TY - JOUR
T1 - Cytosolic pH buffering during exercise and recovery in skeletal muscle of patients with McArdle's disease
AU - Kemp, Graham J.
AU - Tonon, Caterina
AU - Malucelli, Emil
AU - Testa, Claudia
AU - Liava, Alexandra
AU - Manners, David
AU - Trevisi, Enrico
AU - Martinuzzi, Andrea
AU - Barbiroli, Bruno
AU - Lodi, Raffaele
PY - 2009
Y1 - 2009
N2 - 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.
AB - 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.
KW - Acid-base
KW - Buffer capacity
KW - Buffering
KW - McArdle's disease
KW - Muscle glycogenosis
KW - Muscle pH
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U2 - 10.1007/s00421-008-0950-0
DO - 10.1007/s00421-008-0950-0
M3 - Article
C2 - 19066935
AN - SCOPUS:59649124424
VL - 105
SP - 687
EP - 694
JO - European Journal of Applied Physiology
JF - European Journal of Applied Physiology
SN - 1439-6319
IS - 5
ER -