No evidence of mitochondrial abnormality in skeletal muscle of patients with iron‐deficient anaemia

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Abstract
Objectives. Patients with iron deficiency anaemia complain of decreased exercise capacity. We asked whether this is due to defective oxidative ATP synthesis in skeletal muscle as a consequence of reduced blood oxygen content and/or intrinsic mitochondrial abnormalities.Design. We used 31P magnetic resonance spectroscopy to examine skeletal muscle bioenergetics in iron‐deficient patients and in age‐ and sex‐matched controls.Setting. The patients were recruited from the primary care population.Subjects. We studied seven symptomatic female iron‐deficient patients (aged 32–70 years) with haemoglobin (Hb) concentration, [Hb], 8.0 g dl−1. Six had menorrhagia, the cause in the seventh patient remained undiagnosed. Results were compared with those of 8 healthy female controls (aged 25–48 years) with mean [Hb] 13.7 g dl−1.Results. The right calf muscle was by studied 31P magnetic resonance spectroscopy in a 1.9 T superconducting magnet. We measured the intracellular concentrations of phosphocreatine (PCr), inorganic phosphate (Pi), adenosine triphosphate (ATP) and the intracellular pH at rest, during plantar flexion exercise and during recovery from exercise.Exercise duration was reduced in the patients, yet end‐exercise PCr/(PCr + Pi) was higher and adenosine diphosphate (ADP) lower than in controls. After exercise, initial PCr recovery was slowed but this was probably because of the lower cytosolic ADP concentration.Conclusions. Mitochondrial ATP synthesis was not limited by oxygen supply or an intrinsic mitochondrial defect. Therefore, the reduced exercise capacity seen in iron deficiency could be due to central causes and not to skeletal muscle metabolic abnormalities.