title: Neither Hematocrit Normalization nor Exercise Training Restores Oxygen Consumption to Normal Levels in Hemodialysis Patients.
abstract: 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 VO2relative 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.
authors.affiliation: Department of Internal Medicine University of Texas Southwestern Medical Center, Dallas, Texas.
authors.forename: James
authors.initials: J
authors.lastname: Stray-Gundersen
authors.affiliation: Department of Internal Medicine University of Texas Southwestern Medical Center, Dallas, Texas; erinhowden@texashealth.org erin.howden@bakeridi.edu.au.|Institute for Exercise and Environmental Medicine, Texas Health Resources, Dallas, Texas; and.
authors.forename: Erin J
authors.initials: EJ
authors.lastname: Howden
authors.affiliation: Department of Internal Medicine University of Texas Southwestern Medical Center, Dallas, Texas.
authors.forename: Dora Beth
authors.initials: DB
authors.lastname: Parsons
authors.affiliation: Dallas Kidney Specialists, Dallas, Texas.
authors.forename: Jeffrey R
authors.initials: JR
authors.lastname: Thompson
mesh_terms: D000328:Adult; D000368:Aged; D000740:Anemia / Q000097:blood / Q000378:metabolism*; D018592:Cross-Over Studies; D015444:Exercise; D005260:Female; D006400:Hematocrit; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood / Q000378:metabolism* / Q000628:therapy*; D008297:Male; D008875:Middle Aged; D010101:Oxygen Consumption; D012016:Reference Values; D006435:Renal Dialysis; D055815:Young Adult
keywords: VO2 peak; anemia; citrate synthase; end stage kidney disease; erythropoietin; physical activity