D. Laurent et al., EFFECT OF EPINEPHRINE ON MUSCLE GLYCOGENOLYSIS AND INSULIN-STIMULATEDMUSCLE GLYCOGEN-SYNTHESIS IN HUMANS, American journal of physiology: endocrinology and metabolism, 37(1), 1998, pp. 130-138
To examine the effects of a physiological increase in plasma epinephri
ne concentration (similar to 800 pg/ml) on muscle glycogenolysis and i
nsulin-stimulated glycogenesis, we infused epinephrine [1.2 mu g . (m(
2) body surface)(-1) . min(-1)] for 2 h and monitored muscle glycogen
and glucose 6-phosphate (G-6-P) concentrations with C-13/P-31 nuclear
magnetic resonance (NMR) spectroscopy. Epinephrine caused an increase
in plasma glucose (Delta similar to 50 mg/dl), lactate (Delta similar
to 1.4 mM), free fatty acids (Delta similar to 1,200 mu M at peak), an
d whole body glucose oxidation (Delta similar to 0.85 mg . kg(-1) . mi
n(-1)) compared with levels in a group of control subjects (n = 4) in
the presence of slight hyperinsulinemia (similar to 13 mu U/ml, n = 8)
or basal insulin (similar to 7 mu U/ml, n = 7). However, epinephrine
did not induce any detectable changes in glycogen or G-6-P concentrati
ons, whereas muscle inorganic phosphate (P-i) decreased by 35%. Epinep
hrine infusion during a euglycemic-hyperinsulinemic clamp (n = 8) caus
ed a 45% decrease in the glucose infusion rate that could be mostly at
tributed to a 73% decrease in muscle glycogen synthesis rate. After an
initial increase to similar to 160% of basal values, G-6-P levels dec
reased by similar to 30% with initiation of the epinephrine infusion.
We conclude that a physiological increase in plasma epinephrine concen
tration 1) has a negligible effect on muscle glycogenolysis at rest, 2
) decreases muscle P-i, which may maintain phosphorylase activity at a
low level, and 3) causes a major impairment in insulin-stimulated mus
cle glycogen synthesis, possibly due to inhibition of glucose transpor
t-phosphorylation activity.