Limits...
The ergogenic effect of recombinant human erythropoietin on VO2max depends on the severity of arterial hypoxemia.

Robach P, Calbet JA, Thomsen JJ, Boushel R, Mollard P, Rasmussen P, Lundby C - PLoS ONE (2008)

Bottom Line: This implies that there should be a threshold altitude at which VO(2)max is less dependent on CaO(2).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).

View Article: PubMed Central - PubMed

Affiliation: Ecole Nationale de Ski et d'Alpinisme, Chamonix, France. paul.robach@jeunesse-sports.gouv.fr

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.

Show MeSH

Related in: MedlinePlus

Agreement between impedance and dye dilution for cardiac output measurement.This graph shows the agreement (Bland-Altman plot) between the cardiac impedance technique and the indocyanine-green dye dilution method for measuring cardiac output during exercise obtained from 55 measurements in seven subjects. For each measurement, the difference between the two methods is plotted against the average of both techniques. The solid line indicates the mean bias, while the dotted lines indicate the 95% confidence intervals (2×standard deviation).
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC2500186&req=5

pone-0002996-g002: Agreement between impedance and dye dilution for cardiac output measurement.This graph shows the agreement (Bland-Altman plot) between the cardiac impedance technique and the indocyanine-green dye dilution method for measuring cardiac output during exercise obtained from 55 measurements in seven subjects. For each measurement, the difference between the two methods is plotted against the average of both techniques. The solid line indicates the mean bias, while the dotted lines indicate the 95% confidence intervals (2×standard deviation).

Mentions: Validity of cardiac impedance for cardiac output measurement. In order to evaluate the validity of our cardiac impedance method for cardiac output measurement during the non-invasive study, cardiac output during incremental exercise in the invasive study was measured simultaneously by the cardiac impedance technique and the cardio-green dye dilution method. The agreement between the two techniques was assessed by the method of Bland and Altman [19]. The Bland-Altman plot (Fig. 2), obtained from 55 simultaneous measurements, shows that the mean bias was −0.41 l.min−1 with 95% confidence interval ranging between −4.83 and 4.01 l.min−1.


The ergogenic effect of recombinant human erythropoietin on VO2max depends on the severity of arterial hypoxemia.

Robach P, Calbet JA, Thomsen JJ, Boushel R, Mollard P, Rasmussen P, Lundby C - PLoS ONE (2008)

Agreement between impedance and dye dilution for cardiac output measurement.This graph shows the agreement (Bland-Altman plot) between the cardiac impedance technique and the indocyanine-green dye dilution method for measuring cardiac output during exercise obtained from 55 measurements in seven subjects. For each measurement, the difference between the two methods is plotted against the average of both techniques. The solid line indicates the mean bias, while the dotted lines indicate the 95% confidence intervals (2×standard deviation).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2500186&req=5

pone-0002996-g002: Agreement between impedance and dye dilution for cardiac output measurement.This graph shows the agreement (Bland-Altman plot) between the cardiac impedance technique and the indocyanine-green dye dilution method for measuring cardiac output during exercise obtained from 55 measurements in seven subjects. For each measurement, the difference between the two methods is plotted against the average of both techniques. The solid line indicates the mean bias, while the dotted lines indicate the 95% confidence intervals (2×standard deviation).
Mentions: Validity of cardiac impedance for cardiac output measurement. In order to evaluate the validity of our cardiac impedance method for cardiac output measurement during the non-invasive study, cardiac output during incremental exercise in the invasive study was measured simultaneously by the cardiac impedance technique and the cardio-green dye dilution method. The agreement between the two techniques was assessed by the method of Bland and Altman [19]. The Bland-Altman plot (Fig. 2), obtained from 55 simultaneous measurements, shows that the mean bias was −0.41 l.min−1 with 95% confidence interval ranging between −4.83 and 4.01 l.min−1.

Bottom Line: This implies that there should be a threshold altitude at which VO(2)max is less dependent on CaO(2).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).

View Article: PubMed Central - PubMed

Affiliation: Ecole Nationale de Ski et d'Alpinisme, Chamonix, France. paul.robach@jeunesse-sports.gouv.fr

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.

Show MeSH
Related in: MedlinePlus