Mechanism of enhanced insulin sensitivity in athletes. Increased blood flow, muscle glucose transport protein (GLUT-4) concentration, and glycogen synthase activity.
We examined the mechanisms of enhanced insulin sensitivity in 9 male healthy athletes (age, 25 +/- 1 yr; maximal aerobic power [VO2max], 57.6 +/- 1.0 ml/kg per min) as compared with 10 sedentary control subjects (age, 28 +/- 2 yr; VO2max, 44.1 +/- 2.3 ml/kg per min). In the athletes, whole body glucose disposal (240-min insulin clamp) was 32% (P < 0.01) and nonoxidative glucose disposal (indirect calorimetry) was 62% higher (P < 0.01) than in the controls. Muscle glycogen content increased by 39% in the athletes (P < 0.05) but did not change in the controls during insulin clamp. VO2max correlated with whole body (r = 0.60, P < 0.01) and nonoxidative glucose disposal (r = 0.64, P < 0.001). In the athletes forearm blood flow was 64% greater (P < 0.05) than in the controls, whereas their muscle capillary density was normal. Basal blood flow was related to VO2max (r = 0.63, P < 0.05) and glucose disposal during insulin infusion (r = 0.65, P < 0.05). The forearm glucose uptake in the athletes was increased by 3.3-fold (P < 0.01) in the basal state and by 73% (P < 0.05) during insulin infusion. Muscle glucose transport protein (GLUT-4) concentration was 93% greater in the athletes than controls (P < 0.01) and it was related to VO2max (r = 0.61, P < 0.01) and to whole body glucose disposal (r = 0.60, P < 0.01). Muscle glycogen synthase activity was 33% greater in the athletes than in the controls (P < 0.05), and the basal glycogen synthase fractional activity was closely related to blood flow (r = 0.88, P < 0.001).


CONCLUSIONS
(a) athletes are characterized by enhanced muscle blood flow and glucose uptake. (b) The cellular mechanisms of glucose uptake are increased GLUT-4 protein content, glycogen synthase activity, and glucose storage as glycogen. (c) A close correlation between glycogen synthase fractional activity and blood flow suggests that they are causally related in promoting glucose disposal.
Ebeling
P
P
Second Department of Medicine, Helsinki University Central Hospital, Finland.
Bourey
R
R
Koranyi
L
L
Tuominen
J A
JA
Groop
L C
LC
Henriksson
J
J
Mueckler
M
M
Sovijärvi
A
A
Koivisto
V A
VA
D000328:Adult; D000332:Aerobiosis; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism*; D002151:Calorimetry; D004247:DNA / Q000378:metabolism; D015309:Glucose Clamp Technique; D051275:Glucose Transporter Type 4; D006003:Glycogen / Q000378:metabolism; D006006:Glycogen Synthase / Q000096:biosynthesis / Q000378:metabolism*; D006801:Humans; D007328:Insulin / Q000494:pharmacology*; D008297:Male; D009004:Monosaccharide Transport Proteins / Q000096:biosynthesis / Q000378:metabolism*; D009124:Muscle Proteins; D009132:Muscles / Q000098:blood supply / Q000187:drug effects / Q000378:metabolism* / Q000502:physiology*; D010101:Oxygen Consumption / Q000187:drug effects; D012333:RNA, Messenger / Q000378:metabolism; D012016:Reference Values; D012039:Regional Blood Flow / Q000187:drug effects; D013177:Sports
D001786:Blood Glucose; D051275:Glucose Transporter Type 4; D007328:Insulin; D009004:Monosaccharide Transport Proteins; D009124:Muscle Proteins; D012333:RNA, Messenger; C495692:SLC2A4 protein, human; D006003:Glycogen; D004247:DNA; D006006:Glycogen Synthase