Increased muscle glucose uptake after exercise: no need for insulin during exercise

TY - JOUR

T1 - Increased muscle glucose uptake after exercise

T2 - no need for insulin during exercise

AU - Richter, Erik

AU - Ploug, Thorkil

AU - Galbo, Henrik

PY - 1985/10

Y1 - 1985/10

N2 - It has recently been shown that insulin sensitivity of skeletal muscle glucose uptake and glycogen synthesis is increased after a single exercise session. The present study was designed to determine whether insulin is necessary during exercise for development of these changes found after exercise. Diabetic rats and controls ran on a treadmill and their isolated hindquarters were subsequently perfused at insulin concentrations of 0, 100, and 20,000 microU/ml. Exercise increased insulin sensitivity of glucose uptake and glycogen synthesis equally in diabetic and control rats, but insulin responsiveness of glucose uptake was noted only in controls. Analysis of intracellular glucose-6-phosphate, glucose, glycogen synthesis, and glucose transport suggested that the exercise effect on responsiveness might be due to enhancement of glucose disposal. After electrical stimulation of diabetic hindquarters in the presence of insulin antiserum, insulin sensitivity of 3-O-methylglucose transport was increased to the same extent as in muscle from healthy rats stimulated in the presence of insulin at 50 microU/ml. Furthermore, in muscle depleted of glycogen by contractions, transport of 3-O-methylglucose was increased in the presence of insulin antiserum and in the absence of increased regional perfusate flow. It is concluded that after exercise, increased sensitivity of muscle glucose metabolism to insulin can be found in the absence of insulin during exercise, but still involves increased membrane transport of glucose. At maximal insulin concentrations, the enhancing effect of exercise on glucose uptake may involve enhancement of glucose disposal, an effect that is probably less in muscle from diabetic rats.(ABSTRACT TRUNCATED AT 250 WORDS)

AB - It has recently been shown that insulin sensitivity of skeletal muscle glucose uptake and glycogen synthesis is increased after a single exercise session. The present study was designed to determine whether insulin is necessary during exercise for development of these changes found after exercise. Diabetic rats and controls ran on a treadmill and their isolated hindquarters were subsequently perfused at insulin concentrations of 0, 100, and 20,000 microU/ml. Exercise increased insulin sensitivity of glucose uptake and glycogen synthesis equally in diabetic and control rats, but insulin responsiveness of glucose uptake was noted only in controls. Analysis of intracellular glucose-6-phosphate, glucose, glycogen synthesis, and glucose transport suggested that the exercise effect on responsiveness might be due to enhancement of glucose disposal. After electrical stimulation of diabetic hindquarters in the presence of insulin antiserum, insulin sensitivity of 3-O-methylglucose transport was increased to the same extent as in muscle from healthy rats stimulated in the presence of insulin at 50 microU/ml. Furthermore, in muscle depleted of glycogen by contractions, transport of 3-O-methylglucose was increased in the presence of insulin antiserum and in the absence of increased regional perfusate flow. It is concluded that after exercise, increased sensitivity of muscle glucose metabolism to insulin can be found in the absence of insulin during exercise, but still involves increased membrane transport of glucose. At maximal insulin concentrations, the enhancing effect of exercise on glucose uptake may involve enhancement of glucose disposal, an effect that is probably less in muscle from diabetic rats.(ABSTRACT TRUNCATED AT 250 WORDS)

KW - Animals

KW - Diabetes Mellitus, Experimental

KW - Electric Stimulation

KW - Glucose

KW - Glycogen

KW - Insulin

KW - Male

KW - Muscles

KW - Physical Exertion

KW - Rats

KW - Rats, Inbred Strains

U2 - 10.2337/diab.34.10.1041

DO - 10.2337/diab.34.10.1041

M3 - Journal article

C2 - 3899806

SN - 0012-1797

VL - 34

SP - 1041

EP - 1048

JO - Diabetes

JF - Diabetes

IS - 10

ER -