Quadriceps femoris muscle needle biopsies were performed in 21 patients with chronic obstructive lung disease (COLD) and acute respiratory failure (ARF) and in 21 age-matched healthy control subjects. Muscle samples were analysed to obtain intracellular bicarbonate and pH values from total acid-labile carbon dioxide content. Muscle potassium, magnesium and sodium content were also determined, as well as water compartments. Skeletal muscle of COLD patients with ARF showed intracellular acidosis and reduced potassium and magnesium content. Total muscle water increase was linked to extracellular water increment. It was concluded that in COLD patients with ARF an overall derangement of skeletal muscle metabolism is present.

Skeletal muscle biopsies were performed in 16 controls and 15 non-dialysed end-stage chronic renal failure (CRF) patients presenting untreated metabolic acidosis. Intracellular bicarbonate, pH, water compartments and electrolytes were determined. In 8 of 15 patients muscle ATP and lactate were measured. Intracellular bicarbonate (HCO3i) and pH (pHi) were obtained by means of muscle total carbon dioxide method: a significant (p less than 0.001) reduction in both intracellular acid--base indexes was found in all patients (pHi 6.82 +/- 13 vs. 7.04 +/- 0.05; HCO3i 6.28 +/- 2.07 vs. 11.86 +/- 0.87). Total muscle as well as extracellular water was increased. Muscle sodium and chloride contents were also increased, while no change in potassium and magnesium was detected. A significant decrease of both muscle ATP and lactate was found. The data lead to the conclusion that chronic retention of acids in CRF results in a depletion of the muscle buffer pool and consequently in intracellular acidosis: the latter could be the main cause of the cell energy metabolism derangement described in uremia.

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