title: Creatine supplementation in chronic heart failure increases skeletal muscle creatine phosphate and muscle performance.
abstract: BACKGROUND
  Cardiac creatine levels are depressed in chronic heart failure. Oral supplementation of creatine to healthy volunteers has been shown to increase physical performance.
  
  
  OBJECTIVE
  To evaluate the effects of creatine supplementation on ejection fraction, symptom-limited physical endurance and skeletal muscle strength in patients with chronic heart failure.
  
  
  METHODS
  With a double-blind, placebo-controlled design 17 patients (age 43-70 years, ejection fraction < 40) were supplemented with creatine 20 g daily for 10 days. Before and on the last day of supplementation ejection fraction was determined by radionuclide angiography as was symptom-limited 1-legged knee extensor and 2-legged exercise performance on the cycle ergometer. Muscle strength as unilateral concentric knee extensor performance (peak torque, Nm at 180 degrees/s) was also evaluated. Skeletal muscle biopsies were taken for the determination of energy-rich phosphagens.
  
  
  RESULTS
  Ejection fraction at rest and at work did not change. Performance before creatine supplementation did not differ between placebo and creatine groups. While no change was seen in the placebo group compared to baseline, creatine supplementation increased skeletal muscle total creatine and creatine phosphate by 17 +/- 4% (P < 0.05) and 12 +/- 4% (P < 0.05), respectively. Increments were seen only in patients with < 140 mmol total creatine/kg d.w. (P < 0.05). One-legged performance (21%, P < 0.05), 2-legged performance (10%, P < 0.05), and peak torque, Nm (5%, P < 0.05) increased. Both peak torque and 1-legged performance increased linearly with increased skeletal muscle phosphocreatine (P < 0.05). The increments in 1-legged, 2-legged and peak torque were significant compared to the placebo group, (P < 0.05).
  
  
  CONCLUSIONS
  One week of creatine supplementation to patients with chronic heart failure did not increase ejection fraction but increased skeletal muscle energy-rich phosphagens and performance as regards both strength and endurance. This new therapeutic approach merits further attention.
authors.affiliation: Department of Medicine, Karolinska Institute, Huddinge University Hospital, Sweden.
authors.forename: A
authors.initials: A
authors.lastname: Gordon
authors.forename: E
authors.initials: E
authors.lastname: Hultman
authors.forename: L
authors.initials: L
authors.lastname: Kaijser
authors.forename: S
authors.initials: S
authors.lastname: Kristjansson
authors.forename: C J
authors.initials: CJ
authors.lastname: Rolf
authors.forename: O
authors.initials: O
authors.lastname: Nyquist
authors.forename: C
authors.initials: C
authors.lastname: Sylvén
mesh_terms: D000284:Administration, Oral; D000328:Adult; D000368:Aged; D002302:Cardiac Output / Q000187:drug effects; D002908:Chronic Disease; D003401:Creatine / Q000008:administration & dosage* / Q000494:pharmacology; D004311:Double-Blind Method; D006333:Heart Failure / Q000000981:diagnostic imaging / Q000188:drug therapy* / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D010725:Phosphocreatine / Q000378:metabolism*; D010807:Physical Endurance / Q000187:drug effects*; D011875:Radionuclide Angiography
chemical_list: D010725:Phosphocreatine; D003401:Creatine