Effects of exercise on insulin binding and glucose metabolism in muscle

1984 ◽  
Vol 62 (12) ◽  
pp. 1500-1504 ◽  
Author(s):  
A. Bonen ◽  
M. H. Tan ◽  
W. M. Watson-Wright
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Metabolism ◽  
Extensor Digitorum Longus ◽  
Glucose Utilization ◽  
Treadmill Exercise ◽  
Insulin Binding ◽  
Glucose Disposal ◽  
Slow Twitch ◽  
Fast Twitch ◽  
Uptake And Metabolism

To elucidate the mechanism of enhanced insulin sensitivity by muscle after exercise, we studied insulin binding, 2-deoxy-D-[1-14C]glucose (2-DOG) uptake and [5-3H]glucose utilization in glycolysis and glycogenesis in soleus and extensor digitorum longus (EDL) muscles of mice after 60 min of treadmill exercise. In the soleus, glycogenesis was increased after exercise (P < 0.05) and remained sensitive to the action of insulin. Postexercise insulin-stimulated glycolysis was also increased in the soleus (P < 0.05). In the EDL, glycogenesis was increased after exercise (P < 0.05). However, this was already maximal in the absence of insulin and was not further stimulated by insulin (0.1–4 nM). The disposal of glucose occurred primarily via the glycolytic pathway (>60%) in the soleus and EDL at rest and after exercise. The uptake of 2-DOG uptake was not altered in the soleus after exercise (4 h incubation at 18 °C). However, with 1-h incubations at 37 °C, a marked increase in 2-DOG uptake after exercise was observed in the soleus (P < 0.05) in the absence (0 nM) and presence of insulin (0.2–4 nM) (P < 0.05). A similar postexercise increase in 2-DOG uptake occurred in EDL. Despite the marked increase in glucose uptake and metabolism, no changes in insulin binding were apparent in either EDL or soleus at 37 °C or 18 °C. This study shows that the postexercise increase of glucose disposal does not appear to be directly attributable to increments in insulin binding to slow-twitch and fast-twitch muscles. Also, after exercise the increments in glucose metabolism differ markedly in the two types of muscle.

Effects of exercise and glycogen depletion on glyconeogenesis in muscle

1994 ◽  
Vol 76 (4) ◽  
pp. 1753-1758 ◽  
Author(s):  
A. Bonen ◽  
D. A. Homonko
Keyword(s):  
Skeletal Muscle ◽  
Muscle Glycogen ◽  
Extensor Digitorum Longus ◽  
Treadmill Exercise ◽  
Glycogen Depletion ◽  
Epinephrine Injection ◽  
Slow Twitch ◽  
Glycogen Repletion ◽  
Fast Twitch

In the present study, we investigated the hypotheses that 1) skeletal muscle glyconeogenesis will increase after exercise, 2) greater changes in glyconeogenesis will be observed after exercise in fast-twitch muscles than in slow-twitch muscles, and 3) glycogen repletion will reduce the rates of glyconeogenesis. Mouse soleus and extensor digitorum longus (EDL) glycogen depots were reduced to the same levels by treadmill exercise (60 min) or epinephrine injection (75 micrograms/100 g body wt ip). Untreated animals were used as controls. We were able to prevent glycogen repletion by incubating muscles in vitro with sorbitol (75 mM) and to increase glycogen concentrations in vitro by incubating muscles with glucose (75 mM). The experimental results showed that glyconeogenesis was increased by exercise (EDL, +51%; soleus, +82%) when glycogen levels were kept low. When glycogen depots were increased, the rate of glyconeogenesis was lowered in the exercised EDL (P < 0.05) but not in the soleus (P > 0.05). Reductions in muscle glycogen by epinephrine did not change the rate of glyconeogenesis in EDL, either when glycogen depots were kept low or were repleted (P > 0.05). In contrast, in the soleus, epinephrine-induced reductions in glycogen did stimulate glyconeogenesis (P < 0.05). Analyses in EDL showed that in nonexercised muscles glycogen concentrations were minimally effective in altering the rates of glyconeogenesis. A 30% decrement in glycogen increased glyconeogenesis by 5% in resting muscles, whereas the same decrement increased glyconeogenesis by 51% in exercised muscles.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Effect of acetoacetate on glucose metabolism in the soleus and extensor digitorum longus muscles of the rat

1977 ◽  
Vol 162 (3) ◽  
pp. 557-568 ◽  
Author(s):  
E Z Maizels ◽  
N B Ruderman ◽  
M N Goodman ◽  
D Lau
Keyword(s):  
Glucose Metabolism ◽  
Glucose Uptake ◽  
Glucose Oxidation ◽  
Extensor Digitorum Longus ◽  
Similar Rate ◽  
Extensor Digitorum ◽  
Lactate Release ◽  
Red Muscle ◽  
Slow Twitch ◽  
Fast Twitch

1. The effect of acetoacetate on glucose metabolism was compared in the soleus, a slow-twitch red muscle, and the extensor digitorum longus, a muscle composed of 50% fast-twitch red and 50% white fibres. 2. When incubated for 2h in a medium containing 5 mM-glucose and 0.1 unit of insulin/ml, rates of glucose uptake, lactate release and glucose oxidation in the soleus were 19.6, 18.6 and 1.47 micronmol/h per g respectively. Acetoacetate (1.7 mM) diminished all three rates by 25-50%; however, it increased glucose conversion into glycogen. In addition, it caused increases in tissue glucose, glucose 6-phosphate and fructose 6-phosphate, suggesting inhibition of phosphofructokinase. The concentrations of citrate, an inhibitor of phosphofructokinase, and of malate were also increased. 3. Rates of glucose uptake and lactate release in the extensor digitorum longus were 50-80% of those in the soleus. Acetoacetate caused moderate increases in tissue glucose 6-phosphate and possibly citrate, but it did not decrease glucose uptake or lactate release. 4. The rate of glycolysis in the soleus was approximately five times that previously observed in the perfused rat hindquarter, a muscle preparation in which acetoacetate inhibits glucose oxidation, but does not alter glucose uptake or glycolysis. A similar rate of glycolysis was observed when the soleus was incubated with a glucose-free medium. Under these conditions, tissue malate and the lactate/pyruvate ratio in the medium were decreased, and acetoacetate did not decrease lactate release or increase tissue citrate or glucose 6-phosphate. An intermediate rate of glycolysis, which was not decreased by acetoacetate, was observed when the soleus was incubated with glucose, but not insulin. 5. The data suggest that acetoacetate glucose inhibits uptake and glycolysis in red muscle under conditions that resemble mild to moderate exercise. They also suggest that the accumulation of citrate in these circumstances is linked to the rate of glycolysis, possibly through the generation of cytosolic NADH and malate formation.

Effects of thyroidectomy on development of skeletal muscle in fetal sheep

1991 ◽  
Vol 261 (5) ◽  
pp. R1300-R1306 ◽  
Author(s):  
D. I. Finkelstein ◽  
P. Andrianakis ◽  
A. R. Luff ◽  
D. Walker
Keyword(s):  
Skeletal Muscle ◽  
Thyroid Gland ◽  
Extensor Digitorum Longus ◽  
Relaxation Times ◽  
Medial Gastrocnemius ◽  
Fetal Sheep ◽  
Twitch Contraction ◽  
Slow Twitch ◽  
Contraction And Relaxation ◽  
Fast Twitch

The influence of the thyroid gland on the functional and histochemical development of fast- and slow-twitch skeletal muscle of fetal sheep has been studied in euthyroid fetal sheep (n = 6) and athyroid fetuses (n = 4) surgically thyroid-ectomized at 70-75 days of gestation. Two fast-twitch muscles, the medial gastrocnemius and extensor digitorum longus, and the slow-twitch soleus muscle were studied at the fetal age of 140 days gestation. The athyroid fetuses had significantly slower twitch contraction and relaxation times in both the medial gastrocnemius and extensor digitorum longus muscles compared with the euthyroid fetuses. Twitch contraction and relaxation times of the soleus were not different in the two groups. Thyroidectomy resulted in an increase in the proportion of fast (type II) muscle fibers and myosin, as shown histochemically and by gel electrophoresis of heavy-chain myosins. These results indicate that the functional maturation of the fast-twitch muscles of sheep is influenced by the presence of an intact thyroid gland from at least 70 days of gestation. In contrast, the slow-twitch soleus muscle fiber diameter and twitch contraction and relaxation times were not different in the two groups.

Diazepam reveals different rate-limiting processes in rat skeletal muscle contraction

1987 ◽  
Vol 65 (2) ◽  
pp. 272-273 ◽  
Author(s):  
Michael Chua ◽  
Angela F. Dulhunty
Keyword(s):  
Skeletal Muscle ◽  
Sarcoplasmic Reticulum ◽  
Calcium Binding ◽  
Extensor Digitorum Longus ◽  
Calcium Uptake ◽  
Rat Skeletal Muscle ◽  
Skeletal Muscle Contraction ◽  
Slow Twitch ◽  
Fast Twitch ◽  
Rate Limiting

The action of the tranquilizer diazepam on rat skeletal muscle showed that relaxation of isometric twitches is controlled by different processes in extensor digitorum longus (fast-twitch) and soleus (slow-twitch) muscles. Diazepam caused an increase in the amplitude of twitches in fibres from both muscles but increased the twitch duration only in soleus. The amplitude of fused tetani were reduced in both muscles and the rate of relaxation after the tetanus slowed by as much as 34% when the amplitude of the tetanus was reduced by only 11%. The slower tetanic relaxation indicated that calcium uptake by the sarcoplasmic reticulum was slower than normal in slow- and fast-twitch fibres. We conclude therefore that calcium uptake by the sarcoplasmic reticulum is rate limiting for twitch relaxation in slow-twitch but not fast-twitch fibres and suggest that calcium binding to parvalbumin controls relaxation in the fast fibres.

Enhanced muscle glucose metabolism after exercise in the rat: the two phases

1984 ◽  
Vol 246 (6) ◽  
pp. E471-E475 ◽  
Author(s):  
L. P. Garetto ◽  
E. A. Richter ◽  
M. N. Goodman ◽  
N. B. Ruderman
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Metabolism ◽  
Phase I ◽  
Phase Ii ◽  
Muscle Glycogen ◽  
Glucose Utilization ◽  
Glycogen Synthesis ◽  
Moderate Intensity ◽  
Base Line ◽  
Two Phases

Thirty minutes after a treadmill run, glucose utilization and glycogen synthesis in perfused rat skeletal muscle are enhanced due to an increase in insulin sensitivity (Richter et al., J. Clin. Invest. 69: 785-793, 1982). The exercise used in these studies was of moderate intensity, and muscle glycogen was substantially repleted at the time (30 min postexercise) that glucose metabolism was examined. When rats were run at twice the previous rate (36 m/min), muscle glycogen was still substantially diminished 30 min after the run. At this time the previously noted increase in insulin sensitivity was still observed in perfused muscle; however, glucose utilization was also increased in the absence of added insulin (1.5 vs. 4.2 mumol X g-1 X h-1). In contrast 2.5 h after the run, muscle glycogen had returned to near preexercise values, and only the insulin-induced increase in glucose utilization was evident. The data suggest that the restoration of muscle glycogen after exercise occurs in two phases. In phase I, muscle glycogen is depleted and insulin-stimulated glucose utilization and glucose utilization in the absence of added insulin may both be enhanced. In phase II glycogen levels have returned to near base-line values and only the increase in insulin sensitivity persists. It is proposed that phase I corresponds to the period of rapid glycogen repletion that immediately follows exercise and phase II to the period of supercompensation.

Insulin binding and 2-deoxy-D-glucose uptake in fast- and slow-twitch mouse skeletal muscle at 18 and 37 °C

1984 ◽  
Vol 62 (12) ◽  
pp. 1460-1465 ◽  
Author(s):  
Wendy M. Watson-Wright ◽  
Meng H. Tan ◽  
Arend Bonen
Keyword(s):  
Extensor Digitorum Longus ◽  
Insulin Binding ◽  
Extensor Digitorum ◽  
Insulin Degradation ◽  
Response Curves ◽  
Slow Twitch Muscle ◽  
Two Temperatures ◽  
Higher Temperature ◽  
Slow Twitch ◽  
Insulin Responsiveness

Insulin binding, insulin degradation, and 2-deoxyglucose uptake were examined at 18 and 37 °C in soleus and extensor digitorum longus muscles of mice. Insulin binding and degradation were greater in the soleus than in the extensor digitorum longus at both temperatures (p < 0.05). At 37 °C, binding was decreased in both muscles while percentage degradation was increased in comparison with 18 °C (p < 0.05). Dose–response curves (percentage of binding at 4 nM of insulin) remained the same for both muscles at the two temperatures. Basal (no insulin) 2-deoxyglucose uptake was increased at 37 °C in the extensor digitorum longus but not the soleus. Insulin responsiveness in terms of the amount of 2-deoxyglucose taken up per femtomole of insulin bound was almost identical for the two muscles at 18 °C, whereas at 37 °C it was increased more in the soleus than in the extensor digitorum longus. The results indicate that in the presence of physiological concentrations of insulin (0.2–4 nM), insulin binding trends are minimally affected by increased temperature. In contrast, the ability of insulin to stimulate 2-deoxyglucose uptake varies between the two temperatures, and at the higher temperature between fast- and slow-twitch muscle.

Glucose uptake and insulin sensitivity in rat muscle: changes during 3-96 weeks of age

1983 ◽  
Vol 244 (1) ◽  
pp. E93-E100 ◽  
Author(s):  
M. N. Goodman ◽  
S. M. Dluz ◽  
M. A. McElaney ◽  
E. Belur ◽  
N. B. Ruderman
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Glucose Transport ◽  
Early Development ◽  
Glucose Utilization ◽  
Insulin Dose ◽  
Insulin Binding ◽  
Sprague Dawley ◽  
High Insulin ◽  
The Right

It has been demonstrated that aging diminishes the rate of glucose utilization by rat skeletal muscle. To determine the basis for this occurrence as well as its temporal sequence, glucose utilization was examined in isolated hindquarters of 3-, 5-, 8-, 16-, 24-, 48-, and 96-wk-old male Sprague-Dawley rats. Glucose utilization diminished progressively during early development (3-5 wk) and adolescence (5-16 wk) in hindquarters perfused in the absence of added insulin. At the same time there was a progressive shift of the insulin dose-response curve to the right, indicating diminished insulin sensitivity and a marked decrease in maximum insulin responsiveness. In contrast, between 24 and 96 wk of age, insulin sensitivity and the rate of glucose utilization in the absence of added insulin did not decrease, and there was only a small decrease in maximum responsiveness. The rate-limiting step in glucose utilization under all conditions was glucose transport. Even at high insulin concentrations, free glucose was not detected in the muscle cells of young or old rats, the uptake of 2-deoxyglucose diminished in parallel with that of glucose, and there was no evidence of a defect in glucose metabolism. These findings indicate that in the Sprague-Dawley rat glucose transport into skeletal muscle and in particular its sensitivity and responsiveness to insulin diminish progressively during early development and adolescence. No further marked changes occurred up to at least 96 wk of age. To what extent these early age-associated changes are due to insulin binding and to what extent to alterations in the glucose transport system per se remains to be determined.

scholarly journals Insulin action and glucose metabolism in sheep fed on dried-grass or ground, maize-based diets

1985 ◽  
Vol 54 (2) ◽  
pp. 459-471 ◽  
Author(s):  
A. N. Janes ◽  
T. E. C. Weekes ◽  
D. G. Armstrong
Keyword(s):  
Glucose Metabolism ◽  
Insulin Action ◽  
Plasma Insulin ◽  
Glucose Utilization ◽  
Glucose Production ◽  
Endogenous Glucose Production ◽  
Whole Body ◽  
Glucose Disposal ◽  
Metabolic Clearance ◽  
Endogenous Glucose

1. The effect of an exogenous supply of glucose, provided by the digestion of maize starch in the small intestine, on endogenous glucose metabolism and insulin action was studied in sheep using the euglycaemic insulin clamp procedure.2. Insulin was infused intravenously at rates of 0.2, 0.5, 1.0 and 6.0 mU/min per kg live weight for four consecutive periods in each of four sheep fed on dried-grass and maize-based diets. Glucose was also infused intravenously at a variable rate, sufficient to maintain the plasma glucose concentration at basal levels. Whole-body rates of glucose metabolism were determined using a continuous infusion of [6-3H]glucose.3. From the resultinginsulin dose-response curves, it was observed that, when the sheep were fed on the dried-grass diet, the responsiveness of glucose metabolism to insulin was less than that reported for non-ruminants.4. When fed the maize-based diet, the glucose metabolic clearance rates (MCR) observed during insulin infusions were significantly greater (P < 0.05) than those observed for the dried-grass diet. However, after correcting for the non-insulin-mediated glucose disposal, differences between diets were not significant.5. The sensitivity of glucose utilization to insulin was not affected by diet. The plasma insulin concentrations causing half-maximal insulin-mediated glucose MCR were 103 (SE 21) and 85 (SE 11) mU/l for the dried-grass and maize-based diets respectively.6. The sensitivity of endogenous glucose production to insulin was also unaffected by diet. The plasma insulin concentrations resulting in the suppression of endogenous glucose production to half the basal level were 80 (SE 26) and 89 (SE 29) mU/l for the dried-grass and maize-based diets respectively.7. It is concluded that the observed increase in glucose utilization on the maize-based diet was due partly to a slight change in responsiveness to insulin and also partly to a change in the rate of non-insulin-mediated glucose disposal.

Effect of exercise training on whole-body insulin sensitivity and responsiveness

1984 ◽  
Vol 56 (5) ◽  
pp. 1217-1222 ◽  
Author(s):  
D. E. James ◽  
E. W. Kraegen ◽  
D. J. Chisholm
Keyword(s):  
Insulin Sensitivity ◽  
Exercise Training ◽  
Glucose Utilization ◽  
Insulin Receptors ◽  
Whole Body ◽  
Glucose Disposal ◽  
Significant Shift ◽  
Insulin Levels ◽  
Plasma Insulin Levels

Exercise training causes a decline in basal and glucose-stimulated plasma insulin levels and improves glucose tolerance. Furthermore evidence has been presented for effects on both insulin receptors and postreceptor events. However, it is unclear how these changes affect the in vivo dose-response relationship between insulin levels and whole-body glucose utilization. The aim was to examine the effect of exercise training on this relationship and distinguish between changes in insulin sensitivity and responsiveness. Euglycemic clamps were performed in trained (ET, running 1 h/day for 7 wk), sedentary (CON), and sedentary food-restricted ( SFR ) rats. ET rats showed no increase in maximal net glucose utilization in response to insulin (ET 29.5 +/- 0.6 vs. CON 28.2 +/- 1.5 mg X kg-1 X min-1, NS), whereas insulin sensitivity was increased as indicated by the insulin concentration causing half-maximal stimulation (ED50) (49 +/- 20 for ET and 133 +/- 30 mU/l for CON). Thus 7 wk of moderate exercise training resulted in a significant shift of whole-body insulin sensitivity to place ED50 well within the physiological range of insulin concentrations. This would undoubtedly result in improved glucose disposal in the postprandial state and emphasizes the potential benefit of exercise in obesity and type II diabetes.

Increased submaximal insulin-stimulated glucose uptake in mouse skeletal muscle after treadmill exercise

2006 ◽  
Vol 101 (5) ◽  
pp. 1368-1376 ◽  
Author(s):  
Taku Hamada ◽  
Edward B. Arias ◽  
Gregory D. Cartee
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Glucose Uptake ◽  
Extensor Digitorum Longus ◽  
Treadmill Exercise ◽  
Genetically Modified ◽  
Extensor Digitorum ◽  
Exercise Protocol ◽  
Mouse Skeletal Muscle ◽  
Prior Exercise

The primary purpose of this study was to determine the effect of prior exercise on insulin-stimulated glucose uptake with physiological insulin in isolated muscles of mice. Male C57BL/6 mice completed a 60-min treadmill exercise protocol or were sedentary. Paired epitrochlearis, soleus, and extensor digitorum longus (EDL) muscles were incubated with [3H]-2-deoxyglucose without or with insulin (60 μU/ml) to measure glucose uptake. Insulin-stimulated glucose uptake for paired muscles was calculated by subtracting glucose uptake without insulin from glucose uptake with insulin. Muscles from other mice were assessed for glycogen and AMPK Thr172 phosphorylation. Exercised vs. sedentary mice had decreased glycogen in epitrochlearis (48%, P < 0.001), soleus (51%, P < 0.001), and EDL (41%, P < 0.01) and increased AMPK Thr172 phosphorylation ( P < 0.05) in epitrochlearis (1.7-fold), soleus (2.0-fold), and EDL (1.4-fold). Insulin-independent glucose uptake was increased 30 min postexercise vs. sedentary in the epitrochlearis (1.2-fold, P < 0.001), soleus (1.4-fold, P < 0.05), and EDL (1.3-fold, P < 0.01). Insulin-stimulated glucose uptake was increased ( P < 0.05) ∼85 min after exercise in the epitrochlearis (sedentary: 0.266 ± 0.045 μmol·g−1·15 min−1; exercised: 0.414 ± 0.051) and soleus (sedentary: 0.102 ± 0.049; exercised: 0.347 ± 0.098) but not in the EDL. Akt Ser473 and Akt Thr308 phosphorylation for insulin-stimulated muscles did not differ in exercised vs. sedentary. These results demonstrate enhanced submaximal insulin-stimulated glucose uptake in the epitrochlearis and soleus of mice 85 min postexercise and suggest that it will be feasible to probe the mechanism of enhanced postexercise insulin sensitivity by using genetically modified mice.

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