Diabetes, Vol 38, Issue 6 799-807, Copyright © 1989 by American Diabetes Association
Exercise-induced rise in glucagon and ketogenesis during prolonged muscular work
DH Wasserman, JA Spalding, D Bracy, DB Lacy and AD Cherrington
Department of Molecular Physiology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232.
These experiments examined the role of the exercise-induced increment in
glucagon in the control of ketogenesis during prolonged moderate-intensity
(100 m/min, 12% grade) treadmill exercise. Dogs were studied during 150 min
of exercise with saline infusion alone (C; n = 6) with the glucagon levels
clamped at basal values (somatostatin infusion with basal glucagon
replacement and the normal fall in insulin simulated; BG; n = 5) or with
the normal exercise-induced rise in glucagon simulated (somatostatin
infusion with the rise in glucagon and the fall in insulin simulated; SG; n
= 5). Glucose was infused as needed in SG and BG to maintain the glycemic
response seen in C. In all dogs, catheters were inserted into the carotid
artery and the portal and hepatic veins for blood sampling and the vena
cava and the splenic vein for infusions. Glucagon rose from 62 +/- 5 and 57
+/- 4 pg/ml at rest to 104 +/- 20 and 120 +/- 12 pg/ml during exercise in C
and SG but did not deviate from basal in BG (56 +/- 3 pg/ml). Insulin fell
similarly from rest to the end of exercise in C (13 +/- 2 to 5 +/- 1
microU/ml), SG (11 +/- 1 to 6 +/- 1 microU/ml), and BG (10 +/- 1 to 6 +/- 1
microU/ml). In C, SG, and BG, free-fatty acid (FFA) levels rose from 941
+/- 81, 1240 +/- 155, and 938 +/- 36 mu eq/L at rest to 1615 +/- 149, 1558
+/- 175, and 1391 +/- 160 mu eq/L with exercise.2+n C,