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00005768-199712000-0000700005768_1997_29_1588_beidleman_acclimatization_12article< 92_0_7_5 >Medicine & Science in Sports & Exercise©1997The American College of Sports MedicineVolume 29(12)December 1997pp 1588-1595Exercise responses after altitude acclimatization are retained during reintroduction to altitude[Basic Sciences: Original Investigations]BEIDLEMAN, BETH A.; MUZA, STEPHEN R.; ROCK, PAUL B.; FULCO, CHARLES S.; LYONS, TIMOTHY P.; HOYT, REED W.; CYMERMAN, ALLENThermal and Mountain Medicine Division, U.S. Army Research Institute of Environmental Medicine, Natick, MA 01760Submitted for publication January 1997.Accepted for publication August 1997.ABSTRACTExercise responses after altitude acclimatization are retained during reintroduction to altitude. Med. Sci. Sports Exerc., Vol. 29, No. 12, pp. 1588-1595, 1997. 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 ([horizontal bar over]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·min-1;P < 0.05) and remained decreased at RA (157 ± 5 beats·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·L-1; P < 0.05) and remained decreased at RA (2.6 ± 0.6 mmol·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.Acclimatization to altitude is a process, occurring over a 2-3 wk period, that results in systemic adaptations that can be measured as physiological responses. Some of these physiological responses include an increase in ventilation (˙VE) (14) and a decrease in heart rate(HR) (1), plasma volume (PV) (22), and blood lactate accumulation ([La]) during submaximal exercise(32) relative to initial altitude exposure. These responses may contribute to the dramatically improved submaximal exercise capacity observed in the well-acclimatized lowlander(18,25). The time course for each of these responses is variable. Some are fully manifest within days of arriving at altitude while others require 2-3 wk (33). Although the time course for altitude acclimatization has been well studied, the time course for deacclimatization to altitude, a process that results in the loss of systemic adaptations and measured physiological responses associated with acclimatization, has received little attention.Studies examining deacclimatization to altitude have generally performed postexposure measurements only at low altitude. These studies suggest that some degree of altitude acclimatization, measured at low altitude, is retained from as few as 4 d to as long as 45 d after return to low altitude(12,13,21,22,29). However, postexposure measurements were not made at high altitude, and therefore we do not know whether some degree of altitude acclimatization is also retained during a reintroduction to altitude (RA). One study (21) did make resting postexposure measurements at high altitude during a 2-h stepwise reintroduction to altitude in acclimatized mountaineers and nonacclimatized males. They reported a significantly higher ventilation and lower HR during reintroduction to altitude in mountaineers than in nonacclimatized males after a 13-35 d low altitude deacclimatization. The problem with this study is that neither pre-exposure nor chronic exposure measurements were made. Therefore, whether the mountaineers had different physiological responses from the nonacclimatized males before beginning their expedition remains unknown. The data from this study suggest but do not prove that resting ventilatory and cardiovascular responses to acclimatization were retained during reintroduction to altitude after a period of time at low altitude.Retention of altitude acclimatization during RA has never been studied in a systematic and controlled manner. Although retention of acclimatization is likely, the percent retention of physiological responses associated with altitude acclimatization during RA after a defined number of days at low altitude has never been documented. Furthermore, the magnitude of physiological responses retained during exercise during RA has never been studied, and these responses may be different from responses measured at rest because of the added stimulation of hypoxia and exercise. Preservation of some of the physiological responses associated with altitude acclimatization during RA, such as those that dramatically improve submaximal exercise performance, have important implications for people whose work, athletic competition, or recreation schedules involve intermittent sojourns to high elevations. The purpose of this study was to test the hypothesis that some degree of exercise responses associated with altitude acclimatization would be retained upon RA after 8 d at sea level (SL).METHODSVolunteer test subjects. Six male volunteers participated in this study. They had a mean (± SE) age, initial body weight (BW), and height of 31 ± 2 yr, 82.4 ± 4.6 kg, and 180 ± 10 cm. Percent body fat, determined by hydrostatic underwater weighing, was 16.5 ± 1.6%. These men were randomly selected as a subset from 12 volunteers who participated in a larger study on acclimatization and deacclimatization to altitude. Each was a lifelong, low-altitude resident and had no exposure to altitudes greater than 1,000 m for at least 6 months before the study. All were healthy, physically active members of a U.S. Army Special Forces unit. Each provided written acknowledgment of his free and informed voluntary consent and was made aware of his right to withdraw without prejudice at any time. Investigators adhered to AR 70-25 and USAMRDC Regulation 70-25 on the use of volunteers in research.Study protocol. This study used a repeated measures design in which each volunteer served as his own control. The study consisted of four phases: 1) a 10-d SL phase at Natick, MA (50 m); 2) a simulated acute altitude(AA) exposure (<2 h) phase in a hypobaric chamber (4,300 m, 446 mm Hg); 3) an 18-d chronic altitude (CA) phase on the summit of Pikes Peak, CO (4,300 m); and 4) a 3- to 4-h RA phase in a hypobaric chamber (4,300 m, 446 mm Hg) after 8 d at SL. Volunteers were transported to and from Pikes Peak by commercial plane and automobile in approximately 8 h. After the volunteers entered the hypobaric chamber for the AA and RA phases, the chamber was decompressed to the barometric equivalent of 4,300 m over a period of approximately 12 min. All exercise tests in the hypobaric chamber were initiated within 30 min of arriving at 4,300 m. During exercise testing sessions, temperature and relative humidity were maintained at 21 ± 2 °C and 50 ± 5%, respectively. The volunteers had unrestricted access to fluid and food throughout the study.Exercise testing. All volunteers completed a submaximal exercise to exhaustion (EXH) test at SL, AA, CA, and RA and a peak oxygen uptake(˙VO2peak) test at SL, AA, and CA. A fourth ˙VO2peak test was not conducted during RA based on previous reports showing that˙VO2peak does not change from AA to RA after 5 d at SL(7). The ˙VO2peak and EXH tests were separated by at least 48 h. For the CA phase, the ˙VO2peak and EXH tests were performed on days 14 and 16 at 4,300 m, respectively. All exercise testing was performed at the same time of day for each volunteer. Before all exercise tests, the volunteers were required to abstain from alcohol for at least 48 h and not exercise on the actual day of testing. Otherwise, volunteers maintained the same level of physical activity throughout the study.For each exercise testing session, the volunteer was weighed (wearing t-shirt, shorts, and socks) to the nearest 0.1 kg, and electrocardiogram (EKG) electrodes were attached. During exercise, HR was determined from continuous EKG recordings (Cardiovit AT-6C, Schiller Canada, Inc., Nepean, Ontario, Canada). Respiratory gas measurements were made continuously during the˙VO2peak test and intermittently during the EXH test by open circuit calorimetry using an appropriately calibrated metabolic cart (Model 2900, SensorMedics Corp., Anaheim, CA), which provided values for oxygen uptake (˙VO2), carbon dioxide output (˙VCO2), respiratory exchange ratio (RER), and minute ventilation (˙VE(BTPS)). Arterial oxygen saturation (SaO2) was measured by finger pulse oximetry (Oxyshuttle, SensorMedics). The validity of this finger pulse oximeter is ± 2% above 70% SaO2 and ± 3% below 70% SaO2. Cardiorespiratory measurements were made while the volunteer stood at rest for 5 min before the exercise test began and again during exercise testing (see below). The ventilatory equivalent for CO2(˙VE · ˙VCO2-1) was calculated from individual˙VE and ˙VCO2 data to minimize intra-subject variability in˙VE resulting from different body sizes and metabolic rates.For each individual, percent retention of acclimatization-associated response for each variable was calculated as the difference in the CA response from the AA response divided by the difference between the RA response from the AA response, i.e., (RA-AA)/(CA-AA)·100. The fractional contribution of fat and carbohydrate to energy expenditure during exercise testing was calculated using the tables of Lusk (23).Peak exercise testing. The ˙VO2peak was determined by a progressive-intensity, continuous treadmill running test to exhaustion described by Sawka et al. (30). The volunteers performed a warm-up bout of 10 min walking (1.56 m·s-1) at a 10% treadmill grade. At SL, if a volunteer's HR exceeded 140 beats·min-1 during warmup, the treadmill speed was set at 2.68 m·s-1; if HR was ≤ 140 beats·min-1, the speed was set at 3.13 m·s-1. The initial incline was 5% followed by 2.5% increments every 1.5 min for all volunteers. Based on the ≈33% expected reduction in˙VO2peak at altitude (20), volunteers ran at 2.68 m·s-1 at AA, CA, and RA. The highest oxygen uptake achieved for 1 min before reaching voluntary exhaustion was recorded as˙VO2peak. After the ˙VO2peak test, a 4-min postexercise blood sample was drawn by venipuncture for evaluation of blood [La].Submaximal exercise testing. Before the EXH test, a cannula was inserted into a superficial arm vein and kept patent with a dilute heparin solution to allow serial blood samples to be collected without repeat venipuncture. A 20-min equilibration period (standing) was completed before obtaining the 10-mL resting blood sample for evaluation of [La], glucose[GLU], hemoglobin [Hb], hematocrit (Hct), glycerol [GLY], cortisol [COR], and free fatty acids [FFA]. Additional blood samples were taken at 10, 40, and 60 min, and at exhaustion. Two milliliters of whole blood from each sample was immediately assayed for [La], [GLU], [Hb], and Hct. The remaining 8 mL of blood was centrifuged, and the plasma was aliquoted, frozen, and stored at -80°C until final analysis.Each volunteer exercised at 40% of his altitude-specific˙VO2peak for the first 15 min, 75% ˙VO2peak from 15 to 60 min, and 85% ˙VO2peak from 60 min to exhaustion. Treadmill speed and/or grade were adjusted to reach the desired percentage of˙VO2peak for each volunteer. In all cases, the required percentage of ˙VO2peak was obtained within 10 min of the beginning of each stage. The ˙VO2 for each stage of exercise during RA was maintained identically to that during the CA phase. Cardiorespiratory measurements were obtained during the last 10 min of each exercise stage, and the mean value collected during the last 3 min of the test was analyzed. The volunteers were aware of their ongoing exercise time during the EXH test. Volunteers refrained from consuming any nutrients for approximately the same number of hours before each EXH test.Blood analyses. Aliquots of heparinized blood were analyzed for[La], [GLU], [Hb], and Hct. Blood [La] and [GLU] were measured in duplicate using a glucose/lactate analyzer (Model 2300; Yellow Springs Instruments, Yellow Springs, OH). The [Hb] was measured in duplicate using a hemoximeter(Radiometer, Inc., Copenhagen, Denmark). The Hct was measured in triplicate using heparinized microcapillary tubes. Changes in [Hb] and Hct from SL baseline values were used to calculate changes in PV (8). Plasma concentrations of [GLY] and [FFA] (Sigma Chemical Co., St. Louis, MO; Wako Chemicals USA, Inc., Richmond, VA) were determined by enzymatic colorimetric assays in duplicate using a spectrophotometer (Model Lamda 3A; Perkin-Elmer Co., Norwalk, CT). Plasma concentrations of [COR] were determined in duplicate using a solid phase 125I radioimmunoassay (Diagnostic Products Co., Los Angeles, CA) and a gamma counter (Model 5002; Packard Instrument Co., Meriden, CT). Blood [GLU] and plasma [GLY], [FFA], and [COR] were analyzed to determine differences in substrate utilization between the four study phases. The intra-assay variances for [GLY], [FFA], and [COR] were 3.7%, 2.6%, and 4.5%, respectively. All samples for one volunteer were analyzed in the same assay to avoid interassay variations. All samples were thawed once for each assay procedure.Statistical analyses. One way ANOVAs with repeated measures were used to analyze the differences between study phases for all data, except the blood parameters collected during the EXH test, which were analyzed using two-way ANOVAs (study phase, sample time) with repeated measures for both factors. Significant main effects and interactions were analyzed using Tukey's least significant difference test. Statistical significance was set atP < 0.05. All data are presented as means ± SE.RESULTSCardiorespiratory and metabolic responses collected during˙VO2peak testing are presented in Table 1. The≈30% decrease in ˙VO2peak from SL to AA remained decreased at CA. The [La]peak did not change significantly from SL to AA, but decreased ≈45% from AA to CA. As expected, SaO2peak was decreased at AA and CA compared with SL values and tended to increase from AA to CA. Although not statistically significant, ˙VEpeak tended to be higher at CA compared with that at SL and AA. The HRpeak decreased ≈10% from SL to CA, but there was no difference in HRpeak between SL and AA. The RERpeak did not change from SL to AA, but it decreased ≈12% at CA compared with that at both SL and AA values.TABLE 1. Peak cardiorespiratory and metabolic responses at sea level (SL), acute altitude (AA), and chronic altitude (CA).The EXH time was the same at SL (66.0 ± 1.6 min), AA (67.7 ± 7.3 min), CA (79.9 ± 6.2 min), and RA (67.9 ± 1.9 min). The EXH time tended to increase (≈16%) from AA to CA. The cardiorespiratory responses during the EXH test are presented in Figure 1. As expected, absolute ˙VO2 was the same at AA, CA, and RA at all workloads, but was significantly higher at SL since volunteers were tested at their relative percentages of ˙VO2peak. The SaO2 decreased≈30% from SL to AA, but then increased ≈15% from AA to CA and remained increased at RA at all workloads. The ˙VE ·˙VCO2-1 increased ≈40% at all workloads from SL to AA. At 40% ˙VO2peak, ˙VE · ˙VCO2-1 increased≈26% from AA to CA and remained increased at RA. At 75% ˙VO2peak and exhaustion, ˙VE · ˙VCO2-1 tended to increase from AA to CA. There were no differences in HR from SL to AA, but HR decreased≈10% from SL to CA and remained decreased at RA at 75% ˙VO2peak and exhaustion.Figure 1-Oxygen consumption (˙VO2), arterial oxygen saturation (SaO2), ventilatory equivalent for carbon dioxide (˙VE ·˙VCO2-1), and HR at 40% and 75% ˙VO2peak, and exhaustion (EXH) during submaximal exercise at sea level (SL), acute altitude (AA), chronic altitude(CA), and reintroduction to altitude (RA) after 8 d at SL. Values are means± SE; N = 6 for each point.*P < 0.05 from SL.†P < 0.05 from AA.The RER decreased (P <0.005) from SL to CA at 40%˙VO2peak (0.90 ± 0.04 to 0.81 ± 0.01; P< 0.05), but not at 75% ˙VO2peak (0.94 ± 0.01 to 0.90± 0.01), and exhaustion (0.91 ± 0.04 to 0.91 ± 0.02). When compared with that at CA values, RER did not change at RA at 40%˙VO2peak (0.81 ± 0.03), 75% ˙VO2peak (0.89± 0.02), and exhaustion (0.91 ± 0.03). The fractional contribution of fat to total energy expenditure, calculated from˙VO2 and RER data, increased (P < 0.05) from SL (32.0± 6.0%) to CA (61.3 ± 4.5%) and RA (61.0 ± 10.0%) only at 40% ˙VO2peak. However, the tendency for an increased fractional contribution of fat to total energy expenditure at 75% ˙VO2peak at CA (31.5 ± 4.7%) and RA (36.9 ± 5.1%) compared with that at SL(17.5 ± 4.3%) was not significant.The [La] data collected during the EXH test are presented inFigure 2. Blood parameters at minute 40 and minute 60(both at 75% ˙VO2peak) were not significantly different; therefore, the mean value of these two time periods was used to represent values at 75%˙VO2peak. The [La] at 75% ˙VO2peak was ≈63% lower at CA (1.9 ± 0.3 mmol·L-1) compared with that at AA (5.1± 0.6 mmol·L-1). The [La] at exhaustion also decreased≈50% from AA (6.6 ± 0.9 mmol·L-1) to CA (3.3 ± 0.4 mmol·L-1). At RA compared with CA, [La] was similar at both 75% ˙VO2peak (2.6 ± 0.4 mmol·L-1) and exhaustion (3.3 ± 0.6 mmol·L-1).Figure 2-Blood lactate accumulation at rest, 40% and 75%˙VO2peak, and exhaustion (EXH) during submaximal exercise at sea level (SL), acute altitude (AA), chronic altitude(CA), and reintroduction to altitude (RA) after 8 d at SL. Values are means± SE; N = 6 for each point. Values plotted at 75%˙VO2peak are the mean of two exercise blood samples. *P < 0.05 from SL.†P < 0.05 from AA.The [GLU], [GLY], [FFA], and [COR], [Hb] and Hct data collected during the EXH test are presented in Table 2. There were no significant differences in [GLU], [GLY], [FFA], or [COR] between study phases but they all increased with exercise time. The [Hb] and Hct did not change from rest to exhaustion in all study phases but were increased (P< 0.05) at CA compared with SL and AA and remained elevated at RA. Calculated PV during submaximal exercise decreased 6.0 ± 3.5% at AA, 22.3 ± 4.5% at CA, and 15.4 ± 2.4% at RA from SL baseline values.TABLE 2. Blood accumulation data collected at rest and exhaustion (EXH) during the submaximal exercise test to exhaustion at sea level (SL), acute altitude (AA), chronic altitude (CA), and during reintroduction to altitude(RA).The BW did not change from SL (82.4 ± 4.6 kg) to AA (82.1 ± 4.5 kg) but decreased (P < 0.05) from AA to CA (80.5 ± 4.5 kg). BW rebounded at RA to 82.0 ± 3.9 kg, which was similar to values at SL and AA. Figure 3 shows the percent retention of acclimatization-associated responses upon RA after 8 d at SL in variables that showed a significant acclimatization response from AA. The large SES for the percent retention of ˙VE·˙VCO2-1 and [La] was a result of the fact that one volunteer in each case showed a decrease in˙VE·˙VCO2-1 and increase in [La] with acclimatization. These responses were opposite of the expected responses, and thus created a data point for both ˙VE·˙VCO2-1 and [La] percent retention of acclimatization that was negative. These negative data points greatly increased the SEs for these calculated variables.Figure 3-Percent retention of exercise responses associated with acclimatization to 4,300 m for arterial oxygen saturation(SaO2), ventilatory equivalent for carbon dioxide production(˙VE·˙VO2-1), plasma volume (PV), and blood lactate accumulation ([La]) at 40% and 75%˙VO2peak and exhaustion (EXH) during submaximal exercise at sea level (SL), acute altitude (AA), chronic altitude (CA), and reintroduction to altitude (RA) after 8 d at SL. For each individual, percent retention of acclimatization for each variable was calculated as(RA-AA)/(CA-AA)·100.DISCUSSIONTo determine whether exercise responses associated with altitude acclimatization were retained upon RA after 8 d at SL, it was necessary first to examine whether appropriate acclimatization responses were exhibited. Significant increases in peak and submaximal exercise SaO2 and˙VE·˙VCO2-1 from AA to CA, comparable with observations reported by others studying well-acclimatized males at 4,300 m, confirmed the presence of ventilatory acclimatization(4,26). The significant decreases in HR, PV, and[La] from AA to CA during both peak and submaximal exercise were also comparable with results reported by others studying well-acclimatized males at 4,300 m (3,6,22,26). Thus, the similarity between the physiological responses during both peak and submaximal exercise observed in our study and those observed in previous studies of well-acclimatized males at 4,300 m indicates that our volunteers were appropriately acclimatized.Our findings demonstrate that most of the exercise responses associated with acclimatization to 4,300 m were retained to a larger degree upon RA after 8 d at SL than was expected by their reported time course of acquisition during acclimatization. Specifically, during RA, exercise SaO2, and˙VE·˙VCO2-1, which generally follow the same time course and pattern as that of ventilatory acclimatization, were retained 65-92% and 54-86%, respectively, during the three submaximal workloads(Fig. 3). Bender et al. (4) found that the increase in exercise SaO2 and˙VE·˙VCO2-1 were ≈61% and ≈92% complete after 8 d at 4,300 m. Thus, if ventilatory responses are lost at the same rate as they are acquired, exercise SaO2 and˙VE·˙VCO2-1 should only be retained ≈39% and≈8% after 8 d at SL. In our study, the higher retention of exercise ventilatory responses during RA suggests that deacclimatization of exercise ventilatory responses may be slower and perhaps follow a different mechanism than during acclimatization.If ventilatory acclimatization results from increased central and peripheral chemoreceptor sensitivity (5), then deacclimatization should be a reversal of this process. We have reported, for the same group of volunteers, that resting hypoxic and hypercapnic ventilatory responsiveness, measured at SL, had returned to near preacclimatization values by 7-d post acclimatization, suggesting that chemosensitivity had returned to normal (27). However, resting ventilation, measured at SL in this same study, was greater 7 d postacclimatization than preacclimatization values. Since hypoxic stimulation of the carotid chemoreceptors is absent at SL, this elevated resting ventilation was likely a result of the effects of decreased blood and cerebrospinal fluid (CSF) bicarbonate still present from the CA phase (10). The probable persistence of this hypocapnic alkalosis may have set the stage for the greater exercise ventilation upon RA after 8 d at SL than when compared with exercise ventilation at AA.During the three submaximal exercise workloads, 55-79% of the decrease in PV resulting from acclimatization was retained upon RA after 8 d at SL(Fig. 3). Krzywicki et al. (22) reported that 72% of the full reduction in PV was achieved within 8 d at 4,300 m. Thus, only 28% of the decrease in PV that occurs with altitude acclimatization should be retained after an 8-d return to low altitude. Our values were much higher than expected, indicating again that the rate of deacclimatization, as measured by changes in PV, may follow a longer time course than the rate of acclimatization. In contrast, Krzywicki et al.(22) reported that the decrease in PV that was apparent 4 d into a 12-d acclimatization had returned to preacclimatization values after a 4-d return to low altitude. Their results suggest a similar time course for the rate of PV changes during acclimatization and deacclimatization. Reasons for the discrepant results between the two studies may have to do with the fact that our volunteers were under hypoxic stress during the reintroduction to altitude. In our study, the large retention of a decreased PV is unknown but may have to do with changes in vascular permeability that occur with altitude acclimatization (15) that are not quickly reversed upon return to SL.There is conflicting information concerning HR during exercise and acclimatization to altitude. Some studies suggest that HR during exercise decreases with altitude acclimatization(1,13,20), while others suggest no change(4) or an increase (31). We found a trend for HR to decrease at all workloads from AA to CA. The studies that have reported a decrease in exercise HR with acclimatization have found that the decrease was 50-86% complete after 1 wk at high altitude(1,13). Thus, if cardiovascular responses are lost at the same rate that they are acquired, we would expect ≈14-50% retention in exercise HR response upon RA after 8 d at SL. In the present study, HR was retained 50% at 75% ˙VO2peak, indicating that perhaps acclimatization and deacclimatization for HR during exercise follow a similar time course. In support of this conclusion, Grassi et al.(13) found that the decrease in exercise HR observed with altitude acclimatization was retained 17% after 1 wk at low altitude, and Ferretti et al. (11) found no retention of submaximal exercise HR after 3 wk at low altitude. Thus, it appears that the sympathetic and parasympathetic systems controlling the HR response during exercise(16) adapt more readily than other systems when the body is relieved of the hypoxic stress of altitude.The pattern of the metabolic data is similar to the cardiorespiratory data in that [La] was retained between 44-92% during the three submaximal workloads upon RA after 8 d at SL (Fig. 3). Grassi et al.(13) found that 68% of the full reduction in peak [La] was achieved after 1 wk of altitude acclimatization and thus should only be retained ≈32% after a 1-wk return to low altitude. Our 44-92% retention of[La] was much higher than expected as was the 67% retention of peak exercise[La] reported by Grassi et al. (13) following a 1-wk return to low altitude. Thus, deacclimatization responses for [La] may occur over a longer time period than acclimatization responses for [La].One possible explanation for the initial and continued reduction in [La] is an increased glycogen sparing and fat oxidation during exercise with CA and RA exposure (32). Certainly, our RER values during submaximal exercise at CA and RA suggest this as a possibility but our [GLU],[FFA], [GLY], and [COR] data neither support nor refute this as a possibility. However, recent evidence from isotopic tracer studies suggests that simple blood accumulation values often do not accurately reflect substrate uptake and release (28). Furthermore, the decreased RER values in our study may have been caused by the combined effects of hypoxia and anorexia rather than an increase in fat utilization since volunteers did lose BW from SL to CA.Another possible reason for the continued reduction in [La] may be related to the large retention of decreased PV during exercise upon RA after 8 d at SL. In these same test volunteers, a reduced total body water associated with altitude acclimatization was also retained ≈60%, measured at SL, after 6 d at SL (24). Even though other studies have found no change in the oxygen delivery to the working muscle during exercise in acclimatized volunteer subjects (2), there might be an increase in oxygen conductance from the red cell to skeletal muscle mitochondria (9). An increase in oxygen conductance would permit a higher rate of ATP turnover before adenylate breakdown and lactate production. Additionally, the loss of body fluid with altitude acclimatization may improve aerobic metabolism during hypoxemia because of a decrease in the oxygen diffusion distance from the red cell to skeletal muscle mitochondria(17). Since the decrease in PV was retained ≈55-79% during the three submaximal workloads upon RA, there is a strong possibility that this retention may have contributed to the continued depression in [La] values upon RA after 8 d at SL.Although the volunteers in the present study retained a substantial portion of their altitude acclimatization as measured by their physiological responses, we did not see a significant improvement in exercise performance as measured by EXH time. The EXH time tended to increase 19% from AA to CA, but this increase was not maintained at RA. We expected some degree of the improvement in EXH time observed at CA to be maintained at RA, given the significant retention of beneficial physiological responses to exercise. Using EXH time as a measure of exercise performance is problematic. Psychological factors can play a prominent role in determining the point at which a volunteer reaches exhaustion. Furthermore, one study found that the coefficient of variation for an endurance performance test conducted at 70% of maximal power output was 26.6% (19). Therefore, the large intra- and inter-subject variability in the measurement of EXH time makes it difficult to show statistical significance.CONCLUSIONSIn summary, after an 18-d acclimatization to 4,300 m, even though submaximal exercise time to exhaustion was not improved, a large degree of exercise responses associated with acclimatization were retained upon reintroduction to altitude after 8 d at sea level. The observation that these responses were retained to a greater degree than was expected by the time course of their acquisition during acclimatization suggests that deacclimatization to altitude follows a slower time course than acclimatization. Consequently, retention of beneficial exercise responses associated with altitude acclimatization is likely for at least 8 d in individuals whose work, athletic competition, or recreation schedules involve intermittent sojourns to high elevations.We would like to thank the test volunteers for their participation and cooperation in this study. The authors gratefully acknowledge the technical and logistical support provided by Mr. Jim Devine, Mr. James Bogart, SSG Mark Sharp, SGT Sinclair Smith, and PVT Keesha Miller.The views, opinions and/or findings in this report are those of the authors and should not be construed as an official Department of the Army position, policy, or decision, unless so designated by other official documentation.Citations of commercial organizations and trade names in this report do not constitute an official Department of the Army endorsement or approval of the products or services of these organizations.Address for correspondence: Beth A. 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Link]4436221ovid.com:/bib/ovftdb/00005768-199712000-0000700004560_1996_81_1762_roberts_acclimatization_|00005768-199712000-00007#xpointer(id(R28-7))|11065405||ovftdb|SL00004560199681176211065405P79[Medline Link]8904597ovid.com:/bib/ovftdb/00005768-199712000-0000700000461_1988_255_r456_sawka_thermoregulation_|00005768-199712000-00007#xpointer(id(R30-7))|11065405||ovftdb|SL000004611988255r45611065405P81[Medline Link]3414840ovid.com:/bib/ovftdb/00005768-199712000-0000700004529_1982_52_857_young_utilization_|00005768-199712000-00007#xpointer(id(R32-7))|11065405||ovftdb|SL0000452919825285711065405P83[Medline Link]7085419Exercise responses after altitude acclimatization are retained during reintroduction to altitudeBEIDLEMAN, BETH A.; MUZA, STEPHEN R.; ROCK, PAUL B.; FULCO, CHARLES S.; LYONS, TIMOTHY P.; HOYT, REED W.; CYMERMAN, ALLENBasic Sciences: Original Investigations1229