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

This is a minireview of potential wearable physiological sensors and algorithms (process and equations) for detection of acute mountain sickness (AMS). Given the emerging status of this effort, the focus of the review is on the current clinical assessment of AMS, known risk factors (environmental, demographic, and physiological), and current understanding of AMS pathophysiology. Studies that have examined a range of physiological variables to develop AMS prediction and/or detection algorithms are reviewed to provide insight and potential technological roadmaps for future development of real-time physiological sensors and algorithms to detect AMS. Given the lack of signs and nonspecific symptoms associated with AMS, development of wearable physiological sensors and embedded algorithms to predict in the near term or detect established AMS will be challenging. Prior work using [Formula: see text], HR, or HRv has not provided the sensitivity and specificity for useful application to predict or detect AMS. Rather than using spot checks as most prior studies have, wearable systems that continuously measure SpO2 and HR are commercially available. Employing other statistical modeling approaches such as general linear and logistic mixed models or time series analysis to these continuously measured variables is the most promising approach for developing algorithms that are sensitive and specific for physiological prediction or detection 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 (p0.05). Individual values for pre-Pikes Peak sympathetic activity were inversely related to post-altitude sympathoexcitation (r=-0.69, p0.05). There were no differences in neural or cardiovascular responses to tilt between pre and post- Pikes Peak (p0.05). 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.

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

Despite decades of research, the magnitude and time course of hematologic and plasma volume (PV) changes following rapid ascent and acclimation to various altitudes are not precisely described. To develop a quantitative model, we utilized a comprehensive database and general linear mixed models to analyze 1,055 hemoglobin ([Hb]) and hematocrit (Hct) measurements collected at sea level and repeated time points at various altitudes in 393 unacclimatized men ( n = 270) and women ( n = 123) who spent between 2 h and 7 days at 2,500–4,500 m under well-controlled and standardized experimental conditions. The PV change (ΔPV) was calculated from [Hb] and Hct measurements during a time period when erythrocyte volume is stable. The results are 1) ΔPV decreases rapidly (~6%) after the 1st day at 2,500 m and [Hb] and Hct values increase by 0.5 g/dl and 1.5 points, respectively; 2) ΔPV decreases an additional 1%, and [Hb] and Hct increase an additional 0.1 g/dl and 0.2 points every 500-m increase in elevation above 2,500 m after the 1st day; 3) ΔPV continues to decrease over time at altitude, but the magnitude of this decrease and subsequent increase in [Hb] and Hct levels is dependent on elevation and sex; and 4) individuals with high initial levels of [Hb] and Hct and older individuals hemoconcentrate less at higher elevations. This study provides the first quantitative delineation of ΔPV and hematological responses during the first week of exposure over a wide range of altitudes and demonstrates that absolute altitude and time at altitude, as well as initial hematologic status, sex, and age impact the response.

Acute mountain sickness (AMS), characterized by headache, nausea, fatigue, and dizziness when unacclimatized individuals rapidly ascend to high altitude, is exacerbated by exercise and can be disabling. Although AMS is observed in both normobaric (NH) and hypobaric hypoxia (HH), recent evidence suggests that NH and HH produce different physiological responses. We evaluated whether AMS symptoms were different in NH and HH during the initial stages of exposure and if the assessment tool mattered. Seventy-two 8 h exposures to normobaric normoxia (NN), NH, or HH were experienced by 36 subjects. The Environmental Symptoms Questionnaire (ESQ) and Lake Louise Self-report (LLS) were administered, resulting in a total of 360 assessments, with each subject answering the questionnaire 5 times during each of their 2 exposure days. Classification tree analysis indicated that symptoms contributing most to AMS were different in NH (namely, feeling sick and shortness of breath) compared to HH (characterized most by feeling faint, appetite loss, light headedness, and dim vision). However, the differences were not detected using the LLS. These results suggest that during the initial hours of exposure (1) AMS in HH may be a qualitatively different experience than in NH and (2) NH and HH may not be interchangeable environments.

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 O2 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 Pco2, O2 saturation (SaO2), 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 Pco2 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 SaO2 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 SaO2 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 to4000 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.

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.

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.

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·d-1, 5 d·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.

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.

Mountain environments have combined stressors of lower ambient temperature and hypoxia. Cold alone can reduce finger temperature, resulting in discomfort, impaired dexterity, and increased risk of cold injury. Whether hypobaric hypoxia exacerbates these effects is unclear. To examine this, finger temperature responses to two cold water immersion tests were measured at sea level (SL, 99 kPa), 3000 m (70 kPa), and 4675 m (56 kPa) at the same air temperature (22°-23°C). Nine males sat quietly for 30 min, then completed the tests in balanced order. For the cold-induced vasodilation (CIVD) test, middle finger pad temperature was measured during immersion in 4°C water for 30 min. For the Rewarming test, finger temperature was measured for 30 min following a 5 min hand immersion in 16°C water. Average oxygen saturation was 98.6% during SL, 90.7% at 3000 m, and 75.8% at 4657 m. Mean finger temperature during the CIVD test (7.1°C) was similar among trials. There was no difference in CIVD parameters of nadir, apex, or mean finger temperatures; however both onset and apex times were earlier at 3000 m, compared to SL (0.6 min and 1.6 min, respectively). These differences did not persist at 4657 m. Rewarming after hand immersion was similar among trials, reaching 22.7°C after 30 min, compared to an initial finger temperature of 29.3°C. The results of this study provide no evidence that hypobaric hypoxia increases risk of cold injury. Previous findings of blunted finger temperatures at altitude are likely due to the lower ambient temperature that typically occurs at higher elevations.

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 s-carotene, 180 mg of a-tocopherol acetate, 500 mg of ascorbic acid, 100 µg 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.

HAGOBIAN, T. A., K. A. JACOBS, A. W. SUBUDHI, J. A. FATTOR, P. B. ROCK, S. R. MUZA, C. S. FULCO, B. BRAUN, A. GREDIAGIN, R. S. MAZZEO, A. CYMERMAN, and A. L. FRIEDLANDER. Cytokine Responses at High Altitude: Effects of Exercise and Antioxidants at 4300 m. Med. Sci. Sports Exerc., Vol. 38, No. 2, pp. 276–285, 2006. Purpose: This study tested the hypothesis that antioxidant supplementation would attenuate plasma cytokine (IL-6, tumor necrosis factor (TNF)-!), and Creactive 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 "-carotene, 200 IU !-tocopherol acetate, 250 mg ascorbic acid, 50 2g selenium, 15 mg zinc) or placebo was given twice daily. At HA, energy expenditure increased approximately 750 kcalId j1 and energy intake decreased approximately 550 kcalId j1 , resulting in a caloric deficit of approximately 1200–1500 kcalId j1 . At SL and HA day 1 (HA1) and day HA13, subjects exercised at 55% of V u O2peak 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-! 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-! 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. Key Words: IL-6, TNF-!, C-REACTIVE PROTEIN, HYPOXIA, ENERGY DEFICIT

Acute mountain sickness (AMS) is caused by exposure to altitudes exceeding 2500 m and often resolves by acclimatization without further ascent. Statistical models of AMS score and the probability of an AMS diagnosis were developed to allow the combination of dissimilar exposures for simultaneous analysis. The study population was 302 trekkers from a previous investigation who provided self-reported symptoms upon arrival at 3840 m during hikes through altitudes of 1500 to 6200 m. AMS score (Hackett scale) was estimated by linear regression and the probability of an AMS diagnosis (Lake Louise criteria) by logistic regression. AMS score or probability was significantly associated with exposure day and altitude. Increased altitude over the prior 3 days resulted in higher estimated AMS score or probability and decreased altitude in lower score or probability. The odds ratio (OR) of AMS was 3.6 if not on acetazolamide. Females appeared slightly more susceptible than males (1.5 OR). The approach offers the advantages of (1) improved statistical power by combining exposures, (2) insight into the dose-response relationship of altitude exposure and AMS risk, (3) quantitative tests for the significance of factors that might affect AMS susceptibility, and (4) practical tools to track individual climbers and plan operational ascents.

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

The present study assessed the effects of acute hyperoxia on resting-minute ventilation (VE) during altitude acclimatization to 4300 m.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.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.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.

Scientific consensus does not exist regarding hematological responses to moderate to high altitude exposure. The purpose of this study was to quantify the expected changes in hemoglobin concentration [Hb], hematocrit (Hct), and PV changes as a result of a given gain in terrestrial elevation, delineate the time course of these changes, and define baseline demographics and physiologic descriptors that are important in predicting these changes. The overall impact of altitude can be summarized using the following correction factors: 1) 0.1g/dl increase in [Hb] for every 500 m increase in altitude regardless of gender, 2) 1.1% increase in Hct at 2000 m with an additional 2-6% increase for every 500 m increase in altitude depending non the altitude, and 3)rapid 5% loss in PV at 2000 m and additional 0.6% decrease with every 500 m above 2000 m. It is anticipated that results will enhance the ability of sport organizations to detect blood doping in athletes seeking to gain an edge in their athletic performance.

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%, p0.001) and 23 to 24 h (31%, p0.001). 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.

We applied a novel MR imaging technique to investigate the effect of acute mountain sickness on cerebral tissue water. Nine volunteers were exposed to hypobaric hypoxia corresponding to 4572 m altitude for 32 h. Such an exposure may cause acute mountain sickness. We imaged the brains of the volunteers before and at 32 h of hypobaric exposure with two different MRI techniques with subsequent data processing. (1) Brain volumes were calculated from 3D MRI data sets by applying a computerized brain segmentation algorithm. For this specific purpose a novel adaptive 3D segmentation program was used with an automatic correction algorithm for RF field inhomogeneity. (2) T(2) decay rates were analyzed in the white matter. The results demonstrated that a significant brain swelling of 36.2 +/- 19.6 ml (2.77 +/- 1.47%, n = 9, P0.001) developed after the 32-h hypobaric hypoxia exposure with a maximal observed volume increase of 5.8% (71.3 ml). These volume changes were significant only for the gray matter structures in contrast to the unremarkable changes seen in the white matter. The same study repeated 3 weeks later in 6 of 9 original subjects demonstrated that the brains recovered and returned approximately to the initially determined sea-level brain volume while hypobaric hypoxia exposure once again led to a significant new brain swelling (24.1 +/- 12.1 ml, 1.92 +/- 0.96%, n = 6, P0.005). On the contrary, the T(2) mapping technique did not reveal any significant effect of hypobaria on white matter. We present here a technique which is able to detect reversible brain volume changes as they may occur in patients with diffuse brain edema or increased cerebral blood volume, and which may represent a useful noninvasive tool for future evaluations of antiedematous drugs.

Objective To evaluate an ambulatory physiological monitoring system during a mountaineering expedition. We hypothesized that the Environmental Symptoms Questionnaire, combined with frequent measurement of oxygen saturation and core temperature, would accurately identify cases of environmental illness. Methods Twelve military mountaineers took a daily Environmental Symptoms Questionnaire, monitored fingertip oxygen saturations, and recorded core temperatures while climbing a 4,949-m peak. Illnesses identified by the system were compared with those identified by spontaneous reports. Results The system correctly identified one case of high-altitude pulmonary edema and two illnesses that were not reported to the physician (one case of acute mountain sickness and one of self-limited symptomatic desaturation). However, it did not identify two illnesses that were severe enough to preclude further climbing (one case of sinus headache and one of generalized fatigue). Conclusions Our monitoring system may complement, but cannot replace, on-site medical personnel during mountaineering expeditions.

We hypothesized that progesterone-mediated ventilatory stimulation during the midluteal phase of the menstrual cycle would increase exercise minute ventilation (V˙e; l/min) at sea level (SL) and with acute altitude (AA) exposure but would only increase arterial O2 saturation ([Formula: see text], %) with AA exposure. We further hypothesized that an increased exercise[Formula: see text] with AA exposure would enhance O2 transport and improve both peak O2 uptake (V˙o 2 peak; ml ⋅ kg−1 ⋅ min−1) and submaximal exercise time to exhaustion (Exh; min) in the midluteal phase. Eight female lowlanders [33 ± 3 (mean ± SD) yr, 58 ± 6 kg] completed aV˙o 2 peak and Exh test at 70% of their altitude-specificV˙o 2 peak at SL and with AA exposure to 4,300 m in a hypobaric chamber (446 mmHg) in their early follicular and midluteal phases. Progesterone levels increased ( P < 0.05) ∼20-fold from the early follicular to midluteal phase at SL and AA. PeakV˙e (101 ± 17) and submaximalV˙e (55 ± 9) were not affected by cycle phase or altitude. Submaximal[Formula: see text] did not differ between cycle phases at SL, but it was 3% higher during the midluteal phase with AA exposure. NeitherV˙o 2 peak nor Exh time was affected by cycle phase at SL or AA. We conclude that, despite significantly increased progesterone levels in the midluteal phase, exercise V˙e is not increased at SL or AA. Moreover, neither maximal nor submaximal exercise performance is affected by menstrual cycle phase at SL or AA.

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. Language: en

Acute mountain sickness (AMS) is an illness that affects many individuals at altitudes above 2,400 m (8,000 ft) resulting in decreased performance. Models that provide quantitative estimates of AMS risk are expanding, but predictive genetic models for AMS susceptibility are still under investigation. Thirty-four male U.S. Army Soldier volunteers were exposed to baseline, 3,000 m, 3,500 m, or 4,500 m altitude conditions in a hypobaric chamber and evaluated for onset of AMS symptoms. In addition, mice were evaluated at extreme hypoxia conditions equivalent to 7,600 m. Real-time polymerase chain reaction hypoxia response array was used to identify 15 genes that were activated in Soldiers and 46 genes that were activated in mice. We identified angiopoietin-like 4 (ANGPTL4) as a gene that is significantly activated in response to hypoxia (5.8-fold upregulated at 4,500 m in humans). The role of ANGPTL4 in high-altitude response has not been explored. Pretreatment of mice with fenofibrate, an ANGPTL4-activating pharmaceutical, had a considerable effect on overall hypoxia response gene expression and resulted in significantly decreased cerebral edema following exposure to hypoxia. Activation of ANGPTL4 may protect against cerebral edema by inhibiting vascular endothelial growth factor and therefore serve as a potential target for AMS prevention.

Study objective To determine whether urinary leukotriene E 4 (uLTE 4 ) levels increase upon exposure to high altitude, and also to ascertain the relationship between ULTE 4 levels and symptoms of acute mountain sickness (AMS). Design Prospective, unblinded, single-factor (altitude) experimental study. Settings US Army research laboratory facilities at sea level ([SL] 50 m), 1,830 m, and 4,300 m. Participants Eight healthy male subjects ranging in age from 19 to 24 years. Measurements ULTE 4 levels and symptoms of AMS were measured at just above SL (50 m), 3M days after being transported from SL to moderate altitude (MA) (1,830 m), and 1½ days after ascent from 1,830 to 4,300 m (high altitude [HA]). Symptoms of AMS were assessed using standard indexes derived from the Environmental Symptoms Questionnaire weighted toward cerebral (AMS-C) and respiratory (AMS-R) manifestations. Oxygen saturation was measured noninvasively by pulse oximetry at SL and HA. Results The mean (±SEM) ULTE4 levels (pg/mg creatinine) were 67.9 (±13.2) at SL; 82.3 (±5.5) at MA; and 134.8 (±19.4) at HA (p Conclusions We conclude that ULTE 4 levels increase shortly after exposure to HA even after staging for 4 days at MA. Although this study does not clearly demonstrate a relationship between uLTE 4 levels and symptoms of AMS, it supports the hypothesis that leukotrienes may be involved in the pathophysiologic state of AMS.

This study examined the effects of added inspiratory resistance (R5 5 cm H2O.L-1.S-1) on the relationship between exercise breathing pattern and resting hypercapnic ventilatory responsiveness (HCVR). Twelve men completed an HCVR test and two progressive intensity exercise tasks with minimal (R0) and elevated (R5) resistance. Peak oxygen uptake, and peak power output were not different, but peak VE was decreased with the R5 load. Exercise ventilation (VE was tightly coupled to VCO2 (r = 0.97) as was mean inspiratory flow rate (VT/TI, r = 0.95), but not duty cycle (TI/TTOT, r = 0.39). With imposition of R5, VT/TI was depressed (p < 0.05) at mild (approximately 40% VO2peak) to peak exercise intensities, whereas TI/TTOT was relatively unaffected. At both moderate (approximately 60% peak VO2) and peak exercise intensities, VE was positively correlated (r = 0.62, p < 0.05 and r = 0.82, p < 0.01, respectively) to subjects' HCVR. However, when normalized, VE.VCO2(-1) was significantly correlated to HCVR only at peak exercise ventilation during the R0 load. Analysis of the exercise breathing pattern revealed that at both moderate and peak exercise intensities, VT/TI was positively correlated to HCVR, but TI/TTOT was not. The imposition of R5 decreased the slope of the relationship between exercise VT/TI and HCVR at both moderate and peak exercise intensities, and weakened the positive correlation at the moderate exercise intensity. Our analysis indicates that: 1) the positive correlation between exercise hyperpnea and HCVR is mediated by the mean inspiratory flow rate rather than the duty cycle component of the breathing pattern and, 2) at moderate exercise the relationship between mean inspiratory flow rate and resting HCVR is more sensitive to added inspiratory resistance than minute ventilation per se. These findings suggest that the degree of influence resting HCVR has on exercise hyperpnea is dependent upon the magnitudes of both the ventilatory hyperpnea and mechanical loading placed on the ventilatory system.

This study measured sweat rates (msw) during high-altitude summer treks on Mt. Kilimanjaro to evaluate the efficacy of a recently developed fuzzy piecewise sweat prediction equation ( Ṗw,sol) for application to high-altitude conditions. We hypothesized that the Ṗw,sol equation, adjusted for the barometric pressure (Pb) decreasing steadily at high altitude ( Ṗw,sol+Alt), would allow for a more accurate prediction of msw than Ṗw,sol unadjusted for altitude ( Ṗw,solSL). Fifteen men (43 ± 16 yr; 80 ± 22 kg) and seven women (46 ± 16 yr; 77 ± 18 kg) wearing hiking clothes (clo ∼1.15; clothing evaporative potential = 0.27) and carrying light loads (9 ± 2 kg), were studied during morning and afternoon treks (∼2–3 h) while ascending from 2,829 m to 3,505 m. After each trek, msw was measured with specific biophysical parameters at 15-min intervals. During the trek day, Pb progressively declined (530 to 504 Torr), as solar radiation and ambient temperature (°C) rose transiently. During all treks, msw ranged from 68 to 393 g·m−2·h−1 (0.14 to 0.79 l/h). For each subject, derived Ṗw,solSL and Ṗw,sol+Alt model outputs accurately predicted the morning and afternoon average msw within a root mean square error of 0.145 l/h. No differences were found between Ṗw,solSL and Ṗw,sol+Alt values. In conclusion, we report the first msw measured during outdoor high-altitude activities and determined that Ṗw,solSL equation can be used to predict fluid needs during high-altitude activities without alterations for lower Pb. This model prediction provides a valid water planning tool for outdoor activities at high altitude up to 3,500 m.

To test the hypothesis that aging is associated with a reduction in the diaphragm's force-generating capacity, we compared the maximum transdiaphragmatic pressure (Pdimax) obtained during voluntary maximal inspiratory efforts in nine young (19-28 yr) and ten elderly (65-75 yr) subjects. The relationship between Pdi and lung volume was compared in the two groups by having subjects make maximal inspiratory maneuvers at specified lung volumes (i.e., 20, 40, and 80% vital capacity). Subjects underwent symptom-limited exercise tests to characterize their aerobic capacities and evaluate the relationship between aerobic capacity and Pdimax. The average Pdimax of the elderly subjects (128 +/- 9 cm H2O) was significantly lower (p < 0.003) than the average Pdimax of the younger subjects (171 +/- 8 cm H2O). In the elderly, Pdi was lower across the range of lung volumes tested (p < 0.001), and Pdimax occurred at similar relative lung volumes (elderly, at 47% total lung capacity [TLC]; young, at 50% TLC) in both groups. The elderly subjects were quite fit based on their VO2max, and there was no significant relationship between Pdimax and VO2max. This study suggests that diaphragm strength is reduced in elderly individuals. This age-related decrease in diaphragm strength may predispose elderly patients to diaphragm fatigue in the presence of conditions that impair inspiratory muscle function or increase ventilatory load.