The effects of iron stores and supplementation on erythropoietic responses to moderate altitude in endurance athletes were examined. In a retrospective study, red cell compartment volume (RCV) responses to 4 wk at 2,500 m were assessed in athletes with low ( n = 9, ≤20 and ≤30 ng/mL for women and men, respectively) and normal ( n = 10) serum ferritin levels ([Ferritin]) without iron supplementation. In a subsequent prospective study, the same responses were assessed in athletes ( n = 26) with a protocol designed to provide sufficient iron before and during identical altitude exposure. The responses to a 4-wk training camp at sea level were assessed in another group of athletes ( n = 13) as controls. RCV and maximal oxygen uptake (V̇o 2max ) were determined at sea level before and after intervention. In the retrospective study, athletes with low [Ferritin] did not increase RCV (27.0 ± 2.9 to 27.5 ± 3.8 mL/kg, mean ± SD, P = 0.65) or V̇o 2max (60.2 ± 7.2 to 62.2 ± 7.5 mL·kg −1 ·min −1 , P = 0.23) after 4 wk at altitude, whereas athletes with normal [Ferritin] increased both (RCV: 27.3 ± 3.1 to 29.8 ± 2.4 mL/kg, P = 0.002; V̇o 2max : 62.0 ± 3.1 to 66.2 ± 3.7 mL·kg −1 ·min −1 , P = 0.003). In the prospective study, iron supplementation normalized low [Ferritin] observed in athletes exposed to altitude ( n = 14) and sea level ( n = 6) before the altitude/sea-level camp and maintained [Ferritin] within normal range in all athletes during the camp. RCV and V̇o 2max increased in the altitude group but remained unchanged in the sea-level group. Finally, the increase in RCV correlated with the increase in V̇o 2max [( r = 0.368, 95% confidence interval (CI): 0.059–0.612, P = 0.022]. Thus, iron deficiency in athletes restrains erythropoiesis to altitude exposure and may preclude improvement in sea-level athletic performance. NEW & NOTEWORTHY Hypoxic exposure increases iron requirements and utilization for erythropoiesis in athletes. This study clearly demonstrates that iron deficiency in athletes inhibits accelerated erythropoiesis to a sojourn to moderate high altitude and may preclude a potential improvement in sea-level athletic performance with altitude training. Iron replacement therapy before and during altitude exposure is important to maximize performance gains after altitude training in endurance athletes.

Elite endurance athletes typically use “live high - train low” altitude training to enhance sea level performance. Perhaps the most commonly utilized and expected experimental control in altitude training research concerns iron stores and supplementation. Whether elite athletes and coaches independently follow evidence-based best-practice principles regarding iron status and training at altitude, outside of a controlled research setting, is unknown. PURPOSE: To examine logistical decisions elite U.S. distance runners make regarding altitude training and the hematological outcomes that result from those decisions. METHODS: Elite U.S. distance runners (n = 58) completed altitude training (living elevation = 2,000 - 2,600m) at their own cost and volition. Total hemoglobin (tHb) mass was measured using CO rebreathing upon arrival and departure from altitude. Questionnaires asked athletes to self-report pre-altitude serum ferritin values, if iron was taken (pill or liquid) at altitude, and workout specifics. RESULTS: Of the 40 athletes who knew their serum ferritin level at the start of the camp, those with ferritin < 50 ng·ml-1 (n = 11) demonstrated a ΔtHb of 0.6 ± 2.0% (ns) and those with ferritin > 50 ng·ml-1 (n = 29) significantly increased tHb by 3.7 ± 3.0%. Of those with ferritin levels > 50 ng·ml-1, athletes who lived at altitude < 23 days (n = 9) showed a ΔtHb mass of 1.3 ± 1.7% (ns) and those who lived at altitude for > 27 days (n = 20) significantly increased tHb mass by 3.8 ± 2.6%. Of the total cohort, 49 athletes answered questions regarding iron supplementation. Those who supplemented iron in liquid form (n = 27) significantly increased tHb mass by 4.2 ± 3.4%. Those who did not supplement iron (n = 3) or supplemented in pill form (n = 19) showed a ΔtHb mass of 1.5 ± 0.5% (ns) and 1.4 ± 2.7% (ns). Athletes who answered questions regarding training (n = 47) reported completing 8.5 ± 2.5 “higher intensity workouts,” and 3.6 ± 1.1 of those workouts were done at <1,500m. Only 4 of the 47 athletes completed all higher intensity sessions at <1,500m. CONCLUSION: A substantial number of elite U.S. distance runners do not follow what would be considered evidence-based best-practice principles regarding altitude training. Coaches, sport scientists, and clinicians would be prudent to strongly advocate for athletes to follow these principles.

For sea level based endurance athletes who compete at low and moderate altitudes, adequate time for acclimatization to altitude can mitigate performance declines. We asked whether it is better for the acclimatizing athlete to live at the specific altitude of competition or at a higher altitude, perhaps for an increased rate of physiological adaptation. After 4 wk of supervised sea level training and testing, 48 collegiate distance runners (32 men, 16 women) were randomly assigned to one of four living altitudes (1,780, 2,085, 2,454, or 2,800 m) where they resided for 4 wk. Daily training for all subjects was completed at a common altitude from 1,250 to 3,000 m. Subjects completed 3,000-m performance trials on the track at sea level, 28 and 6 days before departure, and at 1,780 m on days 5, 12, 19, and 26 of the altitude camp. Groups living at 2,454 and 2,800 m had a significantly larger slowing of performance vs. the 1,780-m group on day 5 at altitude. The 1,780-m group showed no significant change in performance across the 26 days at altitude, while the groups living at 2,085, 2,454, and 2,800 m showed improvements in performance from day 5 to day 19 at altitude but no further improvement at day 26 The data suggest that an endurance athlete competing acutely at 1,780 m should live at the altitude of the competition and not higher. Living ∼300-1,000 m higher than the competition altitude, acute altitude performance may be significantly worse and may require up to 19 days of acclimatization to minimize performance decrements.

Patients treated with hemodialysis develop severely reduced functional capacity, which can be partially ameliorated by correcting anemia and through exercise training. In this study, we determined perturbations of an erythroid-stimulating agent and exercise training to examine if and where limitation to oxygen transport exists in patients on hemodialysis. Twenty-seven patients on hemodialysis completed a crossover study consisting of two exercise training phases at two hematocrit (Hct) values: 30% (anemic) and 42% (physiologic; normalized by treatment with erythroid-stimulating agent). To determine primary outcome measures of peak power and oxygen consumption (VO2) and secondary measures related to components of oxygen transport and utilization, all patients underwent numerous tests at five time points: baseline, untrained at Hct of 30%, after training at Hct of 30%, untrained at Hct of 42%, and after training at Hct of 42%. Hct normalization, exercise training, or the combination thereof significantly improved peak power and VO2 relative to values in the untrained anemic phase. Hct normalization increased peak arterial oxygen and arteriovenous oxygen difference, whereas exercise training improved cardiac output, citrate synthase activity, and peak tissue diffusing capacity. However, although the increase in arterial oxygen observed in the combination phase reached a value similar to that in healthy sedentary controls, the increase in peak arteriovenous oxygen difference did not. Muscle biopsy specimens showed markedly thickened endothelium and electron-dense interstitial deposits. In conclusion, exercise and Hct normalization had positive effects but failed to normalize exercise capacity in patients on hemodialysis. This effect may be caused by abnormalities identified within skeletal muscle.

Chronic living at altitudes of ∼2,500 m causes consistent hematological acclimatization in most, but not all, groups of athletes; however, responses of erythropoietin (EPO) and red cell mass to a given altitude show substantial individual variability. We hypothesized that athletes living at higher altitudes would experience greater improvements in sea level performance, secondary to greater hematological acclimatization, compared with athletes living at lower altitudes. After 4 wk of group sea level training and testing, 48 collegiate distance runners (32 men, 16 women) were randomly assigned to one of four living altitudes (1,780, 2,085, 2,454, or 2,800 m). All athletes trained together daily at a common altitude from 1,250-3,000 m following a modified live high-train low model. Subjects completed hematological, metabolic, and performance measures at sea level, before and after altitude training; EPO was assessed at various time points while at altitude. On return from altitude, 3,000-m time trial performance was significantly improved in groups living at the middle two altitudes (2,085 and 2,454 m), but not in groups living at 1,780 and 2,800 m. EPO was significantly higher in all groups at 24 and 48 h, but returned to sea level baseline after 72 h in the 1,780-m group. Erythrocyte volume was significantly higher within all groups after return from altitude and was not different between groups. These data suggest that, when completing a 4-wk altitude camp following the live high-train low model, there is a target altitude between 2,000 and 2,500 m that produces an optimal acclimatization response for sea level performance.

23 Chronic living at altitudes ~2500m causes consistent hematological acclimatization in most, but 24 not all, groups of athletes; however, responses of erythropoietin (EPO) and red cell mass to a 25 given altitude show substantial individual variability. We hypothesized that athletes living at 26 higher altitudes would experience greater improvements in sea level performance, secondary to 27 greater hematological acclimatization, compared to athletes living at lower altitudes. After 4 28 weeks of group sea level training and testing, 48 collegiate distance runners (32M, 16W) were 29 randomly assigned to one of four living altitudes (1780m, 2085m, 2454m, or 2800m). All 30 athletes trained together daily at a common altitude from 1250m 3000m following a modified 31 Live High – Train Low model. Subjects completed hematological, metabolic, and performance 32 measures at sea level, before and after altitude training; EPO was assessed at various time points 33 while at altitude. Upon return from altitude, 3000m time trial performance was significantly 34 improved in groups living at the middle two altitudes (2085m and 2454m) but not in groups 35 living at 1780m and 2800m. EPO was significantly higher in all groups at 24h and 48h, but 36 returned to sea level baseline after 72h in the 1780m group. Erythrocyte volume was 37 significantly higher within all groups after return from altitude, and was not different between 38 groups. These data suggest that when completing a 4 week altitude camp following the Live 39 High – Train Low model, there is a target altitude between 2000m and 2500m that produces an 40 optimal acclimatization response for sea level performance. 41

In their intriguing study of peak oxygen uptake in patients with end-stage renal disease, Painter et al 1Painter P. Krasnoff J.B. Kuskowske M. Frassetto L. Johansen K.L. Effects of modality change and transplant on peak oxygen uptake in patients with kidney failure.Am J Kidney Dis. 2010; 57: 113-122Abstract Full Text Full Text PDF PubMed Scopus (26) Google Scholar discuss factors that may limit the extraction of oxygen from the blood by working skeletal muscle. These include abnormal blood flow to muscle, decreased capillary density within muscle, increased diffusion distances from capillary to myofibril, and abnormal oxidative enzyme level or activity. During a study of anemia correction and exercise training among patients receiving hemodialysis, 2Stray-Gundersen J. Sams B. Goodkin D. Holloway D. Wang C. Thompson J. Improvement in functional capacity in dialysis patients with regular exercise and correction of anemia [abstract].J Am Soc Nephrol. 1997; 8: 212AGoogle Scholar we performed muscle biopsies and utilized electron microscopy in addition to standard histology. We identified thickened capillary endothelium, thickened basement membranes, and interstitial electron-dense deposits, all of which may further impede the diffusion of oxygen from the circulation to the mitochondria of myocytes. We suspect that the interstitial deposits may have been amyloid. We would not expect such deposits to disappear shortly following kidney transplant, exercise training, or increases in hemoglobin concentration. In their intriguing study of peak oxygen uptake in patients with end-stage renal disease, Painter et al 1Painter P. Krasnoff J.B. Kuskowske M. Frassetto L. Johansen K.L. Effects of modality change and transplant on peak oxygen uptake in patients with kidney failure.Am J Kidney Dis. 2010; 57: 113-122Abstract Full Text Full Text PDF PubMed Scopus (26) Google Scholar discuss factors that may limit the extraction of oxygen from the blood by working skeletal muscle. These include abnormal blood flow to muscle, decreased capillary density within muscle, increased diffusion distances from capillary to myofibril, and abnormal oxidative enzyme level or activity. During a study of anemia correction and exercise training among patients receiving hemodialysis, 2Stray-Gundersen J. Sams B. Goodkin D. Holloway D. Wang C. Thompson J. Improvement in functional capacity in dialysis patients with regular exercise and correction of anemia [abstract].J Am Soc Nephrol. 1997; 8: 212AGoogle Scholar we performed muscle biopsies and utilized electron microscopy in addition to standard histology. We identified thickened capillary endothelium, thickened basement membranes, and interstitial electron-dense deposits, all of which may further impede the diffusion of oxygen from the circulation to the mitochondria of myocytes. We suspect that the interstitial deposits may have been amyloid. We would not expect such deposits to disappear shortly following kidney transplant, exercise training, or increases in hemoglobin concentration. Financial Disclosure: Dr Goodkin has consulted for Affymax Inc, AMAG Pharmaceuticals, Amgen Inc, FibroGen Inc, and Xenon Pharmaceuticals Inc. The study described in this letter was sponsored by Amgen Inc, and Dr Goodkin was an employee and shareholder of Amgen at the time the study was conducted. Dr Stray-Gundersen declares that he has no relevant financial interests. Effects of Modality Change and Transplant on Peak Oxygen Uptake in Patients With Kidney FailureAmerican Journal of Kidney DiseasesVol. 57Issue 1PreviewExercise capacity as measured by peak oxygen uptake (Vo2peak) is low in hemodialysis patients. The present study assesses determinants of VO2peak in patients with chronic kidney failure who either changed kidney replacement modality to frequent hemodialysis therapy or received a kidney transplant. Full-Text PDF

UNLABELLED:The decline in maximal oxygen uptake (ΔVO(2)max) with acute exposure to moderate altitude is dependent on the ability to maintain arterial oxyhemoglobin saturation (SaO2). PURPOSE:This study examined if factors related to ΔVO(2)max at altitude are also related to the decline in race performance of elite athletes at altitude. METHODS:Twenty-seven elite distance runners (18 men and 9 women, VO(2)max = 71.8 ± 7.2 mL·kg(-1)·min(-1)) performed a treadmill exercise at a constant speed that simulated their 3000-m race pace, both in normoxia and in 16.3% O2 (∼2100 m). Separate 3000-m time trials were completed at sea level (18 h before altitude exposure) and at 2100 m (48 h after arrival at altitude). Statistical significance was set at P ≤ 0.05. RESULTS:Group 3000-m performance was significantly slower at altitude versus sea level (48.5 ± 12.7 s), and the declines were significant in men (48.4 ± 14.6 s) and women (48.6 ± 8.9 s). Athletes grouped by low SaO2 during race pace in normoxia (SaO2 < 91%, n = 7) had a significantly larger ΔVO(2) in hypoxia (-9.2 ± 2.1 mL·kg(-1)·min(-1)) and Δ3000-m time at altitude (54.0 ± 13.7 s) compared with athletes with high SaO2 in normoxia (SaO2 > 93%, n = 7, ΔVO(2) = -3.5 ± 2.0 mL·kg(-1)·min(-1), Δ3000-m time = 38.9 ± 9.7 s). For all athletes, SaO2 during normoxic race pace running was significantly correlated with both ΔVO(2) (r = -0.68) and Δ3000-m time (r = -0.38). CONCLUSIONS:These results indicate that the degree of arterial oxyhemoglobin desaturation, already known to influence ΔVO(2)max at altitude, also contributes to the magnitude of decline in race performance at altitude.

Ventilation is typically higher during exercise at altitude compared to sea level. However, many elite endurance athletes demonstrate expiratory flow limitation (EFL) during heavy exercise and are mechanically constrained from increasing ventilation at high workloads in a hypoxic environment. PURPOSE: To retrospectively examine the hypothesis that EFL attenuates ventilatory acclimatization and endurance performance following altitude training in elite athletes. METHODS: Eleven elite male distance runners [4 flow limited (FL; 40.1 ± 15.7%) and 7 non flow limited (NFL)] were retrospectively categorized based on the presence of EFL in flow volume loops collected during the final minute of an incremental exercise bout to exhaustion at sea level. Runners completed a 28d altitude training intervention at 2500m, following a "Live High - Train Low" (HiLo) training model. During the initial exhaustive exercise bout, and also upon return from altitude, maximal oxygen uptake (VO2 max) and ventilation (VE max) were measured. Isocapnic hypoxic ventilatory response (HVR) and endurance performance at sea level using a 3km time trial were also measured before and after HiLo training. RESULTS: HVR significantly increased (p<0.05) by a similar amount in both groups, demonstrating an increase in ventilatory chemoresponsiveness. Upon return from altitude, FL runners did not significantly increase VE max (161.7 ± 13.6 vs. 164.2 ± 12.8 L·min-1) or VO2 max (4.80 ± 0.25 vs. 4.78 ± 0.25 L·min-1) compared to pre-altitude, whereas both variables significantly increased in the NFL runners (VE max: 168.2 ± 10.3 vs. 186.3 ± 9.6 L·min-1; VO2 max: 4.97 ± 0.19 vs. 5.25 ± 0.19 L·min-1). Mean 3k time did not change from pre-to post-altitude in FL runners (-0.6 ± 8.2 s), but was 8.1 ± 3.4 s (1.6%) faster in NFL runners. CONCLUSIONS: The data suggest that EFL may impair the possible beneficial effects of HiLo training, resulting in no improvements in VO2 max or performance in flow limited athletes. More research is needed to determine how EFL may influence training at altitude. Supported by U.S. Olympic Committee grant SST97-ATH-007, a grant from USA Track and Field, and institutional support from Presbyterian Hospital of Dallas and Indiana University.

Research suggests that individuals with strong hypoxic ventilatory responsiveness are better suited for mountain climbing performance at high altitudes. We asked if this relationship between hypoxic ventilatory response (HVR) and endurance exercise performance would extend to racing performance of elite distance runners at moderate altitude. PURPOSE: To test the hypothesis that endurance performance at moderate altitude is related to initial levels of and/or changes in HVR in a group of elite distance runners. METHODS: Twenty-one national class U.S. distance runners (13 M, 8 F) completed a 28-day altitude training intervention in Deer Valley, Utah, elevation 2500m, following a "Live High - Train Low" training model. Isocapnic HVR was measured in the one week prior to and within 72 hours upon return from altitude. Endurance performance was measured using 3km time trials completed on 400m all-weather tracks at sea-level (SL) one day prior to departure for altitude, and twice at an altitude of 2100m - 48 hours after arrival to altitude (ALT1), and on day 23 of the altitude intervention (ALT4). RESULTS: HVR was significantly increased from pre- to post-altitude (0.21±0.04 vs. 0.40±0.06 ΔL·min-1·Δ%SaO2-1, p<0.05). ALT1 3km performance time was significantly slower than that measured at SL (9.53±0.68 vs. 8.76±0.63 min). ALT4 3km time was significantly faster than ALT1 3km time (9.34 ± 0.68 min but remained significantly slower than SL 3km time. HVR was not significantly correlated with 3km performance time at either ALT1 (r = -0.25 M; r = -0.14 F) or ALT4 (r = 0.05 M; r = -0.32 F). In addition, pre-altitude HVR was not significantly related to the change in 3km time from SL to ALT1 (r = -0.28 M; r = 0.34 F). The change in HVR after chronic altitude exposure (pre- to post-altitude) was not significantly correlated with the change in 3km performance time from ALT1 to ALT4 (r = 0.24). CONCLUSIONS: In contrast to the positive HVR-performance relationship seen in mountain climbers at high altitude, it appears that the performance of elite distance runners at moderate altitude does not depend on initial levels of or changes in hypoxic ventilatory response. Supported by US Olympic Committee grant SST97-ATH-007, a grant from USA Track and Field, and institutional support from Presbyterian Hospital of Dallas and Indiana University.

The level of circulating erythropoietin (EPO) in response to a fixed level of hypoxia shows substantial inter-individual variability, the source of which is undetermined. Arterial PO(2) at altitude is regulated in part by the hypoxic ventilatory response, which also shows a wide inter-individual variability. We asked if the ventilatory response to hypoxia is related to the magnitude of EPO release at moderate altitude. Twenty-six national class US distance runners (17 M, 9 F) participated in a test of isocapnic hypoxic ventilatory response (HVR) at sea level, 2-7 days prior to departure to altitude. EPO measures were obtained at sea level and after 20 h at 2500 m. HVR for all subjects was 0.21±0.16 L min⁻¹ %SaO₂⁻¹ (range 0.01-0.61 L min⁻¹ %SaO₂⁻¹), with no significant difference between men and women. EPO was significantly increased from pre-altitude (8.6±2.6 ng ml(-1), range 4.0-14.6 ng ml⁻¹) to acute altitude (16.6±4.4 ng ml⁻¹, range 5.0-27.0 ng ml⁻¹), an increase of 92.2±70.1%. There was no significant sex difference in the EPO increase. ΔEPO for all subjects was not correlated with HVR (r=-0.17). Similarly, a statistically or physiologically significant correlation was not present between ΔEPO and HVR within the group of men (r=-0.22) or women (r=-0.19). The variability in the acute EPO response to moderate altitude is not explained by differences in peripheral chemoresponsiveness in elite distance runners. These results suggest that factors acting downstream from the lung influence the magnitude of the acute EPO response to altitude.

Athletic competitions involving endurance exercise at moderate altitude are characterized by impaired performances compared to sea level. The decline in maximal oxygen uptake (VO2max) with acute exposure to moderate altitude has been shown to be dependent on both the magnitude of VO2max at sea level, as well as the ability to maintain arterial oxyhemoglobin saturation (SaO2) during exercise. Whether these relationships extend to influence racing performance with acute altitude exposure is unknown. PURPOSE: This study examined if SaO2 and VO2 maintenance during heavy exercise in acute hypoxia are related to the acute decline in racing performance of elite athletes at altitude. METHODS: Twenty-seven elite distance runners (18 M, 9 F, VO2max = 71.8 + 7.2 ml/kg/min) performed a treadmill exercise bout at a constant speed which simulated their 3000m race pace, both in normoxia (elevation 230m) and breathing 16.3 % O2 (simulating 2100m). Separate 3000m time trials were completed on 400m all-weather outdoor tracks at elevations of 230m (SL), 18 hrs prior to exposure to altitude, and 2100m (ALT), 48 hrs after arrival at altitude. Statistical significance was set at P < 0.05. RESULTS: Group 3000m time trial performance was significantly slower at ALT versus SL (D3000m race time = +48.5 + 12.7 s or 9.2%), and the declines in performances were similar in men (+48.4 + 14.6 s) and women (+48.6 + 8.9 s). Athletes grouped as low SaO2 during race pace treadmill running in normoxia (SaO2 < 91%, n = 7) had a significantly larger decline in race pace VO2 in hypoxia (-9.2 + 2.1 ml/kg/min) and slowing of 3000m race time at altitude (+54.0 + 13.7 s) compared to athletes grouped with high SaO2 during race pace running in normoxia (SaO2 > 93%, n = 7, DVO2 = -3.5 + 2.0 ml/kg/min, D3000m race time = +38.9 + 9.7 s). SaO2 during normoxic race pace running was significantly correlated with both the decline in VO2 from normoxia to hypoxia during race pace running (r = -0.68), as well as the decline in 3000m race time at ALT (r = -0.38). CONCLUSION: These results indicate that the degree of arterial oxyhemoglobin desaturation during heavy exercise, already known to influence the decline in VO2max at altitude, also contributes to the magnitude of the decline in racing performance with acute altitude exposure. Supported by a grant from the US Olympic Committee and USA Track and Field

The level of erythropoietin (EPO) release by the kidney has been directly related to the severity of hypoxic stress. However, the acute EPO response to a fixed altitude shows substantial variability between subjects. Arterial PO2 with acute altitude exposure is regulated in part by the hypoxic ventilatory response (HVR), which also shows a wide inter-subject variability. PURPOSE: We asked if the ventilatory response to hypoxia influences the magnitude of EPO release with acute exposure to moderate altitude. METHODS: Twenty-six national class U.S. distance runners (17 M, 9 F) participated in a test of isocapnic HVR at sea level, 2-7 days prior to departure to an altitude training camp. Plasma EPO concentrations were determined by radio-immuno assay on samples collected at sea level and after 20 hours of residence at 2500m. RESULTS: HVR for all subjects was 0.21 + 0.16 L.min-1.%SaO2 (range 0.01 to 0.61 L.min-1.%SaO2). No significant difference was observed between the HVR of the male athletes (0.23 + 0.16 L.min-1.%SaO2) and female athletes (0.17 + 0.16 L.min-1.%SaO2). EPO was significantly increased 92.2 + 70.1% (range -19.9 to 415.4%) from pre-altitude (8.6 + 2.6 IU/mL, range 4.0 to 14.6 IU/mL) to acute altitude (16.6 + 4.4 IU/mL, range 5.0 to 27.0 IU/mL). There was no significant gender difference in the magnitude of the EPO increase (either in absolute terms or in percentage change), despite the women having lower baseline hemoglobin levels and O2 carrying capacity. The acute increase in EPO with altitude exposure for all subjects was not correlated with HVR (r = -0.17), and no correlation was present between ΔEPO and HVR within the group of men (r = -0.22) or women (r = -0.19). CONCLUSIONS: The variability in the acute EPO response to moderate altitude is not explained by differences in peripheral chemoresponsiveness in elite distance runners. These results suggest that factors acting downstream from the lung influence the magnitude of the acute EPO response to altitude in this population. Supported by US Olympic Committee grant SST97-ATH-07, a grant from USA Track and Field, and institutional support from Presbyterian Hospital of Dallas and Indiana University.

This double-blind, randomized, placebo-controlled trial examined the effects of 4 wk of resting exposure to intermittent hypobaric hypoxia (IHE, 3 h/day, 5 days/wk at 4,000-5,500 m) or normoxia combined with training at sea level on performance and maximal oxygen transport in athletes. Twenty-three trained swimmers and runners completed duplicate baseline time trials (100/400-m swims, or 3-km run) and measures for maximal oxygen uptake (VO(2max)), ventilation (VE(max)), and heart rate (HR(max)) and the oxygen uptake at the ventilatory threshold (VO(2) at VT) during incremental treadmill or swimming flume tests. Subjects were matched for sex, sport, performance, and training status and divided randomly between hypobaric hypoxia (Hypo, n = 11) and normobaric normoxia (Norm, n = 12) groups. All tests were repeated within the first (Post1) and third weeks (Post2) after the intervention. Time-trial performance did not improve in either group. We could not detect a significant difference between groups for a change in VO(2max), VE(max), HR(max), or VO(2) at VT after the intervention (group x test interaction P = 0.31, 0.24, 0.26, and 0.12, respectively). When runners and swimmers were considered separately, Hypo swimmers appeared to increase VO(2max) (+6.2%, interaction P = 0.07) at Post2 following a precompetition taper and increased VO(2) at VT (+8.9 and +12.1%, interaction P = 0.007 and 0.006, at Post1 and Post2). We conclude that this "dose" of IHE was not sufficient to improve performance or oxygen transport in this heterogeneous group of athletes. Whether there are potential benefits of this regimen for specific sports or training/tapering strategies may require further study.

To evaluate the effect of intermittent hypobaric hypoxia combined with sea level training on exercise economy, 23 well-trained athletes (13 swimmers, 10 runners) were assigned to either hypobaric hypoxia (simulated altitude of 4,000-5,500 m) or normobaric normoxia (0-500 m) in a randomized, double-blind design. Both groups rested in a hypobaric chamber 3 h/day, 5 days/wk for 4 wk. Submaximal economy was measured twice before (Pre) and after (Post) the treatment period using sport-specific protocols. Economy was estimated both from the relationship between oxygen uptake (V(.-)o2) and speed, and from the absolute V(.-)o2 at each speed using sport-specific protocols. V(.-)o2 was measured during the last 60 s of each (3-4 min) stage using Douglas bags. Ventilation (V(.-)E), heart rate (HR), and capillary lactate concentration ([La(-)]) were measured during each stage. Velocity at maximal V(.-)o2 (velocity at V(.-)o2max) was used as a functional indicator of changes in economy. The average V(.-)o2 for a given speed of the Pre values was used for Post test comparison using a two-way, repeated-measures ANOVA. Typical error of measurement of V(.-)o2 was 4.7% (95% confidence limits 3.6-7.1), 3.6% (2.8-5.4), and 4.2% (3.2-6.9) for speeds 1, 2, and 3, respectively. There was no change in economy within or between groups (ANOVA interaction P = 0.28, P = 0.23, and P = 0.93 for speeds 1, 2, and 3). No differences in submaximal HR, [La-], Ve, or velocity at V(.-)o2(max) were found between groups. It is concluded that 4 wk of intermittent hypobaric hypoxia did not improve submaximal economy in this group of well-trained athletes.