Influence of recent altitude exposure on sea level sympathetic neural & hemodynamic responses to orthostasis.

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 (p<0.05). Individual values for pre-Pikes Peak sympathetic activity were inversely related to post-altitude sympathoexcitation (r=-0.69, p<0.05). There were no differences in neural or cardiovascular responses to tilt between pre and post- Pikes Peak (p>0.05). 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.

Carbohydrate supplementation improves time-trial cycle performance during energy deficit at 4,300-m altitude.

Carbohydrate supplementation (CHOS) typically improves prolonged time-trial (TT) performance at sea level (SL). This study determined whether CHOS also improves TT performance at high altitude (ALT; 4,300 M) despite increased hypoxemia and while in negative energy balance (approximately 1,250 kcal/day). Two groups of fasting, fitness-matched men performed a 720-kJ cycle TT at SL and while living at ALT on days 3 (ALT3) and 10 (ALT10). Eight men drank a 10% carbohydrate solution (0.175 g/kg body wt) and eight drank a placebo (PLA; double blind) at the start of and every 15 min of the TT. Blood glucose during each TT was higher (P < 0.05) for CHOS than for PLA. At SL, TT duration (approximately 59 min) and watts (approximately 218 or approximately 61% of peak watts; %SL Wpeak) were similar for both groups. At ALT, the TT was longer for both groups (P < 0.01) but was shorter for CHOS than for PLA on ALT3 (means +/- SE: 80 +/- 7 vs. 105 +/- 9 min; P < 0.01) and ALT10 (77 +/- 7 vs. 90 +/- 5 min; P < 0.01). At ALT, %SL Wpeak was reduced (P < 0.01) with the reduction on ALT3 being larger for PLA (to 33 +/- 3%) than for CHOS (to 43 +/- 2%; P < 0.05). On ALT3, O2 saturation fell similarly from 84 +/- 2% at rest to 73 +/- 1% during the TT for both groups (P < 0.05), and on ALT10 O2 saturation fell more (P < 0.02) for CHOS (91 +/- 1 to 76 +/- 2%) than for PLA (90 +/- 1 to 81 +/- 1%). %SL Wpeak and O2 saturation were inversely related during the TT for both groups at ALT (r > or = -0.76; P < or = 0.03). It was concluded that, despite hypoxemia exacerbated by exercise, CHOS greatly improved TT performance at ALT in which there was a negative energy balance.

Dexamethasone as prophylaxis for acute mountain sickness. Effect of dose level.

Rapid exposure of unacclimatized persons to high altitude causes the syndrome acute mountain sickness (AMS). Prophylactic treatment with frequent high doses of dexamethasone has been shown to prevent AMS. To determine whether lower, less frequent doses were effective in preventing AMS, 28 men between the ages of 18 and 32 were exposed to a simulated altitude of 4,570 m for 45 h in a hypobaric chamber on two occasions while taking one of three doses of dexamethasone (4 mg, 1 mg, or .25 mg every 12 h) or a placebo in a double-blind, crossover design. The 4-mg dose of dexamethasone reduced the incidence of AMS symptoms compared with placebo and the other dose levels. Dexamethasone did not alter fluid balance or plasma volume changes, but treatment with 1 mg and 4 mg suppressed cortisol secretion. There was no evidence of adrenal cortical suppression after treatment with dexamethasone or placebo 48 h after discontinuing altitude exposure and drug treatment. The results indicate that 4 mg of dexamethasone twice daily is an effective prophylactic treatment for AMS, while lower doses are relatively ineffective.

Operation Everest. II: Nutrition and body composition.

Progressive body weight loss occurs during high mountain expeditions, but whether it is due to hypoxia, inadequate diet, malabsorption, or the multiple stresses of the harsh environment is unknown. To determine whether hypoxia due to decompression causes weight loss, six men, provided with a palatable ad libitum diet, were studied during progressive decompression to 240 Torr over 40 days in a hypobaric chamber where hypoxia was the major environmental variable. Caloric intake decreased 43.0% from 3,136 to 1,789 kcal/day (P less than 0.001). The percent carbohydrate in the diet decreased from 62.1 to 53.2% (P less than 0.001). Over the 40 days of the study the subjects lost 7.4 +/- 2.2 (SD) kg and 1.6% (2.5 kg) of the total body weight as fat. Computerized tomographic scans indicated that most of the weight loss was derived from fat-free weight. The data indicated that prolonged exposure to the increasing hypoxia was associated with a reduction in carbohydrate preference and body weight despite access to ample varieties and quantities of food. This study suggested that hypoxia can be sufficient cause for the weight loss and decreased food consumption reported by mountain expeditions at high altitude.

Use of bioelectrical impedance to assess body composition changes at high altitude.

This study determined the feasibility of using bioelectrical impedance analysis (BIA) to assess body composition alterations associated with body weight (BW) loss at high altitude. The BIA method was also evaluated relative to anthropometric assessments. Height, BW, BIA, skinfold (SF, 6 sites), and circumference (CIR, 5 sites) measurements were obtained from 16 males (23-35 yr) before, during, and after 16 days of residence at 3,700-4,300 m. Hydrostatic weighings (HW) were performed pre- and postaltitude. Results of 13 previously derived prediction equations using various combinations of height, BW, age, BIA, SF, or CIR measurements as independent variables to predict fat-free mass (FFM), fat mass (FM), and percent body fat (%Fat) were compared with HW. Mean BW decreased from 84.74 to 78.84 kg (P less than 0.01). As determined by HW, FFM decreased by 2.44 kg (P less than 0.01), FM by 3.46 kg (P less than 0.01), and %Fat by 3.02% (P less than 0.01). The BIA and SF methods overestimated the loss in FFM and underestimated the losses in FM and %Fat (P less than 0.01). Only the equations utilizing the CIR measurements did not differ from HW values for changes in FFM, FM, and %Fat. It was concluded that the BIA and SF methods were not acceptable for assessing body composition changes at altitude.

Altitude acclimatization attenuates plasma ammonia accumulation during submaximal exercise.

This study examined the effects of acclimatization to 4,300 m altitude on changes in plasma ammonia concentrations with 30 min of submaximal [75% maximal O2 uptake (VO2max)] cycle exercise. Human test subjects were divided into a sedentary (n = 6) and active group (n = 5). Maximal uptake (VO2max) was determined at sea level and at high altitude (HA; 4,300 m) after acute (t less than 24 h) and chronic (t = 13 days) exposure. The VO2max of both groups decreased 32% with acute HA when compared with sea level. In the sedentary group, VO2max decreased an additional 16% after 13 days of continuous residence at 4,300 m, whereas VO2max in the active group showed no further change. In both sedentary and active subjects, plasma ammonia concentrations were increased (P less than 0.05) over resting levels immediately after submaximal exercise at sea level as well as during acute HA exposure. With chronic HA exposure, the active group showed no increase in plasma ammonia immediately after submaximal exercise, whereas the postexercise ammonia in the sedentary group was elevated but to a lesser extent than at sea level or with acute HA exposure. Thus postexercise plasma ammonia concentration was decreased with altitude acclimatization when compared with ammonia concentrations following exercise performed at the same relative intensity at sea level or acute HA. This decrease in ammonia accumulation may contribute to enhanced endurance performance and altered substrate utilization with exercise following acclimatization to altitude.

Effects of altitude acclimatization on fluid regulatory hormone response to submaximal exercise.

To determine the effect of altitude acclimatization on plasma levels of atrial natriuretic peptide (ANP) during submaximal exercise and its relationship with renin and aldosterone, seven male volunteers aged 17-23 yr exercised to exhaustion on a cycle ergometer at 80-85% of their maximum O2 uptake at sea level (SL; 50 m), during 1 h in a hypobaric chamber [acute altitude (AA); 4,300 m], and after 14 or 16 days of residence on the summit of Pikes Peak, CO [chronic altitude (CA); 4,300 m]. Plasma samples taken before exercise, 10 min after the start of exercise, and 5 min postexercise were analyzed for ANP, plasma renin activity (PRA), and aldosterone (ALDO). ANP showed a progressive increase from rest to postexercise [7.49 +/- 1.63 to 11.32 +/- 1.80 (SE) pmol/ml and 6.05 +/- 2.55 to 10.38 +/- 7.20 pmol/ml; P = 0.049, exercise] at SL and AA, respectively, but not at CA (P = 0.039, altitude). Similarly, PRA and ALDO rose from rest to postexercise (P < 0.001, exercise), but the rise in ALDO with exercise was less during AA than during SL and CA (P = 0.002, phase). The decreased ANP levels during exercise after altitude acclimatization, with no change in PRA and ALDO, suggest that ANP has little effect on PRA and ALDO under these conditions.

Adductor pollicis muscle fatigue during acute and chronic altitude exposure and return to sea level.

Large muscle exercise performance is impaired during acute exposure to normobaric or hypobaric hypoxia, but the effects of hypoxic conditions on fatigue of isolated smaller muscle groups per se are poorly defined. We studied how acute and chronic altitude (ALT) exposure and post-ALT return to sea level (SL) affects voluntary strength and fatigue of the adductor pollicis muscle. Eight healthy men (mean age 28 yr) were studied on five separate occasions: at SL, on days 1 (acute) and 13 (chronic) at ALT (4,300 m), and on days 1 (post 1) and 3 or 4 (post 2) at SL after 20 days of residence at ALT. On each day, maximal voluntary contractions (MVCs) of the adductor pollicis were obtained before and at the end of each minute of submaximal intermittent contractions of the adductor pollicis (50% of MVC of rested muscle, 5 s of contraction/5 s of rest) until exhaustion, defined as the inability to exert or maintain 50% of rested MVC. MVC of rested muscle did not differ among days. Time to exhaustion was shorter at acute ALT [5.1 +/- 0.5 (SE) min] than at SL (7.4 +/- 0.8 min, P < 0.05) and tended to be shorter than at chronic ALT (6.6 +/- 0.7 min, P > 0.05). Compared with acute and chronic ALT, time to exhaustion was prolonged during post 1 (9.0 +/- 1.2 min, P < 0.05) but not post 2 (6.1 +/- 0.5 min, P > 0.05). We conclude that 1) MVC of rested adductor pollicis muscle is not impaired during or after ALT exposure, 2) compared with SL conditions, acute but not chronic ALT exposure leads to a more rapid decline in adductor pollicis MVC associated with submaximal contractions, and 3) time to exhaustion is prolonged for > or = 1 day after return from ALT.

Exercise VE and physical performance at altitude are not affected by menstrual cycle phase.

We hypothesized that progesterone-mediated ventilatory stimulation during the midluteal phase of the menstrual cycle would increase exercise minute ventilation (VE; l/min) at sea level (SL) and with acute altitude (AA) exposure but would only increase arterial O2 saturation (SaO2, %) with AA exposure. We further hypothesized that an increased exercise SaO2 with AA exposure would enhance O2 transport and improve both peak O2 uptake (VO2 peak; ml x kg-1 x 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 a VO2 peak and Exh test at 70% of their altitude-specific VO2 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) approximately 20-fold from the early follicular to midluteal phase at SL and AA. Peak VE (101 +/- 17) and submaximal VE (55 +/- 9) were not affected by cycle phase or altitude. Submaximal SaO2 did not differ between cycle phases at SL, but it was 3% higher during the midluteal phase with AA exposure. Neither VO2 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 VE is not increased at SL or AA. Moreover, neither maximal nor submaximal exercise performance is affected by menstrual cycle phase at SL or AA.

Muscle fatigue and exhaustion during dynamic leg exercise in normoxia and hypobaric hypoxia.

Using an exercise device that integrates maximal voluntary static contraction (MVC) of knee extensor muscles with dynamic knee extension, we compared progressive muscle fatigue, i.e., rate of decline in force-generating capacity, in normoxia (758 Torr) and hypobaric hypoxia (464 Torr). Eight healthy men performed exhaustive constant work rate knee extension (21 +/- 3 W, 79 +/- 2 and 87 +/- 2% of 1-leg knee extension O2 peak uptake for normoxia and hypobaria, respectively) from knee angles of 90-150 degrees at a rate of 1 Hz. MVC (90 degrees knee angle) was performed before dynamic exercise and during < or = 5-s pauses every 2 min of dynamic exercise. MVC force was 578 +/- 29 N in normoxia and 569 +/- 29 N in hypobaria before exercise and fell, at exhaustion, to similar levels (265 +/- 10 and 284 +/- 20 N for normoxia and hypobaria, respectively; P > 0.05) that were higher (P < 0.01) than peak force of constant work rate knee extension (98 +/- 10 N, 18 +/- 3% of MVC). Time to exhaustion was 56% shorter for hypobaria than for normoxia (19 +/- 5 vs. 43 +/- 7 min, respectively; P < 0.01), and rate of right leg MVC fall was nearly twofold greater for hypobaria than for normoxia (mean slope = -22.3 vs. -11.9 N/min, respectively; P < 0.05). With increasing duration of dynamic exercise for normoxia and hypobaria, integrated electromyographic activity during MVC fell progressively with MVC force, implying attenuated maximal muscle excitation. Exhaustion, per se, was postulated to related more closely to impaired shortening velocity than to failure of force-generating capacity.

Gender alters impact of hypobaric hypoxia on adductor pollicis muscle performance.

Recently, we reported that, at similar voluntary force development during static submaximal intermittent contractions of the adductor pollicis muscle, fatigue developed more slowly in women than in men under conditions of normobaric normoxia (NN) (Acta Physiol Scand 167: 233-239, 1999). We postulated that the slower fatigue of women was due, in part, to a greater capacity for muscle oxidative phosphorylation. The present study examined whether a gender difference in adductor pollicis muscle performance also exists during acute exposure to hypobaric hypoxia (HH; 4,300-m altitude). Healthy young men (n = 12) and women (n = 21) performed repeated static contractions at 50% of maximal voluntary contraction (MVC) force of rested muscle for 5 s followed by 5 s of rest until exhaustion. MVC force was measured before and at the end of each minute of exercise and at exhaustion. Exhaustion was defined as an MVC force decline to 50% of that of rested muscle. For each gender, MVC force of rested muscle in HH was not significantly different from that in NN. MVC force tended to decline at a faster rate in HH than in NN for men but not for women. In both environments, MVC force declined faster (P < 0.01) for men than for women. For men, endurance time to exhaustion was shorter (P < 0.01) in HH than in NN [6.08 +/- 0.7 vs. 8.00 +/- 0.7 (SE) min]. However, for women, endurance time to exhaustion was similar (not significant) in HH (12.86 +/- 1.2 min) and NN (13.95 +/- 1.0 min). In both environments, endurance time to exhaustion was longer for women than for men (P < 0.01). Gender differences in the impact of HH on adductor pollicis muscle endurance persisted in a smaller number of men and women matched (n = 4 pairs) for MVC force of rested muscle and thus on submaximal absolute force and, by inference, ATP demand in both environments. In contrast to gender differences in the impact of HH on small-muscle (adductor pollicis) exercise performance, peak O(2) uptake during large-muscle exercise was lower in HH than in NN by a similar (P > 0.05) percentage for men and women (-27.6 +/- 2 and -25.1 +/- 2%, respectively). Our findings are consistent with the postulate of a higher adductor pollicis muscle oxidative capacity in women than in men and imply that isolated performance of muscle with a higher oxidative capacity may be less impaired when the muscle is exposed to HH.

Women at altitude: ventilatory acclimatization at 4,300 m.

Women living at low altitudes or acclimatized to high altitudes have greater effective ventilation in the luteal (L) compared with follicular (F) menstrual cycle phase and compared with men. We hypothesized that ventilatory acclimatization to high altitude would occur more quickly and to a greater degree in 1) women in their L compared with women in their F menstrual cycle phase, and 2) in women compared with men. Studies were conducted on 22 eumenorrheic, unacclimatized, sea-level (SL) residents. Indexes of ventilatory acclimatization [resting ventilatory parameters, hypoxic ventilatory response, hypercapnic ventilatory response (HCVR)] were measured in 14 women in the F phase and in 8 other women in the L phase of their menstrual cycle, both at SL and again during a 12-day residence at 4,300 m. At SL only, ventilatory studies were also completed in both menstrual cycle phases in 12 subjects (i.e., within-subject comparison). In these subjects, SL alveolar ventilation (expressed as end-tidal PCO(2)) was greater in the L vs. F phase. Yet the comparison between L- and F-phase groups found similar levels of resting end-tidal PCO(2), hypoxic ventilatory response parameter A, HCVR slope, and HCVR parameter B, both at SL and 4,300 m. Moreover, these indexes of ventilatory acclimatization were not significantly different from those previously measured in men. Thus female lowlanders rapidly ascending to 4,300 m in either the L or F menstrual cycle phase have similar levels of alveolar ventilation and a time course for ventilatory acclimatization that is nearly identical to that reported in male lowlanders.

Quantitation of progressive muscle fatigue during dynamic leg exercise in humans.

There is virtually no published information on muscle fatigue, defined as a gradual decline in force-generating capacity, during conventional dynamic (D) leg exercise. To quantitate progression of fatigue, we developed 1) a model featuring integration of maximal voluntary static contraction (MVC) of knee extension (KE) muscles with ongoing DKE and 2) a device that allows frequent rapid transfer between DKE isolated to the quadriceps femoris muscles and measurement of KE MVC. Eight healthy men performed graded and submaximal constant work rate one-leg DKE to exhaustion while seated. Work rate, a product of a contraction rate (1 Hz), force measured at the ankle, and distance of ankle movement from 90 degrees to 150 degrees of KE, was precisely controlled. Lack of rise in myoelectric activity in biceps femoris of the active leg during DKE and MVC was consistent with restriction of muscle action to quadriceps femoris. The slope of the linear relationship between O2 uptake and work rate was 13.7 ml O2/W (r = 0.93). This slope and the increase of heart rate relative to increasing work intensity agreed with published values for D leg exercise. Test-retest values for O2 uptake were similar (P > 0.05) for matched DKE work rates. To track fatigue, MVC (90 degrees knee angle) was performed every 2 min of DKE. After 4 min of DKE at work rates corresponding to (mean +/- SE) 66 +/- 2, 78 +/- 2, and 100% of peak DKE O2 uptake, MVC fell to 95 +/- 3, 90 +/- 5, and 65 +/- 7%* of MVC of rested muscle, respectively (*P < 0.01 from previous work rates). Virtually identical declines in MVC were observed by the end of graded work rate DKE and submaximal constant work rate DKE tests. Quantitation of progressive muscle fatigue during D leg exercise provides a framework to study the effects of a variety of interventions on the fatigue process and may permit unique insights into the involved mechanisms.

Women at altitude: short-term exposure to hypoxia and/or alpha(1)-adrenergic blockade reduces insulin sensitivity.

After short-term exposure to high altitude (HA), men appear to be less sensitive to insulin than at sea level (SL). We hypothesized that the same would be true in women, that reduced insulin sensitivity would be directly related to the rise in plasma epinephrine concentrations at altitude, and that the addition of alpha-adrenergic blockade would potentiate the reduction. To test the hypotheses, 12 women consumed a high-carbohydrate meal at SL and after 16 h at simulated 4,300-m elevation (HA). Subjects were studied twice at each elevation: once with prazosin (Prz), an alpha(1)-adrenergic antagonist, and once with placebo (Pla). Mathematical models were used to assess insulin resistance based on fasting [homeostasis model assessment of insulin resistance (HOMA-IR)] and postprandial [composite model insulin sensitivity index (C-ISI)] glucose and insulin concentrations. Relative to SL-Pla (HOMA-IR: 1.86 +/- 0.35), insulin resistance was greater in HA-Pla (3.00 +/- 0.45; P < 0.05), SL-Prz (3.46 +/- 0.51; P < 0.01), and HA-Prz (2.82 +/- 0.43; P < 0.05). Insulin sensitivity was reduced in HA-Pla (C-ISI: 4.41 +/- 1.03; P < 0.01), SL-Prz (5.73 +/- 1.01; P < 0.05), and HA-Prz (4.18 +/- 0.99; P < 0.01) relative to SL-Pla (8.02 +/- 0.92). Plasma epinephrine was significantly elevated in HA-Pla (0.57 +/- 0.08 ng/ml; P < 0.01), SL-Prz (0.42 +/- 0.07; P < 0.05), and HA-Prz (0.82 +/- 0.07; P < 0.01) relative to SL-Pla (0.28 +/- 0.04), but correlations with HOMA-IR, HOMA-beta-cell function, and C-ISI were weak. In women, short-term exposure to simulated HA reduced insulin sensitivity compared with SL. The change does not appear to be directly mediated by a concurrent rise in plasma epinephrine concentrations.

Influence of altitude and caffeine during rest and exercise on plasma levels of proenkephalin peptide F.

The purpose of this study was to examine the resting and exercise response patterns of plasma Peptide F immunoreactivity (ir) to altitude exposure (4300 m) and caffeine ingestion (4 mg.kg b.w.-1). Nine healthy male subjects performed exercise tests to exhaustion (80-85% VO2max) at sea level (50 m), during an acute altitude exposure (1 hr, hypobaric chamber, 4300 m) and after a chronic (17-day sojourn, 4300 m) altitude exposure. Using a randomized, double-blind/placebo experimental design, a placebo or caffeine drink was ingested 1 hour prior to exercise. Exercise (without caffeine) significantly (p less than 0.05) increased plasma Peptide F ir values during exercise at chronic altitude only. Caffeine ingestion significantly increased plasma Peptide F ir concentrations during exercise and in the postexercise period at sea level. Conversely caffeine ingestion at altitude resulted in significant reductions in the postexercise plasma Peptide F ir values. The results of this study demonstrate that the exercise and recovery response patterns of plasma Peptide F ir may be significantly altered by altitude exposure and caffeine ingestion. These data support further study examining relationships between Peptide F (and other enkephalin-containing polypeptides) and epinephrine release in response to these types of physiological stresses.

Exercise responses after altitude acclimatization are retained during reintroduction to altitude.

Following 2 to 3 wk of altitude acclimatization, ventilation is increased and heart rate (HR), plasma volume (PV), and lactate accumulation ([La]) are decreased during submaximal exercise. The objective of this study was to determine whether some degree of these exercise responses associated with acclimatization would be retained upon reintroduction to altitude (RA) after 8 d at sea level (SL). Six male lowlanders (X +/- SE; 31 +/- 2 yr, 82.4 +/- 4.6 kg) exercised to exhaustion at the same relative percentages of peak oxygen uptake (VO2peak) at SL, on acute altitude (AA) exposure, after a 16-d chronic altitude (CA) exposure on Pikes Peak (4,300 m), and during a 3- to 4-h RA in a hypobaric chamber (4,300 m; 446 mm Hg) after 8 d at SL. The submaximal exercise to exhaustion time (min) was the same at SL (66.0 +/- 1.6), AA (67.7 +/- 7.3), CA (79.9 +/- 6.2), and RA (67.9 +/- 1.9). At 75% VO2peak: (1) arterial oxygen saturation (SaO2) increased from AA to CA (67.0 +/- 1.5 vs 78.5 +/- 1.8%; P < 0.05) and remained increased at RA (77.0 +/- 2.0%); (2) HR decreased from SL to CA (171 +/- 6 vs 152 +/- 9 beats x min-1; P < 0.05) and remained decreased at RA (157 +/- 5 beats x min-1); (3) calculated PV decreased 6.9 +/- 10.0% at AA, 21.3 +/- 11.1% at CA, and 16.7 +/- 5.4% at RA from SL baseline values, and (4) [La] decreased from AA to CA (5.1 +/- 0.9 vs 1.9 +/- 0.4 mmol x L-1; P < 0.05) and remained decreased at RA (2.6 +/- 0.6 mmol x L-1). Upon RA after 8 d at SL, the acclimatization responses were retained 92 +/- 9% for SaO2, 74 +/- 8% for PV, and 58 +/- 3% for [La] at 75% VO2peak. In conclusion, although submaximal exercise to exhaustion time is not improved upon reintroduction to altitude after 8 d at sea level, retention of beneficial exercise responses associated with altitude acclimatization is likely in individuals whose work, athletic competition, or recreation schedules involve intermittent sojourns to high elevations.

The effect of naproxen on acute mountain sickness and vascular responses to hypoxia.

The role of prostaglandins in the pathogenesis of acute mountain sickness and two hypoxia-induced vascular responses was evaluated using the cyclooxygenase inhibitor naproxen. Eleven men spent 24 hours at sea level, followed by 34 hours of decompression to 428 mm Hg while receiving naproxen (N), 250 mg twice daily or placebo (P) in a double-blind crossover trial. Serum naproxen levels measured by high pressure liquid chromatography were not changed by hypoxia. The severity of acute mountain sickness (AMS) by the Environmental Symptom Questionnaire scores and observer assessment were unaffected by drug treatment. Retinal artery diameter measured from projected fundus photographs was increased after 27 hours at altitude (11.4 +/- .5 mm) vs. sea level (9.4 +/- .5 mm, p less than 0.05) during both trials. Upright mean arterial pressure fell after 6 hours at altitude (79 +/- 3 mm Hg during N and P vs. 92 +/- 3 at sea level, p less than 0.01). Minute ventilation, end expiratory alveolar PO2 and PCO2 did not differ between drug trials. This study suggests vasodilating prostaglandins do not have a major role in the genesis of AMS, hypoxia-induced retinal vasodilatation, or postural blood pressure responses in man.

Postural instability and acute mountain sickness during exposure to 24 hours of simulated altitude (4300 m).

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%, p < 0.001) and 23 to 24 h (31%, p < 0.001). 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.

A software package for administering and monitoring the Environmental Symptoms Questionnaire (ESQ-III).

The latest version of the Environmental Symptoms Questionnaire (ESQ-III) contains 67 symptoms designed to allow researchers to evaluate a broad range of environmental stresses. We have developed an interactive computer software package that administers and monitors the ESQ-III. This package, written in a format maximizing clarity, provides consistency of administration from one test or day to another, checks for response inconsistencies, maintains subject motivation, provides feedback to the subject and allows an investigator to quickly inspect raw and computed results. Further, because there is no interaction between investigators and subjects, no experimenter bias can be introduced. This package can be adapted to almost any computer system having a CRT and at least one disc drive.

Maximal and submaximal exercise performance at altitude.

BACKGROUND: Exercise performance data of numerous altitude research studies and competitive sporting events of the last four decades are reviewed. METHODS: The primary focus is on the wide interindividual variation associated with maximal and submaximal exercise performance that occurs at different altitudes and for different periods of time at altitude. RESULTS: Fitness level, pre-exposure resident altitude, gender, and duration of altitude exposure are qualitatively assessed to determine their contribution to the overall variability. Of these, pre-altitude exposure fitness level difference contributes the most variability and gender difference contributes the least. It is also determined that beginning at an altitude of 580 m, maximal aerobic power (VO2max reduced and does not improve with extended exposure as long as the individual's level of fitness level is not altered significantly by increases in activity, exercise training or by altitude-induced physical deterioration. Submaximal exercise performance is also impaired at altitude. CONCLUSION: By assessing the performance of elite athletes, who are performing at an "all-out" effort in precisely timed events for which they are trained, it is determined that: a) the magnitude of submaximal exercise impairment is proportional to both the elevation and exercise duration at a given altitude; and b) submaximal exercise performance at altitude can improve with continued exposure without an increase in VO2max. Muscle strength, maximal muscle power, and anaerobic performance at altitude are not affected as long as muscle mass is maintained. In addition, performance is not impaired in athletic activities that have a minimal aerobic component and can be performed at high velocity (e.g., sprints).