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 and endurance performance of moderate altitude residents at 4300 m.

Recent work from our laboratory demonstrated that carbohydrate supplementation (CHOS) during exercise improved prolonged time-trial (TT) performance of sea-level residents (SLR) living at 4300 m while they were in daily negative energy balance (- 1250 kcal x day (-1); [ ]). The purposes of the current study were to determine during initial exposure to 4300 m:1) whether CHOS also improves TT performance of moderate altitude residents (MAR) who are in energy balance and 2) if acclimatization to moderate elevations benefits TT performance. Fifteen Air Force Academy (AFA) active duty members (age: 30 +/- 1 yrs; mean +/- SE), who had been living at approximately 2000 m for 21 +/- 3 months performed a maximal-effort 720-kJ cycle TT at the AFA and at Pikes Peak (PP), CO, (4300 m) on days 1 (PP1) and 3 (PP3). Daily energy intake and expenditure were maintained similarly at the AFA and PP. At the start of the TTs at PP, and then every 15 min thereafter, 9 subjects drank a 10 % CHO solution (0.175 g x kg (-1) body weight) and 6 subjects drank a placebo (PLA) solution. All subjects were allowed to freely adjust the power output of the cycle ergometer and drank water AD LIBITUM. Performance time did not differ between groups on PP1 (CHOS vs. PLA; 101 +/- 8 vs. 116 +/- 10 min) or PP3 (95 +/- 8 vs. 107 +/- 12 min). For both groups, cycle times on PP1 and PP3 were longer compared to the AFA (p<0.01) and were improved from PP1 to PP3 (p<0.05). Exercise intensity (i.e., % peak oxygen uptake) was maintained similarly at approximately 62 % during the TTs at the AFA and PP. Blood glucose was 1.5 to 2.0 mmol x L (-1) higher for CHOS vs. PLA (p<0.01). It was concluded that CHOS provided no TT performance benefit for MAR at 4300 m when energy balance was maintained. However, the decrements in TT performance and exercise intensity were attenuated at 4300 m in MAR compared to those of SLR as a result of acclimatization attained while living for nearly 2 years at approximately 2000 m.

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.

Energy intake deficit and physical performance at altitude.

BACKGROUND: Physical performance of sea-level (SL) residents acutely exposed to altitude (ALT) is diminished and may improve somewhat with ALT acclimatization. HYPOTHESIS: A large reduction in lean body mass (LBM), due to severe energy intake deficit during the first 21 d of ALT (4300 m) acclimatization, will adversely affect performance. METHODS: At ALT, 10 men received a deficit (DEF) of 1500 kcal x d(-1) below body weight (BW) maintenance requirements and 7 men received adequate (ADQ) kcal x d(-1) to maintain BW. Performance was assessed by: 1) maximal oxygen uptake (VO2max); 2) time to complete 50 cycles of a lift and carry task (L+C); 3) number of one-arm elbow flexions (10% BW at 22 flexions x min(-1); and 4) adductor pollicis (AP) muscle strength and endurance time (repeated 5-s static contractions at 50% of maximal force followed by 5-s rest, to exhaustion). Performance and body composition (using BW and circumference measures) were determined at SL and at ALT on days 2 through 21. RESULTS: At SL, there were no between-group differences (p > 0.05) for any of the performance measures. From SL to day 21 at ALT, BW and LBM declined by 6.6 +/- 3 kg and 4.6 kg, respectively, for the DEF group (both p < 0.01), but did not change (both p > 0.05) for the ADQ group. Performance changes from day 2 or 3 to day 20 or 21 at ALT were as follows (values are means +/- SD): VO2max (ml x min(-1)): DEF = +97 +/- 237, ADQ = +159 +/- 156; L + C (s): DEF = -62 +/- 35*, ADQ = -35 +/- 20* (*p < 0.05; improved from day 3); arm flex (reps): DEF = -2 +/- 7, ADQ = +2 +/- 8; AP endurance (min): DEF = +1.4 +/- 2, ADQ = + 1.9 +/- 2; AP strength (kg): DEF = -0.7 +/- 4, ADQ = -1.2 +/- 2. There were no differences in performance between groups. CONCLUSIONS: A significant BW and LBM loss due to underfeeding during the first 21 d of ALT acclimatization does not impair physical performance at ALT.

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.

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.

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.

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.

Circulatory responses to orthostasis during alpha1-adrenergic receptor blockade at high altitude.

BACKGROUND: Increased blood level of norepinephrine, a primary alpha-adrenergic agonist, is associated with high-altitude exposure, and may help regulate key physiological functions (e.g., blood pressure). We hypothesized that blocking alpha1-adrenergic receptors would impair circulatory compensation for an orthostatic challenge to a greater extent at altitude than at sea level. METHODS: Sixteen healthy women (23 +/- 2 yr) were randomly assigned to receive either 2 mg prazosin (n = 8) or placebo (n = 8) t.i.d. (double-blind design) for 12 d at sea level and during the first 12 d of altitude residence (4300 m). Passive 60 degrees upright tilt was performed at sea level (10 d of treatment), and after 3 and 10 d at altitude. Mean arterial BP (MABP, via auscultation) and heart rate (HR, via ECG) were measured every min during 10 min each of supine rest and tilt. RESULTS: For the prazosin group compared with the placebo group: 1.) Supine and tilt MABP were consistently lower (p < 0.05) at sea level; 2.) MABP did not differ (p > 0.05) for either day at altitude; 3.) HR was similar for both positions at sea level and altitude; and 4.) MABP was consistently less only at sea level and HR was consistently greater only at altitude (both p < 0.05) in response to tilt. CONCLUSIONS: alpha1-adrenergic blockade altered MABP and HR responses to tilt at sea level and altitude, but circulatory responses to orthostasis were well maintained in both environments. At altitude, BP during tilt was sufficiently maintained by a compensatory increase in heart rate, likely mediated by parasympathetic withdrawal.

Intraocular pressure and acclimatization to 4300 M altitude.

BACKGROUND: Studies were conducted to determine the effect of altitude exposure on intraocular pressure (IOP) and any relationship with the severity of acute mountain sickness (AMS). HYPOTHESES: a) IOP is decreased during exposure to 4300 m altitude; b) there is a positive correlation between IOP and AMS; and c) there is a correlation between changes in urinary catecholamines and IOP. METHODS: IOP (noncontact tonometry) was measured in 11 resting males during acute simulated altitude (446 mmHg, < 2 h, hypobaric chamber), during altitude acclimatization (15 d at 4300 m), and in 6 of the 11 volunteers during re-exposure in the chamber after 8 d at sea level (Study A). In a second study (Study B) of 12 females, IOP (contact tonometry) and 24-h urinary catecholamines were measured during a 50-h chamber exposure (446 mmHg). AMS severity was assessed using the Environmental Symptoms Questionnaire (ESQ-C). RESULTS: IOP decreased 25% after 2 d at altitude and returned toward sea level values by 15 d (Study A). IOP was reduced 13% after 5 h of exposure followed by return toward sea level values (Study B). Significant correlation was found between the sea level IOP and ESQ-C (Study A); significant correlation was found between the reduction in IOP and the ESQ-C and urinary epinephrine concentrations (Study B). CONCLUSIONS: Altitude exposure resulted in a reduction in IOP that occurred within hours and recovered during acclimatization. This reduction may be related to increases in epinephrine concentration. Measurement of IOP before and during altitude exposure may provide an objective method of assessing an individual's response to hypoxic stress.

Reproducible voluntary muscle performance during constant work rate dynamic leg exercise.

During constant intensity treadmill or cycle exercise, progressive muscle fatigue is not readily quantified and endurance time is poorly reproducible. However, integration of dynamic knee extension (DKE) exercise with serial measurement of maximal voluntary contraction (MVC) force of knee extensor muscles permits close tracking of leg fatigue. We studied reproducibility of four performance indices: MVC force of rested muscle (MVC(rest)) rate of MVC force fall, time to exhaustion, and percentage of MVC(rest) (%MVC(rest)) at exhaustion in 11 healthy women (22+/-1 yrs) during identical constant work rate 1-leg DKE (1 Hz) on 2 separate days at sea level (30 m). Means+/-SD for the two test days, and the correlations (r), standard estimate errors and coefficients of variation (CV%) between days were, respectively: a) MVC(rest)(N), 524+/-99 vs 517+/-111, 0.91, 43.0, 4.9%; b) MVC force fall (N x min(-1)), -10.77+/-9.3 vs -11.79+/-12.1, 0.94, 3.6, 26.5 %; c) Time to exhaustion (min), 22.6+/-12 vs 23.9+/-14, 0.98, 2.7, 7.5 %; and d) %MVC(rest) at exhaustion, 65+/-13 vs 62+/-14, 0.85, 7.8, 5.6%. There were no statistically significant mean differences between the two test days for any of the performance measures. To demonstrate the potential benefits of evaluating multiple effects of an experimental intervention, nine of the women were again tested within 24hr of arriving at 4,300 m altitude using the identical force, velocity, power output, and energy requirement during constant work rate dynamic leg exercise. Low variability of each performance index enhanced the ability to describe the effects of acute altitude exposure on voluntary muscle function.

Improving athletic performance: is altitude residence or altitude training helpful?

Exercise training studies conducted at different altitudes (1250-5700 m) of varying durations (30 min to 19 wk) are critically reviewed to determine the efficacy of using altitude as a training stimulus to enhance sea level and altitude exercise performance. Four strategies are discussed: a) exercise training while residing at the same altitude; b) exercise training at altitude but residing at sea level; c) exercise training at low altitude but residing at a higher altitude; and d) exercise training under sea level and altitude conditions but only after altitude acclimatization has occurred. Residing at altitude causes a multitude of potentially beneficial physiological, ventilatory, hematological and metabolic changes that theoretically should induce a potentiating effect on endurance exercise performance. While it is accepted that endurance performance is greatly enhanced at altitude, there is less support for the view that altitude training while residing at altitude improves subsequent sea level endurance performance. There is some evidence, though also not universally accepted, that training at altitude but residing at sea level may benefit sea level endurance performance. Most recently, the combination of "living high" (e.g., at 2500 m) to obtain beneficial physiological changes associated with altitude acclimatization and "training low" (e.g., at 1250 m) to allow maintenance of high-intensity training is accumulating scientific and popular support as the most advantageous strategy to improve subsequent sea level exercise performance in well-trained, competitive runners.

Slower fatigue and faster recovery of the adductor pollicis muscle in women matched for strength with men.

In previous gender comparisons of muscle performance, men and women rarely have been closely matched, absolute force has not been equalized, and rates of fatigue and early recovery have not been determined. We compared adductor pollicis muscle performance at a similar absolute force development in healthy men and women (both n=9) matched for adductor pollicis maximal voluntary contraction (MVC) force (132 +/- 5 N for women and 136 +/- 4 N for men, mean +/- SE, P > 0.05). Subjects repeated static contractions at a target force of approximately 50% of MVC force of rested muscle (68 +/- 3 N or 51.9 +/- 1.0% MVC for women and 72 +/- 2 N or 53.0 +/- 2.0% MVC for men, P > 0.05) for 5 s followed by 5 s rest until exhaustion, i. e. inability to maintain the target force for 5 s. MVC force was measured following each minute of exercise, at exhaustion, and after each minute for 3 min of passive recovery. For women compared with men: MVC force fell less after 1 min of exercise (to 93 +/- 1% vs. 80 +/- 3% of MVC force of rested muscle, respectively, P < 0.05); MVC force (N min-1) fell approximately 2-fold slower (P < 0.05); and endurance time to exhaustion was nearly two times longer (14.7 +/- 1. 6 min vs. 7.9 +/- 0.7 min, P < 0.05). After declining to a similar level of MVC force of rested muscle at exhaustion (56 +/- 1% for women and 56 +/- 3% for men), MVC force rose faster in women than in men (to 71 +/- 2% vs. 65 +/- 3% of MVC force of rested muscle, respectively; P < 0.05) during the first minute of recovery. The findings are consistent with the hypothesis that slower adductor pollicis muscle fatigue in women is linked with differences between men and women both in impairment of force generating capacity, per se, and in rates of recovery between contractions.

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.

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).

Ventilatory capacities at sea level and high altitude.

Because air is less dense at high altitude (HA), airway resistance is reduced and maximum inspiratory and expiratory flows are greater than at sea level (SL). Despite the reduction in airway resistance, ventilatory muscle endurance may be decreased by hypobaric hypoxia and, thus, may be a factor in limiting exercise at HA. To explore the effects of HA on ventilatory capacities and their relation to ventilatory demands of exercise, we measured 15-s maximum voluntary ventilation (MVV), 15-min maximum sustainable ventilation (MSV), and maximum airway pressures (Plmax and PEmax) in 18 healthy young men at SL and HA (Pikes Peak, 4300 m, or hypobaric chamber, PB approximately 460 mmHg). In eight of these subjects ventilatory capacities were compared with exercise ventilations. We also measured the effects of 36% O2 on the MSV in 12 of the subjects exposed to simulated altitude. Similar results were obtained at either simulated or actual HA. We found that MVV increased (p < 0.001) by 20% and the MSV (p < 0.001) by 15% at HA. Administration of 36% O2 at HA increased MSV further by 5% with no effect on MVV. No effect of HA on maximum inspiratory and expiratory pressures was found. We confirmed previous findings of modest increases in forced 1-s expired volume (FEV1) and slight decreases in forced vital capacity (FVC) at HA. At both SL and HA, the MSV exceeded the ventilatory demands of submaximal cycle exercise that could be sustained for about 30 min. During progressive cycle exercise to exhaustion, however, peak VE was not different from MVV, either at SL or HA. We conclude that the small, but significant, increase in MSV with 36% O2 administration at HA suggests that hypoxia decreases ventilatory endurance for flow loads as determined by the MSV. Thus, the possibility that ventilatory limits have a role in cessation of exercise at high altitude cannot be ruled out.

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.

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.

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.