Wilkerson, D. P., Rittweger, J., Berger, N. J., Naish, P. F., & Jones, A. M. (2005). Influence of recombinant human erythropoietin treatment on pulmonary O2 uptake kinetics during exercise in humans. Journal of Physiology, 568(Part 2), 639-652.

This study evaluated the hypotheses that four weeks of recombinant human erythropoietin (RhEPO) treatment would result in a significant increase in hemoglobin concentration and arterial blood O2-carrying capacity and that this would (1) increase peak pulmonary oxygen uptake VO2 during ramp incremental exercise, and (2) speed VO2 kinetics during ‘severe’-, but not ‘moderate’- or ‘heavy’-intensity, step exercise. Ss (N = 15) were randomly assigned to either an experimental group (N = 8) which received a weekly subcutaneous injection of RhEPO, or a control group (N = 7) which received a weekly subcutaneous injection of sterile saline as a placebo, for four weeks. Ss and the principal researchers were blind with respect to the group assignment. Before and after the intervention period, Ss completed a ramp test for determination of the gas exchange threshold and VO2peak, and a number of identical ‘step’ transitions from ‘unloaded’ cycling to work rates requiring 80% gas exchange threshold (moderate), 70% of the difference between the gas exchange threshold and VO2peak (heavy), and 105% VO2peak severe) as determined from the initial ramp test.

There were no significant differences between the two groups for any of the measurements of interest - hemoglobin concentration, VO2peak, and VO2 kinetics before the intervention. Four weeks of RhEPO treatment resulted in a 7% increase both in hemoglobin concentration and VO2peak with no significant change in the control group. RhEPO had no significant effect on VO2 kinetics for moderate, heavy, or severe step exercise.

Recombinant human erythropoietin enhanced the O2-carrying capacity of the blood and thus the potential for muscle O2 delivery, and enhanced the VO2peak but did not influence VO2 kinetics. It is the VO2 kinetics that determines if the extra oxygen potential is used in exercise and it was not. Thus, the intracellular (metabolic) factors in the periphery govern the exercise response and it does not employ the hypothetical "benefits" of added recombinant human erythropoietin.

Implication. Additional recombinant human erythropoietin would not alter the response to moderate, heavy, or severe exercise intensities because its effects stop short of influencing VO2 kinetics at the cellular level.

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