A non-invasive selective assessment of type I fibre mitochondrial function using31PNMR spectroscopy Evidence for impaired oxidative phosphorylation rate in skeletal muscle in patients with chronic heart failure

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Abstract
Background Skeletal muscle abnormalities contribute considerably to the clinical expression of heart failure. Deconditioning, underperfusion and an increased number of type IIb glycolytical fibres lead to early lactate production and muscle fatigue at low exercise levels. Aerobic muscle metabolism may also be impaired, as suggested by biopsy studies. Thus far, no data are available from non-invasive studies to indicate the extent of aerobic muscle dysfunction during low-grade exercise which does not induce acidosis. Methods and results Mitochondrial function of skeletal muscle during fibre type I activation was studied in 22 patients with chronic heart failure [NYHA class III, left ventricular ejection fraction 28±2%, (patients)] on ACE inhibitors, diuretics and digoxin, and in 20 normal subjects, using31PNMR spectroscopy of a single right forearm flexor muscle during three mild intermittent exercise levels (0–40% of maximum voluntary contraction) and recovery time. At rest, the inorganic phosphate/phosphocreatine ratio was different [0·13±0·005 (patients) vs 0·09±0·002 (normal subjects),P=0·0001]. However, intracellular pH was comparable. Local acidosis (tissue pH PPConclusions In heart failure, oxidative fibre mitochondrial function in skeletal muscle is impaired, as reflected by the reduced phosphate potential and oxidative phosphorylation rate, early exhaustion and slowed recovery of intracellular energy reserve at workloads, which do not affect intracellular pH.

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