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ABSTRACT: Abstract Staab, Janet E., Beth A. Beidleman, Stephen R. Muza, Charles S. Fulco, Paul B. Rock, and Allen Cymerman. Efficacy of residence at moderate versus low altitude on reducing acute mountain sickness in men following rapid ascent to 4300 m. High Alt Med Biol 14:13-18, 2013.-To determine if residence at moderate (∼2000 m) compared to low (<50 m) altitude reduces acute mountain sickness (AMS) in men during subsequent rapid ascent to a higher altitude. Nine moderate-altitude residents (MAR) and 18 sea-level residents (SLR) completed the Environmental Symptoms Questionnaire (ESQ) at their respective baseline residence and again at 12, 24, 48, and 72 h at 4300 m to assess the severity and prevalence of AMS. AMS cerebral factor score (AMS-C) was calculated from the ESQ at each time point. AMS was judged to be present if AMS-C was ≥0.7. Resting end-tidal CO2 (PETco2) and arterial oxygen saturation (Sao2) were assessed prior to and at 24, 48, and 72 h at 4300 m. Resting venous blood samples were collected prior to and at 72 h at 4300 m to estimate plasma volume (PV) changes. MAR compared to SLR: 1) AMS severity at 4300 was lower (p<0.05) at 12 h (0.50±0.69 vs. 1.48±1.28), 24 h (0.15±0.19 vs. 1.39±1.19), 48 h (0.10±0.18 vs. 1.37±1.49) and 72 h (0.08±0.12 vs. 0.69±0.70); 2) AMS prevalence at 4300 was lower (p<0.05) at 12 h (22% vs. 72%), 24 h (0% vs. 56%), 48 h (0% vs. 56%), and 72 h (0% vs. 45%); 3) resting Sao2 (%) was lower (p<0.05) at baseline (95±1 vs. 99±1) but higher (p<0.05) at 4300 at 24 h (86±2 vs. 81±5), 48 h (88±3 vs. 83±6), and 72 h (88±2 vs. 83±5); and 4) PV (%) did not differ at 72 h at 4300 m in the MAR (4.5±6.7) but was reduced for the SLR (-8.1±10.4). These results suggest that ventilatory and hematological acclimatization acquired while living at moderate altitude, as indicated by a higher resting Sao2 and no reduction in PV during exposure to a higher altitude, is associated with greatly reduced AMS after rapid ascent to high altitude.
High altitude medicine & biology 03/2013; 14(1):13-8. · 1.58 Impact Factor
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ABSTRACT: PURPOSE: Despite decades of research, no predictive models of acute mountain sickness (AMS) exist which identify the time course of AMS severity and prevalence following rapid ascent to various altitudes. METHODS: Using general linear and logistic mixed models and a comprehensive database, we analyzed 1,292 AMS Cerebral factor scores in 308 unacclimatized men and women who spent between 4-48 h at altitudes ranging from 1659-4501 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 (BMI), race, sex, and smoking status. RESULTS: AMS severity increased (P<0.05) nearly 2-fold (i.e., 179%) for every 1000 m increase in altitude at 20 h of exposure, peaked between 18-22 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 to 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 (OR 1.72, CI 1.03-3.08) of AMS compared to low actives. There was also a tendency (P=0.10) for men to demonstrate greater odds of AMS (OR 1.65, CI 0.84-3.25) compared to women. Age, BMI, race, and smoking status were not significantly associated with AMS. CONCLUSION: 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.
Medicine and science in sports and exercise 11/2012; · 3.71 Impact Factor
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ABSTRACT: Acute mountain sickness (AMS) and large decrements in endurance exercise performance occur when unacclimatized individuals rapidly ascend to high altitude. Six altitude and hypoxia pre-acclimatization strategies were evaluated to determine their effectiveness for minimizing AMS and improving performance during altitude exposure. Strategies using hypobaric chambers or true altitude were much more effective overall than those using normobaric hypoxia (breathing <20.9% oxygen).
Exercise and sport sciences reviews 05/2012; · 3.23 Impact Factor
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ABSTRACT: 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.
AJP Regulatory Integrative and Comparative Physiology 02/2011; 300(2):R428-36. · 3.34 Impact Factor
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ABSTRACT: 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.
Journal of Applied Physiology 12/2010; 109(6):1792-800. · 3.75 Impact Factor
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ABSTRACT: For many low-altitude (<1500 m) residents, their travel itineraries may cause them to ascend rapidly to high (>2400 m) altitudes without having the time to develop an adequate degree of altitude acclimatization. Prior to departing on these trips, low-altitude residents can induce some degree of altitude acclimatization by ascending to moderate (>1500 m) or high altitudes during either continuous or intermittent altitude preexposures. Generally, the degree of altitude acclimatization developed is proportional to the altitude attained and the duration of exposure. The available evidence suggests that continuous residence at 2200 m or higher for 1 to 2 days or daily 1.5- to 4-h exposures to >4000 m induce ventilatory acclimatization. Six days at 2200 m substantially decreases acute mountain sickness (AMS) and improves work performance after rapid ascent to 4300 m. There is evidence that 5 or more days above 3000 m within the last 2 months will significantly decrease AMS during a subsequent rapid ascent to 4500 m. Exercise training during the altitude preexposures may augment improvement in physical performance. The persistence of altitude acclimatization after return to low altitude appears to be proportional to the degree of acclimatization developed. The subsequent ascent to high altitude should be scheduled as soon as possible after the last altitude preexposure.
High altitude medicine & biology 01/2010; 11(2):87-92. · 1.58 Impact Factor
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Aaron L Baggish, Charles S Fulco,
Stephen Muza,
Paul B Rock,
Beth Beidleman,
Allen Cymerman,
Kibar Yared,
Peter Fagenholz,
David Systrom,
Malissa J Wood,
Arthur E Weyman,
Michael H Picard,
N Stuart Harris
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ABSTRACT: Staged ascent (SA), temporary residence at moderate altitude en route to high altitude, reduces the incidence and severity of noncardiopulmonary altitude illness such as acute mountain sickness. To date, the impact of SA on pulmonary arterial pressure (PAP) is unknown. We tested the hypothesis that SA would attenuate the PAP increase that occurs during rapid, direct ascent (DA). Transthoracic echocardiography was used to estimate mean PAP in 10 healthy males at sea level (SL, P(B) approximately 760 torr), after DA to simulated high altitude (hypobaric chamber, P(B) approximately 460 torr), and at 2 times points (90 min and 4 days) during exposure to terrestrial high altitude (P(B) approximately 460 torr) after SA (7 days, moderate altitude, P(B) approximately 548 torr). Alveolar oxygen pressure (Pao(2)) and arterial oxygenation saturation (Sao(2)) were measured at each time point. Compared to mean PAP at SL (mean +/- SD, 14 +/- 3 mmHg), mean PAP increased after DA to 37 +/- 8 mmHg (Delta = 24 +/- 10 mmHg, p < 0.001) and was negatively correlated with both Pao(2) (r(2) = 0.57, p = 0.011) and Sao(2) (r(2) = 0.64, p = 0.005). In comparison, estimated mean PAP after SA increased to only 25 +/- 4 mmHg (Delta = 11 +/- 6 mmHg, p < 0.001), remained unchanged after 4 days of high altitude residence (24 +/- 5 mmHg, p = not significant, or NS), and did not correlate with either parameter of oxygenation. SA significantly attenuated the PAP increase associated with continuous direct ascent to high altitude and appeared to uncouple PAP from both alveolar hypoxia and arterial hypoxemia.
High altitude medicine & biology 01/2010; 11(2):139-45. · 1.58 Impact Factor
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ABSTRACT: 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.
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).
Hemoglobin concentration ([Hb]), hematocrit (Hct), arterial oxygen saturation (SaO2), ratings of perceived exertion (RPE), and heart rate (HR) were measured before and during exercise.
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).
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.
Aviation Space and Environmental Medicine 11/2009; 80(11):955-61. · 0.88 Impact Factor
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ABSTRACT: 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.
High altitude medicine & biology 01/2009; 10(3):253-60. · 1.58 Impact Factor
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ABSTRACT: Warfighter exposure to high terrestrial altitude continues to be a reality for the modern fighting force. Understanding the negative effects of altitude on cognitive performance is essential as the cognitive demands of many warfighting tasks are becoming increasingly complex. To date, little research has investigated the performance of multiple cognitive tasks in a high altitude environment. The work reported here was designed to investigate the performance of Soldiers on a multi-task cognitive assessment at sea-level and high altitude (4300m) both before (hypobaric chamber) and after (terrestrial altitude) living for six days at moderate altitude (2200m). Results indicate that multi-task performance declined during initial, unacclimatized high altitude exposure compared to sea-level. In contrast, performance at high altitude after staging did not differ from sea-level. While these results suggest that the stay at moderate altitude produced acclimatization which worked to sustain cognitive performance, the effects of task learning and individual differences in response to altitude are also discussed.
11/2008;
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ABSTRACT: 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.
High Altitude Medicine & Biology 02/2008; 9(4):281-7. · 1.77 Impact Factor
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Charles S. Fulco,
Stephen R. Muza,
Beth Beidleman,
Juli Jones,
Eric Lammi,
Janet Staab,
Paul B. Rock,
Kenneth Kambis,
Ellen Glickman,
Brandon K. Doan,
Michael D. Brothers,
Michael F. Zupan,
Allen Cymerman
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ABSTRACT: The overall objective of the current project was to determine in previously unacclimatized SLR the effectiveness of staging in minimizing impairments in physical and cognitive performances and reducing acute mountain sickness incidence and severity during subsequent high altitude exposure The data presented here will be focused on the effects of staging at moderate altitude on prolonged endurance performance of SLR during exposure to 4300 m The results from the current study also will be compared to those of our previous two Pikes Peak studies to determine the relative effectiveness of short-term staging to no prior altitude acclimatization and to full moderate altitude acclimatization respectively.
01/2008;
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ABSTRACT: 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.
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.
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).
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.
Medicine & Science in Sports & Exercise 01/2008; 40(1):141-8. · 4.43 Impact Factor
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ABSTRACT: We sought to describe cerebrovascular responses to incremental exercise and test the hypothesis that changes in cerebral oxygenation influence maximal performance. Eleven men cycled in three conditions: 1) sea level (SL); 2) acute hypoxia [AH; hypobaric chamber, inspired Po(2) (Pi(O(2))) 86 Torr]; and 3) chronic hypoxia [CH; 4,300 m, Pi(O(2)) 86 Torr]. At maximal work rate (W(max)), fraction of inspired oxygen (Fi(O(2))) was surreptitiously increased to 0.60, while subjects were encouraged to continue pedaling. Changes in cerebral (frontal lobe) (C(OX)) and muscle (vastus lateralis) oxygenation (M(OX)) (near infrared spectroscopy), middle cerebral artery blood flow velocity (MCA V(mean); transcranial Doppler), and end-tidal Pco(2) (Pet(CO(2))) were analyzed across %W(max) (significance at P < 0.05). At SL, Pet(CO(2)), MCA V(mean), and C(OX) fell as work rate rose from 75 to 100% W(max). During AH, Pet(CO(2)) and MCA V(mean) declined from 50 to 100% W(max), while C(OX) fell from rest. With CH, Pet(CO(2)) and C(OX) dropped throughout exercise, while MCA V(mean) fell only from 75 to 100% W(max). M(OX) fell from rest to 75% W(max) at SL and AH and throughout exercise in CH. The magnitude of fall in C(OX), but not M(OX), was different between conditions (CH > AH > SL). Fi(O(2)) 0.60 at W(max) did not prolong exercise at SL, yet allowed subjects to continue for 96 +/- 61 s in AH and 162 +/- 90 s in CH. During Fi(O(2)) 0.60, C(OX) rose and M(OX) remained constant as work rate increased. Thus cerebral hypoxia appeared to impose a limit to maximal exercise during hypobaric hypoxia (Pi(O(2)) 86 Torr), since its reversal was associated with improved performance.
AJP Heart and Circulatory Physiology 01/2008; 294(1):H164-71. · 3.71 Impact Factor
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ABSTRACT: 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.
High Altitude Medicine & Biology 01/2007; 8(3):192-9. · 1.77 Impact Factor
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ABSTRACT: Recent studies have demonstrated that brief daily IAE (intermittent altitude exposure) was equally as effective as continuous altitude residence in inducing physiological adaptations consistent with altitude acclimatization. Although the positive benefits of IAE have been clearly defined, the potential negative consequences of IAE on health, specifically the immune system, remain undefined. The present study determined the effects of IAE on WBC (white blood cell) and hormonal responses during rest and exercise at 4300 m altitude. Six lowlanders (age, 23+/-2 years; body weight, 77+/-6 kg; values are means+/-S.E.M.) completed a VO(2)max (maximal O(2) uptake) and submaximal cycle ergometer test during a 30-h SL (sea level) exposure and during a 30 h exposure to 4300 m altitude-equivalent once before (PreIAE) and once after (PostIAE) a 3-week period of IAE (4 hxday(-1), 5 daysxweek(-1), 4300 m). The submaximal cycle ergometer test consisted of two consecutive 15-min work bouts at 40% and 70% of altitude-specific VO(2)max. Blood samples were obtained at rest and during both exercise work bouts for measurements of WBC count, leucocyte subset counts, cortisol, adrenaline (epinephrine) and noradrenaline (norepinephrine). WBC, neutrophil and lymphocyte counts increased significantly (P<0.05) during rest and exercise from SL to PreIAE and decreased (P<0.05) during rest and exercise from PreIAE to PostIAE. Monocyte counts decreased (P<0.05) during rest and exercise from PreIAE to PostIAE, but eosinophil and basophil counts did not change. Cortisol, adrenaline and noradrenaline did not change during rest or exercise from SL to PreIAE or PostIAE, but all increased significantly (P<0.05) from rest during the two work bouts. In conclusion, this type of IAE stimulus did not induce a hormonal stress response and did no harm in terms of activation of the immune system at altitude, as measured by WBC and leucocyte subset counts. This method of pre-acclimatization can therefore be highly recommended for inducing altitude acclimatization without the 'altitude residency' requirement.
Clinical Science 09/2006; 111(2):163-9. · 4.61 Impact Factor
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ABSTRACT: To determine whether creatine (Cr) supplementation improves muscle performance during exposure to acute hypobaric hypoxia.
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).
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).
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.
Medicine & Science in Sports & Exercise 08/2006; 38(8):1418-24. · 4.43 Impact Factor
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ABSTRACT: To investigate the effects of prolonged hypoxia and antioxidant supplementation on ventilatory threshold (VT) during high-altitude (HA) exposure (4300 m).
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).
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.
VT decreases upon acute HA exposure but improves with acclimatization. Prior AO supplementation improves VT upon acute, but not chronic altitude exposure.
Medicine & Science in Sports & Exercise 08/2006; 38(8):1425-31. · 4.43 Impact Factor
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ABSTRACT: Acetazolamide can be taken at sea level to prevent acute mountain sickness during subsequent altitude exposure. Acetazolamide causes metabolic acidosis at sea level and altitude, and increases SaO2 (arterial oxygen saturation) at altitude. The aim of the present study was to determine whether acetazolamide impairs muscle endurance at sea level but not simulated altitude (4300 m for <3 h). Six subjects (20+/-1 years of age; mean+/-S.E.M.) performed exhaustive constant work rate one-leg knee-extension exercise (25+/-2 W) once a week for 4 weeks, twice at sea level and twice at altitude. Each week, subjects took either acetazolamide (250 mg) or placebo orally in a double-blind fashion (three times a day) for 2 days. On day 2, all exercise bouts began approx. 2.5 h after the last dose of acetazolamide or placebo. Acetazolamide caused similar acidosis (pH) in all subjects at sea level (7.43+/-0.01 with placebo compared with 7.34+/-0.01 with acetazolamide; P<0.05) and altitude (7.48+/-0.03 with placebo compared with 7.37+/-0.01 with acetazolamide; P<0.05). However, endurance performance was impaired with acetazolamide only at sea level (48+/-4 min with placebo compared with 36+/-5 min with acetazolamide; P<0.05), but not altitude (17+/-2 min with placebo compared with 20+/-3 min with acetazolamide; P = not significant). In conclusion, lack of impairment of endurance performance by acetazolamide compared with placebo at altitude was probably due to off-setting secondary effects resulting from acidosis, e.g. ventilatory induced increase in SaO2 for acetazolamide compared with placebo (89+/-1 compared with 86+/-1% respectively; P<0.05), which resulted in an increased oxygen pressure gradient from capillary to exercising muscle.
Clinical Science 07/2006; 110(6):683-92. · 4.61 Impact Factor
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ABSTRACT: High-altitude anorexia leads to a hormonal response pattern modulated by both hypoxia and caloric restriction (CR). The purpose of this study was to compare altitude-induced neuroendocrine changes with or without energy imbalance and to explore how energy sufficiency alters the endocrine acclimatization process. Twenty-six normal-weight, young men were studied for 3 wk. One group [hypocaloric group (HYPO), n = 9] stayed at sea level and consumed 40% fewer calories than required to maintain body weight. Two other groups were deployed to 4,300 meters (Pikes Peak, CO), where one group (ADQ, n = 7) was adequately fed to maintain body weight and the other [deficient group (DEF), n = 10] had calories restricted as above. HYPO experienced a typical CR-induced reduction in many hormones such as insulin, testosterone, and leptin. At altitude, fasting glucose, insulin, and epinephrine exhibited a muted rise in DEF compared with ADQ. Free thyroxine, thyroid-stimulating hormone, and norepinephrine showed similar patterns between the two altitude groups. Morning cortisol initially rose higher in DEF than ADQ at 4,300 meters, but the difference disappeared by day 5. Testosterone increased in both altitude groups acutely but declined over time in DEF only. Adiponectin and leptin did not change significantly from sea level baseline values in either altitude group regardless of energy intake. These data suggest that hypoxia tends to increase blood hormone concentrations, but anorexia suppresses elements of the endocrine response. Such suppression results in the preservation of energy stores but may sacrifice the facilitation of oxygen delivery and the use of oxygen-efficient fuels.
AJP Endocrinology and Metabolism 07/2006; 290(6):E1078-88. · 4.75 Impact Factor
