Question 1
During ischemic forearm exercise, a patient with deficiency of muscle glycogen phosphorylase shows almost no rise in venous lactate, whereas a healthy person shows a large rise. Which explanation is correct?
- A.
Muscle glycogen cannot be broken down to glucose 1-phosphate, so little substrate enters glycolysis and less lactate forms.
- B.
Glycolysis is blocked at phosphofructokinase-1, so glycogen accumulates in the muscle and glucose is not used for lactate formation.
- C.
Lactate is formed normally but is taken up by the liver faster in these patients.
- D.
Pyruvate cannot be reduced to lactate, because lactate dehydrogenase requires no NADH in muscle.
Answer: A. Muscle glycogen cannot be broken down to glucose 1-phosphate, so little substrate enters glycolysis and less lactate forms.
Without phosphorylase, muscle glycogen cannot supply glucose 1-phosphate for glycolysis during ischemic exercise, so anaerobic glycolysis and lactate production are low and patients tire quickly (McArdle disease). A PFK-1 block (B) would be a different disorder, rapid hepatic uptake (C) is not the mechanism, and lactate dehydrogenase requires NADH (D).