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J Appl Physiol 84: 1573-1580, 1998;
8750-7587/98 $5.00
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Vol. 84, Issue 5, 1573-1580, May 1998

Metabolic and hemodynamic responses of lower limb during exercise in patients with COPD

François Maltais1, Jean Jobin2, Martin J. Sullivan3, Sarah Bernard1, François Whittom1, Kieran J. Killian4, Marc Desmeules1, Marthe Bélanger1, and Pierre LeBlanc1

1 Unité de Recherche en Pneumologie, Centre de Pneumologie de l'Hôpital Laval, and 2 Institut de Cardiologie de Québec, Hôpital Laval, Université Laval, Quebec, Canada G1V 4G5; 3 Department of Medicine, Division of Cardiology, Duke University Medical Center, Durham, North Carolina 27710; and 4 Department of Medicine, McMaster University Medical Centre, Hamilton, Ontario, Canada L8N 3Z5

Premature lactic acidosis during exercise in patients with chronic obstructive pulmonary disease (COPD) may play a role in exercise intolerance. In this study, we evaluated whether the early exercise-induced lactic acidosis in these individuals can be explained by changes in peripheral O2 delivery (DO2). Measurements of leg blood flow by thermodilution and of arterial and femoral venous blood gases, pH, and lactate were obtained during a standard incremental exercise test to capacity in eight patients with severe COPD and in eight age-matched controls. No significant difference was found between the two groups in leg blood flow at rest or during exercise at the same power outputs. Blood lactate concentrations and lactate release from the lower limb were greater in COPD patients at all submaximal exercise levels (all P < 0.05). Leg DO2 at a given power output was not significantly different between the two groups, and no significant correlation was found between this parameter and blood lactate concentrations. COPD patients had lower arterial and venous pH at submaximal exercise, and there was a significant positive correlation between venous pH at 40 W and the peak O2 uptake (r = 0.91, P < 0.0001). The correlation between venous pH and peak O2 uptake suggests that early muscle acidosis may be involved in early exercise termination in COPD patients. The early lactate release from the lower limb during exercise could not be accounted for by changes in peripheral DO2. The present results point to skeletal muscle dysfunction as being responsible for the early onset of lactic acidosis in COPD.

chronic obstructive pulmonary disease; metabolism; skeletal muscle; leg blood flow


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