Impaired resting metabolism in peripheral muscles potentially contributes to exercise intolerance in
chronic obstructive pulmonary disease (
COPD). This study investigated the cytosolic energy metabolism of the quadriceps, from
glycogen degradation to
lactate accumulation, in exercising patients with
COPD, in comparison to healthy controls. We measured, in 12 patients with
COPD and 10 control subjects, resting and post-cycling exercise quadriceps levels of 1) energy substrates and end products of glycolysis (
glycogen,
glucose,
pyruvate, and
lactate) and intermediate markers of glycolysis (
glucose-6-phosphate,
glucose-1-phosphate,
fructose-6-
phosphate) and 2) the activity of key
enzymes involved in the regulation of glycolysis (
phosphofructokinase,
lactate dehydrogenase). Exercise intensity (P < 0.01), duration (P = 0.049), and total work (P < 0.01) were reduced in patients with
COPD. The variations in energy substrates and end products of glycolysis after cycling exercise were of similar magnitude in patients with
COPD and controls.
Glucose-6-phosphate (P = 0.036) and
fructose-6-
phosphate (P = 0.042) were significantly elevated in patients with
COPD after exercise.
Phosphofructokinase (P < 0.01) and
lactate dehydrogenase (P = 0.02) activities were greater in
COPD. Muscle
glycogen utilization (P = 0.022) and
lactate accumulation (P = 0.025) per unit of work were greater in
COPD. We conclude that cycling exercise induced changes in quadriceps metabolism in patients with
COPD that were of similar magnitude to those of healthy controls. These intramuscular events required a much lower exercise work load and time to occur in
COPD. Our data suggest a greater reliance on glycolysis during exercise in
COPD, which may contribute to exercise intolerance in
COPD.