Uremic myopathy limits aerobic capacity in hemodialysis patients

G. E. Moore, D. B. Parsons, J. Stray-Gundersen, P. L. Painter, K. R. Brinker, J. H. Mitchell

Research output: Contribution to journalArticle

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Abstract

Eleven end-stage renal disease patients trained by stationary cycling during their hemodialysis treatments. After a 6-week control period, 12 weeks of training began and was increased to 30 to 60 minutes at ≥70% of peak heart rate. Baseline, pretraining and, posttraining exercise tests were performed. Workload (WL), oxygen uptake (V̇O(2peak)), cardiac output (Q̇), heart rate (HR), and arterial oxygen content (CaO2) were measured. Stroke volume (SV), arteriovenous oxygen difference ((a-v)O2), and mixed-venous oxygen content (CvO2) were calculated. Rectus femoris biopsies were obtained pretraining and posttraining. At peak exercise, WL increased from 60 ± 4 to 70 ± 6 W (P < 0.05), V̇O(2peak) showed an upward trend from 14.8 ± 0.9 to 16.8 ± 1.3 mL/kg/min (P < 0.1), and Q̇, HR, SV, CaO2, CvO2, and (a-v)O2 were unchanged. Ten of the 11 patients increased WL, but only six increased V̇O(2peak) (five of 11 patients decreased V̇O(2peak)). The difference between groups (P < 0.02) was attributable to (a-v)O2, which increased in those who increased V̇O(2peak) (P < 0.02). There was an upward trend for succinate dehydrogenase activity (P < 0.06), and phosphofructokinase activity increased (P < 0.05). However, the rectus femoris capillary to fiber ratio, type I and II fiber areas, and fiber area variability were unchanged, and neither histomorphologic nor enzymatic activity changes were related to change in V̇O(2peak). We conclude that not all dialysis patients increase V̇O(2peak) after training, but most can improve exercise capacity. Patients who improved V̇O(2peak) widened their (a-v)O2 difference, increasing oxygen extraction and showing that oxygen delivery is not always the limiting factor. Thus, the limitation of V̇O(2peak) in dialysis patients is a complex interaction of central and peripheral factors. Muscle therapies, such as exercise training, are needed in addition to increased oxygen delivery in rehabilitation of dialysis patients.

Original languageEnglish (US)
Pages (from-to)277-287
Number of pages11
JournalAmerican Journal of Kidney Diseases
Volume22
Issue number2
StatePublished - 1993

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Muscular Diseases
Renal Dialysis
Oxygen
Workload
Dialysis
Heart Rate
Quadriceps Muscle
Exercise
Stroke Volume
Phosphofructokinases
Succinate Dehydrogenase
Exercise Test
Cardiac Output
Chronic Kidney Failure
Rehabilitation
Biopsy
Muscles
Therapeutics

ASJC Scopus subject areas

  • Nephrology

Cite this

Moore, G. E., Parsons, D. B., Stray-Gundersen, J., Painter, P. L., Brinker, K. R., & Mitchell, J. H. (1993). Uremic myopathy limits aerobic capacity in hemodialysis patients. American Journal of Kidney Diseases, 22(2), 277-287.

Uremic myopathy limits aerobic capacity in hemodialysis patients. / Moore, G. E.; Parsons, D. B.; Stray-Gundersen, J.; Painter, P. L.; Brinker, K. R.; Mitchell, J. H.

In: American Journal of Kidney Diseases, Vol. 22, No. 2, 1993, p. 277-287.

Research output: Contribution to journalArticle

Moore, GE, Parsons, DB, Stray-Gundersen, J, Painter, PL, Brinker, KR & Mitchell, JH 1993, 'Uremic myopathy limits aerobic capacity in hemodialysis patients', American Journal of Kidney Diseases, vol. 22, no. 2, pp. 277-287.
Moore GE, Parsons DB, Stray-Gundersen J, Painter PL, Brinker KR, Mitchell JH. Uremic myopathy limits aerobic capacity in hemodialysis patients. American Journal of Kidney Diseases. 1993;22(2):277-287.
Moore, G. E. ; Parsons, D. B. ; Stray-Gundersen, J. ; Painter, P. L. ; Brinker, K. R. ; Mitchell, J. H. / Uremic myopathy limits aerobic capacity in hemodialysis patients. In: American Journal of Kidney Diseases. 1993 ; Vol. 22, No. 2. pp. 277-287.
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AU - Parsons, D. B.

AU - Stray-Gundersen, J.

AU - Painter, P. L.

AU - Brinker, K. R.

AU - Mitchell, J. H.

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N2 - Eleven end-stage renal disease patients trained by stationary cycling during their hemodialysis treatments. After a 6-week control period, 12 weeks of training began and was increased to 30 to 60 minutes at ≥70% of peak heart rate. Baseline, pretraining and, posttraining exercise tests were performed. Workload (WL), oxygen uptake (V̇O(2peak)), cardiac output (Q̇), heart rate (HR), and arterial oxygen content (CaO2) were measured. Stroke volume (SV), arteriovenous oxygen difference ((a-v)O2), and mixed-venous oxygen content (CvO2) were calculated. Rectus femoris biopsies were obtained pretraining and posttraining. At peak exercise, WL increased from 60 ± 4 to 70 ± 6 W (P < 0.05), V̇O(2peak) showed an upward trend from 14.8 ± 0.9 to 16.8 ± 1.3 mL/kg/min (P < 0.1), and Q̇, HR, SV, CaO2, CvO2, and (a-v)O2 were unchanged. Ten of the 11 patients increased WL, but only six increased V̇O(2peak) (five of 11 patients decreased V̇O(2peak)). The difference between groups (P < 0.02) was attributable to (a-v)O2, which increased in those who increased V̇O(2peak) (P < 0.02). There was an upward trend for succinate dehydrogenase activity (P < 0.06), and phosphofructokinase activity increased (P < 0.05). However, the rectus femoris capillary to fiber ratio, type I and II fiber areas, and fiber area variability were unchanged, and neither histomorphologic nor enzymatic activity changes were related to change in V̇O(2peak). We conclude that not all dialysis patients increase V̇O(2peak) after training, but most can improve exercise capacity. Patients who improved V̇O(2peak) widened their (a-v)O2 difference, increasing oxygen extraction and showing that oxygen delivery is not always the limiting factor. Thus, the limitation of V̇O(2peak) in dialysis patients is a complex interaction of central and peripheral factors. Muscle therapies, such as exercise training, are needed in addition to increased oxygen delivery in rehabilitation of dialysis patients.

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