Cytosolic pH buffering during exercise and recovery in skeletal muscle of patients with McArdle's disease

Cellular pH control is important in muscle physiology, and for interpretation of ³¹P magnetic resonance spectroscopy (MRS) data. Cellular acidification in exercise results from coupled glycolytic ATP production mitigated by cytosolic buffering, 'consumption' of H⁺ by phosphocreatine (PCr) breakdown, and membrane transport processes. Ex vivo methods for cytosolic buffer capacity are vulnerable to artefact, and MRS methods often require assumptions. ³¹P MRS of early exercise, when pH increases unopposed by glycolysis, is conceptually simple, but limited in normal muscle by time resolution and signal-to-noise. A therapeutic trial (Martinuzzi A et al. Musc Nerve 37: 350-357, 2007) in McArdle's disease (glycogen phosphorylase deficiency), where pH does not decrease with exercise, offered the opportunity to test ³¹P MRS data obtained throughout incremental plantar flexion exercise and recovery in ten McArdle's patients against the simple model of cellular pH control. Changes in pH, [Pi] and [PCr] throughout exercise and recovery were quantitatively consistent with mean ± SEM buffer capacity of 10 ± 1 mM/(pH unit), which was not significantly different from the control subjects under the initial-exercise conditions where the comparison could be made. The simple model of cellular acid-base balance therefore gives an adequate account of cellular pH changes during both exercise and recovery in McArdle's disease.