Abstract
The purpose was to determine the effects of exercise training (ExT) on skeletal muscle metabolism in patients with heart failure. Twenty eight patients with heart failure (Etiology: Ischemic Heart Disease; NYHA: II or III) were randomly assigned to ExT (n=14, age:58±5yrs, LVEF=29%±10) or no-training (NEx) (n=14, age:60±5yrs, LVEF=28%±10). ExT consisted of walking 3d/wk for 16 wks. Muscle metabolism was evaluated with 31P-MRS during low (LO;25%MVC; 10:00 min) and high (HI;85%MVC;To fatigue) intensity calf flexion (1 contract/4s). Following ExT exercise capacity (VO2peak) and exercise time increased 24% (13.0±3.5 to 16.2±4.0 ml·kg-1·min-1) and 32% (12.3±3.5min to 16.25±4.3min), respectively (pλ0.05). The inorganic phosphate / phosphocreatine ratio (Pi/PCr) decreased 18% (0.62±0.09 to 0.51±0.08) at peak LO exercise after ExT (pλ0.05). During HI accumulation of the diprotonated form of inorganic phosphate(H2PO4-) decreased 30% (659%±145 to 394%±98) whereas time to fatigue increased 53% (228±38 to 349±53s) (pλ0.05), despite a similar pH response. No changes were noted in the NEx group. The decreased Pi/PCr ratio during LO indicates an increased capacity for oxidative synthesis of ATP and is in part supported by an increase in VO2peak. Increased time to fatigue during HI may in part be due to decreased cross-bridge interference by H2PO4-. Increased oxidative potential and decreased H2PO4- accumulation during exercise play a significant role in the improved VO2peak and exercise time following ExT in patients with heart failure.
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