Am. J. Respir. Crit. Care Med., Vol 155, No. 2, 02 1997, 615-621.
Abnormal skeletal muscle oxidative capacity after lung transplantation by 31P-MRS
AB Evans, AJ Al-Himyary, MI Hrovat, P Pappagianopoulos, JC Wain, LC Ginns and DM Systrom
Pulmonary and Critical Care Unit, Massachusetts General Hospital and Harvard Medical School, Boston 02114, USA.
Although lung transplantation improves exercise capacity by removal of a
ventilatory limitation, recipients' postoperative maximum oxygen uptake
(VO2max) remains markedly abnormal. To determine if abnormal skeletal
muscle oxidative capacity contributes to this impaired aerobic capacity,
nine lung transplant recipients and eight healthy volunteers performed
incremental quadriceps exercise to exhaustion with simultaneous
measurements of pulmonary gas exchange, minute ventilation, blood lactate,
and quadriceps muscle pH and phosphorylation potential by 31P-magnetic
resonance spectroscopy (31P- MRS). Five to 38 mo after lung
transplantation, peak VO2 was decreased compared with that of normal
control subjects (6.7 +/- 0.4 versus 12.3 +/- 1.0 ml/min/kg, p < 0.001),
even after accounting for differences in age and lean body weight. Neither
ventilation, arterial O2 saturation nor mild anemia could account for the
decrease in aerobic capacity. Quadriceps muscle intracellular pH (pH(i))
was more acidic at rest (7.07 +/- 0.01 versus 7.12 +/- 0.01 units, p <
0.05) and fell during exercise from baseline values at a lower metabolic
rate (282 +/- 21 versus 577 +/- 52 ml/min, p < 0.001). Regressions for
pH(i) versus VO2, phosphocreatine/inorganic phosphate ratio (PCr/Pi) versus
VO2, and blood lactate versus pH(i) were not different. Among transplant
recipients, the metabolic rate at which pH(i) fell correlated closely with
VO2max (r = 0.87, p < 0.01). The persistent decrease in VO2max after
lung transplantation may be related to abnormalities of skeletal muscle
oxidative capacity.
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Copyright © 1997 American Thoracic Society
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