Effect of simulated altitude erythrocythemia in women on hemoglobin flow rate during exercise
Human Energy Research Laboratory, School of Medicine, University of Pittsburgh, Pennsylvania 15261. Journal of Applied Physiology
(Impact Factor: 3.06).
The effect of simulated altitude erythrocythemia on hemoglobin flow rate and maximal O2 uptake (VO2max) was determined for nine women sea-level residents. Test conditions included normoxia and normobaric hypoxia (16% O2-84% N2). Cycle tests were performed under normoxia (T1-N) and hypoxia (T1-H) at prereinfusion control and under hypoxia 48 h after a placebo infusion (T2-H) and 48 h after autologous infusion of 334 ml of erythrocytes (T3-H). Hematocrit (38.1-44.9%) and hemoglobin concentration (12.7-14.7 g.dl-1) increased from control to postreinfusion. At peak exercise, VO2max decreased from T1-N (2.40 l.min-1) to T1-H (2.15 l.min-1) then increased at T3-H (2.37 l.min-1). Maximal arterial-mixed venous O2 difference decreased from T1-N to T1-H and increased at T3-H. Cardiac output (Q), stroke volume, heart rate, and total peripheral resistance during maximal exercise were unchanged from T1-N through T3-H. Hemoglobin flow rate (Hb flow) at maximum did not change from T1-N to T1-H but increased at T3-H. When compared with submaximal values for T1-N, VO2 was unchanged at T1-H and T3-H; Q increased at T1-H and decreased at T3-H; arterial-mixed venous O2 difference decreased at T1-H and increased at T3-H; Hb flow did not change at T1-N but increased at T3-H. For young women, simulated altitude erythrocythemia increased peak Hb flow and decreased physiological altitude (227.8 m) but did not affect maximum cardiac output (Qmax).
Available from: Robert Boushel
- "To our knowledge, only one research group has previously evaluated the effect of an acute rise in CaO2 and red blood cell volume on V̇O2max during moderate acute hypoxia. Their studies showed that after autologous blood re-infusion V̇O2max was increased by 9.3% at 2278 m  and by 13% at 3566 m . It has also recently been reported that at moderate altitude of 2340 m, the 15% increase in hemoglobin concentration induced by three weeks of acclimatization in athletes resulted in a progressive rise in CaO2 that was associated with a 8.9% increase in V̇O2max from acute to chronic exposure to 2340 m . "
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ABSTRACT: Treatment with recombinant human erythropoietin (rhEpo) induces a rise in blood oxygen-carrying capacity (CaO(2)) that unequivocally enhances maximal oxygen uptake (VO(2)max) during exercise in normoxia, but not when exercise is carried out in severe acute hypoxia. This implies that there should be a threshold altitude at which VO(2)max is less dependent on CaO(2). To ascertain which are the mechanisms explaining the interactions between hypoxia, CaO(2) and VO(2)max we measured systemic and leg O(2) transport and utilization during incremental exercise to exhaustion in normoxia and with different degrees of acute hypoxia in eight rhEpo-treated subjects. Following prolonged rhEpo treatment, the gain in systemic VO(2)max observed in normoxia (6-7%) persisted during mild hypoxia (8% at inspired O(2) fraction (F(I)O(2)) of 0.173) and was even larger during moderate hypoxia (14-17% at F(I)O(2) = 0.153-0.134). When hypoxia was further augmented to F(I)O(2) = 0.115, there was no rhEpo-induced enhancement of systemic VO(2)max or peak leg VO(2). The mechanism highlighted by our data is that besides its strong influence on CaO(2), rhEpo was found to enhance leg VO(2)max in normoxia through a preferential redistribution of cardiac output toward the exercising legs, whereas this advantageous effect disappeared during severe hypoxia, leaving augmented CaO(2) alone insufficient for improving peak leg O(2) delivery and VO(2). Finally, that VO(2)max was largely dependent on CaO(2) during moderate hypoxia but became abruptly CaO(2)-independent by slightly increasing the severity of hypoxia could be an indirect evidence of the appearance of central fatigue.
Available from: Mark A Stoove
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ABSTRACT: This thesis investigated the relationship of ratings of perceived exertion (RPE) with heart rate (HR) and blood lactate (La) that involved four studies. The first study concerned comparing RPE relationships with elite swimmers during exercise tests performed during in-season (IS) and off-season (OS) periods of training. The second study examined the effect of high ambient temperatures on the HRRPE and La-RPE relationship in elite cyclists during self-paced cycle tests. The third study investigated the effect of acute simulated moderate altitude (1800m) exposure on the HR-RPE and La-RPE relationship in highly trained cross-country skiers during incremental ski-striding treadmill tests. The fourth, and final study, was concerned with RPE relationships during upper and lower body work with elite kayakers and elite cyclists.
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ABSTRACT: Physical training at high altitude improves performance at high altitude. However, studies assessing performance improvements at sea level after training at higher altitudes have produced ambiguous and inconclusive results. Hypoxia-induced secondary polycythemia is a major contributor to increased work capacity at altitude.
The common finding upon exposure to hypoxia is a transient increase in haemoglobin concentration and haematocrit because of a rapid decrease in plasma volume followed by an increase in erythropoiesis per se. Both nonathletes and elite endurance athletes have maximal reticulo-cytosis after about 8 to 10 days at moderate altitude. Training periods of 3 weeks at moderate altitudes result in individual increase of haemoglobin concentration of about 1 to 4%. A more accentuated increase in haemoglobin can be obtained with longer sojourns at moderate altitude.
The normal erythropoietin reaction upon exposure to hypoxia comprises initially increased levels followed by a decrease after about 1 week. Thus, the maintenance of a high erythropoietin concentration is not a prerequisite for a sustained increase in erythrocyte formation at high altitude. The main pharmacological modulator of erythropoietin production seems to be adenosine. But modulators such as growth hormone and catecholamines may also potentiate the effect of hypoxia per se on erythropoietin production. On the other hand, there is a risk that the stress hormones may induce a relative depression of the bone marrow particularly in the early phase of altitude training when the adaptation is minimal and the stress reaction is most accentuated.
The most important ‚erythropoiesis-specific’ nutrition factor is iron availability which can modulate erythropoiesis over a wide range in humans. Adequate iron stores are a necessity for haematological adaptation to hypoxia. However, at moderate altitude, there is a need for rapid mobilisation of iron and even if the stores are normal there is a risk that they cannot be mobilised fast enough for an optimal synthesis of haemoglobin.
Data from healthy athletes training at moderate altitudes suggest a true increase in haemoglobin concentration of about 1% per week. Complete haematological adaptation occurred when sea level residents have similar haemoglobin concentrations at moderate altitude compared with residents. The normal difference in haemoglobin concentrations can be estimated to be about 12% between permanent residents at sea level and at 2500m above sea level. This difference indicates a necessary adaptation time of about 12 weeks. If the training period at moderate altitude must be shorter, several sojourns at short intervals are recommended. The important factor in haematological adaptation in athletes at moderate altitude is hypoxia. Training itself, particularly intense training, can constitute a risk early on during adaptation, but it is necessary for optimal long term adaptation to secure a possible synergistic effect of hypoxia and physical training on the erythropoietic response.
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