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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 (V̇o2max) 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 V̇o2max (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; V̇o2max: 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 V̇o2max increased in the altitude group but remained unchanged in the sea-level group. Finally, the increase in RCV correlated with the increase in V̇o2max [(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.

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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.

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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.

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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.

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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.

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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.

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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.

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Live high-train low (LH+TL) altitude training was developed in the early 1990s in response to potential training limitations imposed on endurance athletes by traditional live high-train high (LH+TH) altitude training. The essence of LH+TL is that it allows athletes to "live high" for the purpose of facilitating altitude acclimatization, as manifest by a profound and sustained increase in endogenous erythropoietin (EPO) and ultimately an augmented erythrocyte volume, while simultaneously allowing athletes to "train low" for the purpose of replicating sea-level training intensity and oxygen flux, thereby inducing beneficial metabolic and neuromuscular adaptations. In addition to "natural/terrestrial" LH+TL, several simulated LH+TL devices have been developed to conveniently bring the mountain to the athlete, including nitrogen apartments, hypoxic tents, and hypoxicator devices. One of the key questions regarding the practical application of LH+TL is, what is the optimal hypoxic dose needed to facilitate altitude acclimatization and produce the expected beneficial physiological responses and sea-level performance effects? The purpose of this paper is to objectively answer that question, on the basis of an extensive body of research by our group in LH+TL altitude training. We will address three key questions: 1) What is the optimal altitude at which to live? 2) How many days are required at altitude? and 3) How many hours per day are required? On the basis of consistent findings from our research group, we recommend that for athletes to derive the physiological benefits of LH+TL, they need to live at a natural elevation of 2000-2500 m for >or=4 wk for >or=22 h.d(-1).

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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.

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INTRODUCTION: Maximal oxygen uptake (.VO2max) was defined by Hill and Lupton in 1923 as the oxygen uptake attained during maximal exercise intensity that could not be increased despite further increases in exercise workload, thereby defining the limits of the cardiorespiratory system. This concept has recently been disputed because of the lack of published data reporting an unequivocal plateau in .VO2 during incremental exercise. PURPOSE: The purpose of this investigation was to test the hypothesis that there is no significant difference between the .VO2max obtained during incremental exercise and a subsequent supramaximal exercise test in competitive middle-distance runners. We sought to determine conclusively whether .VO2 attains a maximal value that subsequently plateaus or decreases with further increases in exercise intensity. METHODS: Fifty-two subjects (36 men, 16 women) performed three series of incremental exercise tests while measuring .VO2 using the Douglas bag method. On the day after each incremental test, the subjects returned for a supramaximal test, during which they ran at 8% grade with the speed chosen individually to exhaust the subject between 2 and 4 min. .VO2 at supramaximal exercise intensities (30% above incremental .VO2max) was measured continuously. RESULTS: .VO2max measured during the incremental test (63.3 +/- 6.3 mL.kg(-1).min(-1); mean +/- SD) was indistinguishable from the .VO2max during the supramaximal test (62.9 +/- 6.2, N = 156; P = 0.77) despite a sufficient duration of exercise to demonstrate a plateau in .VO2 during continuous supramaximal exercise. These data provide strong support for the hypothesis that there is indeed a peak and subsequent plateau in .VO2 during maximal exercise intensity. CONCLUSIONS: .VO2max is a valid index measuring the limits of the cardiorespiratory systems' ability to transport oxygen from the air to the tissues at a given level of physical conditioning and oxygen availability.

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Intermittent hypoxia (IH), which refers to the discontinuous use of hypoxia to reproduce some key features of altitude acclimatization, is commonly used in athletes to improve their performance. However, variations of IH are also used as a model for sleep apnea, causing sustained sympathoexcitation and hypertension in animals and, thus, raising concerns over the safety of this model. We tested the hypothesis that chronic IH at rest alters autonomic control of arterial pressure in healthy trained individuals. Twenty-two young athletes (11 men and 11 women) were randomly assigned to hypobaric hypoxia (simulated altitude of 4,000-5,500 m) or normoxia (500 m) in a double-blind and placebo-controlled design. Both groups rested in a hypobaric chamber for 3 h/day, 5 days/wk for 4 wk. In the sitting position, resting hemodynamics, including heart rate (HR), blood pressure (BP), cardiac output (Q(c), C(2)H(2) rebreathing), stroke volume (SV = Q(c)/HR), and total peripheral resistance (TPR = mean BP/Q(c)), were measured, dynamic cardiovascular regulation was assessed by spectral and transfer function analysis of cardiovascular variability, and cardiac-vagal baroreflex function was evaluated by a Valsalva maneuver, twice before and 3 days after the last chamber exposure. We found no significant differences in HR, BP, Q(c), SV, TPR, cardiovascular variability, or cardiac-vagal baroreflex function between the groups at any time. These results suggest that exposure to intermittent hypobaric hypoxia for 4 wk does not cause sustained alterations in autonomic control of BP in young athletes. In contrast to animal studies, we found no secondary evidence for sustained physiologically significant sympathoexcitation in this model.

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Altitude training continues to be a key adjunctive aid for the training of competitive athletes throughout the world. Over the past decade, evidence has accumulated from many groups of investigators that the "living high--training low" approach to altitude training provides the most robust and reliable performance enhancements. The success of this strategy depends on two key features: 1) living high enough, for enough hours per day, for a long enough period of time, to initiate and sustain an erythropoietic effect of high altitude; and 2) training low enough to allow maximal quality of high intensity workouts, requiring high rates of sustained oxidative flux. Because of the relatively limited access to environments where such a strategy can be practically applied, numerous devices have been developed to "bring the mountain to the athlete," which has raised the key issue of the appropriate "dose" of altitude required to stimulate an acclimatization response and performance enhancement. These include devices using molecular sieve technology to provide a normobaric hypoxic living or sleeping environment, approaches using very high altitudes (5,500m) for shorter periods of time during the day, and "intermittent hypoxic training" involving breathing very hypoxic gas mixtures for alternating 5 minutes periods over the course of 60-90 minutes. Unfortunately, objective testing of the strategies employing short term (less than 4 hours) normobaric or hypobaric hypoxia has failed to demonstrate an advantage of these techniques. Moreover individual variability of the response to even the best of living high--training low strategies has been great, and the mechanisms behind this variability remain obscure. Future research efforts will need to focus on defining the optimal dosing strategy for these devices, and determining the underlying mechanisms of the individual variability so as to enable the individualized "prescription" of altitude exposure to optimize the performance of each athlete.

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This study tested the hypothesis that athletes exposed to 4 wk of intermittent hypobaric hypoxia exposure (3 h/day, 5 days/wk at 4,000-5,500 m) or double-blind placebo increase their red blood cell volume (RCV) and hemoglobin mass (Hbmass) secondary to an increase in erythropoietin (EPO). Twenty-three collegiate level athletes were measured before (Pre) and after (Post) the intervention for RCV via Evans blue (EB) dye and in duplicate for Hbmass using CO rebreathing. Hematological indexes including EPO, soluble transferrin receptor, and reticulocyte parameters were measured on 8-10 occasions spanning the intervention. The subjects were randomly divided among hypobaric hypoxia (Hypo, n = 11) and normoxic (Norm, n = 12) groups. Apart from doubling EPO concentration 3 h after hypoxia there was no increase in any of the measures for either Hypo or Norm groups. The mean change in RCV from Pre to Post for the Hypo group was 2.3% (95% confidence limits = -4.8 to 9.5%) and for the Norm group was -0.2% (-5.7 to 5.3%). The corresponding changes in Hbmass were 1.0% (-1.3 to 3.3%) for Hypo and -0.3% (-2.6 to 3.1%) for Norm. There was good agreement between blood volume (BV) from EB and CO: EB BV = 1.03 x CO BV + 142, r2 = 0.85, P < 0.0001. Overall, evidence from four independent techniques (RCV, Hbmass, reticulocyte parameters, and soluble transferrin receptor) suggests that intermittent hypobaric hypoxia exposure did not accelerate erythropoiesis despite the increase in serum EPO.

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The aim of this study was to examine the influence of several explanatory factors: anthropometry, buoyancy, passive underwater torque, drag and swimming technique on the energy cost of swimming front crawl in children and adults. Submaximal V(.)O(2) was measured in ten children (age 12) and 13 adults (age 21), as well as body length (BL), body mass, arm length, propelling size, active drag, hydrostatic lift, passive torque, intracyclic velocity fluctuation, hand slip, stroke length and body angle. The results show that body length ( r=0.74), body mass ( r=0.86) propelling size ( r=0.61), arm length ( r=0.66), distance between the center of mass and the center of volume (Delta d, r=0.74) and body angle during swimming ( r=-0.56) all showed significant linear relationships with the cost of swimming at 1.0 m x s(-1) (CS(1.0)). When normalizing the cost of swimming to body size (CS(1.0) x BL(-1)) there were no differences between the two groups. The conclusions of this study are that the combination of BL, body mass, active drag factor, passive torque, drag efficiency and hydrostatic lift were able to explain 97% of the variation in the cost of swimming for the whole group of swimmers. The size-independent factors of torque and floating abilities (density and Delta d in % of BL), together with swimming technique and active drag were found to explain 75% of the variations in CS(1.0) x BL(-1). The identical values for CS(1.0) x BL(-1) for children and adults are explained through the opposing effects of a better swimming technique in the adults, and a better passive torque in the children.

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The purpose of this study was to examine the effect of passive underwater torque on active body angle with the horizontal during front crawl swimming and to assess the effect of body size on passive torque and active body angle. Additionally, the effects of passive torque, body angle and hydrostatic lift on maximal sprinting performance were addressed. Ten boys [aged 11.7 (0.8) years] and 12 male adult [aged 21.4 (3.7) years] swimmers volunteered to participate. Their body angle with the horizontal was measured at maximal velocity, and at two submaximal velocities using an underwater video camera system. Passive torque and hydrostatic lift were measured during an underwater weighing procedure, and the center of mass and center of volume were determined. The results showed that passive torque correlated significantly with the body angle at a velocity 63% of v(max) ( alpha(63) r=-0.57), and that size-normalized passive torque correlated significantly with the alpha(63) and alpha(77) (77% of v(max)) with r=-0.59 and r=-0.54 respectively. Hydrostatic lift correlated with alpha(63) with r=-0.45. The negative correlation coefficients are suggested to be due to the adults having learned to overcome passive torque when swimming at submaximal velocities by correcting their body angle. It is concluded that at higher velocities the passive torque and hydrostatic lift do not influence body angle during swimming. At a velocity of 63% of v(max), hydrostatic lift and passive torque influences body angle. Passive torque and size-normalized passive torque increases with body size. When corrected for body size, hydrostatic lift and passive torque did not influence the maximal sprinting velocity.

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There is little information available about the swimming economy of children. The aim of this study was to examine any possible differences in swimming economy in children and adults, swimming front crawl submaximally. Swimming economy was compared in adults [ n=13, aged 21.4 (3.7) years] and children [n=10, aged 11.8 (0.8) years] tested at four submaximal 6-min workloads. Oxygen consumption (VO2) was measured with Douglas bags in a 25-m pool and pacer lights were used to control the velocities. Swimming economy was scaled to body size using mass (BM), body surface area (BSA) and body length (BL). Children had lower VO2 (litres per minute) at a given velocity than the adults, with 1.86 (0.28) and 2.39 (0.20) l min(-1) respectively (at 1.00 m s(-1)). When scaling for size, children had higher VO2 measured in litres per square metre per minute and millilitres per kilogram per minute (divided by BSA and BM) than adults. The VO2 divided by BL was found not to differ between the two groups. The O2 cost of swimming 1 m at a velocity of 1.00 m s(-1) was lower in the children [31.0 (4.6) ml m(-1)] than in the adults [39.9 (3.3) ml m(-1) P<0.01], probably due to a lower total drag in the children. The results also showed that for children a relationship between swimming velocity cubed and VO2 exists as shown earlier for adults. It is concluded that, when scaling for BSA and BM, children are less economical than adults, when scaling for BL, children are equally economical, and when considering energy cost per metre and absolute VO2, children are more economical than the adults.

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This study was designed to test the hypothesis that intermittent normobaric hypoxia at rest is a sufficient stimulus to elicit changes in physiological measures associated with improved performance in highly trained distance runners. Fourteen national-class distance runners completed a 4-wk regimen (5:5-min hypoxia-to-normoxia ratio for 70 min, 5 times/wk) of intermittent normobaric hypoxia (Hyp) or placebo control (Norm) at rest. The experimental group was exposed to a graded decline in fraction of inspired O2: 0.12 (week 1), 0.11 (week 2), and 0.10 (weeks 3 and 4). The placebo control group was exposed to the same temporal regimen but breathed fraction of inspired O2 of 0.209 for the entire 4 wk. Subjects were matched for training history, gender, and baseline measures of maximal O2 uptake and 3,000-m time-trial performance in a randomized, balanced, double-blind design. These parameters, along with submaximal treadmill performance (economy, heart rate, lactate, and ventilation), were measured in duplicate before, as well as 1 and 3 wk after, the intervention. Hematologic indexes, including serum concentrations of erythropoietin and soluble transferrin receptor and reticulocyte parameters (flow cytometry), were measured twice before the intervention, on days 1, 5, 10, and 19 of the intervention, and 10 and 25 days after the intervention. There were no significant differences in maximal O2 uptake, 3,000-m time-trial performance, erythropoietin, soluble transferrin receptor, or reticulocyte parameters between groups at any time. Four weeks of a 5:5-min normobaric hypoxia exposure at rest for 70 min, 5 days/wk, is not a sufficient stimulus to elicit improved performance or change the normal level of erythropoiesis in highly trained runners.

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