Glycogen depletion and increased insulin sensitivity and responsiveness in muscle after exercise

1986 ◽  
Vol 251 (6) ◽  
pp. E664-E669 ◽  
Author(s):  
A. Zorzano ◽  
T. W. Balon ◽  
M. N. Goodman ◽  
N. B. Ruderman
Keyword(s):  
Insulin Sensitivity ◽  
Glucose Utilization ◽  
Treadmill Exercise ◽  
Moderate Intensity ◽  
Glycogen Depletion ◽  
Increase Insulin Sensitivity ◽  
Enhanced Sensitivity ◽  
Prior Exercise ◽  
Insulin Responsiveness ◽  
The Relationship

As judged by its ability to stimulate glucose uptake and alpha-aminoisobutyric acid (AIB) transport, the sensitivity and the responsiveness of perfused rat muscle to insulin are enhanced after moderately intense treadmill exercise. In fed rats, these enhanced effects of insulin are predominantly restricted to muscles that performed work as evidenced by glycogen depletion. The present study was designed to examine the relationship between glycogen depletion per se and the postexercise changes in insulin action. Toward this end, fed and 48-h starved rats were run on a treadmill for 45 min at moderate intensity, and glucose and AIB uptake were then assessed using the isolated perfused hindquarter preparation. Glycogen is depleted in red muscles such as the soleus and red fibers of the gastrocnemius in fed rats immediately after such exercise, whereas, in starved rats, muscle glycogen is unchanged. As previously shown, the stimulation by insulin of glucose utilization by the hindquarter and AIB transport into red muscles was substantially increased in fed rats after the treadmill run. This was due to increases in both insulin sensitivity and responsiveness. In starved rats, the treadmill run also enhanced the ability of insulin to stimulate these processes; however, this was solely due to an increase in insulin sensitivity. No change in insulin responsiveness was observed. The results indicate that the enhanced sensitivity of muscle to insulin after exercise is not dependent on glycogen depletion, whereas increased insulin responsiveness does not occur in its absence. They also suggest that the mechanisms by which prior exercise acts to increase insulin sensitivity and responsiveness are different.

Epinephrine inhibits exogenous glucose utilization in exercising horses

2000 ◽  
Vol 88 (5) ◽  
pp. 1777-1790 ◽  
Author(s):  
Raymond J. Geor ◽  
Kenneth W. Hinchcliff ◽  
Laura Jill McCutcheon ◽  
Richard A. Sams
Keyword(s):  
Muscle Glycogen ◽  
Glucose Utilization ◽  
Treadmill Exercise ◽  
Moderate Intensity ◽  
Oral Glucose ◽  
Moderate Intensity Exercise ◽  
Epinephrine Infusion ◽  
Glucose Administration ◽  
Exogenous Glucose ◽  
Glycogen Utilization

This study examined the effects of preexercise glucose administration, with and without epinephrine infusion, on carbohydrate metabolism in horses during exercise. Six horses completed 60 min of treadmill exercise at 55 ± 1% maximum O2 uptake 1) 1 h after oral administration of glucose (2 g/kg; G trial); 2) 1 h after oral glucose and with an intravenous infusion of epinephrine (0.2 μmol ⋅ kg− 1 ⋅ min− 1; GE trial) during exercise, and 3) 1 h after water only (F trial). Glucose administration (G and GE) caused hyperinsulinemia and hyperglycemia (∼8 mM). In GE, plasma epinephrine concentrations were three- to fourfold higher than in the other trials. Compared with F, the glucose rate of appearance was ∼50% and ∼33% higher in G and GE, respectively, during exercise. The glucose rate of disappearance was ∼100% higher in G than in F, but epinephrine infusion completely inhibited the increase in glucose uptake associated with glucose administration. Muscle glycogen utilization was higher in GE [349 ± 44 mmol/kg dry muscle (dm)] than in F (218 ± 28 mmol/kg dm) and G (201 ± 35 mmol/kg dm). We conclude that 1) preexercise glucose augments utilization of plasma glucose in horses during moderate-intensity exercise but does not alter muscle glycogen usage and 2) increased circulating epinephrine inhibits the increase in glucose rate of disappearance associated with preexercise glucose administration and increases reliance on muscle glycogen for energy transduction.

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.

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.

Muscle alpha-aminoisobutyric acid transport after exercise: enhanced stimulation by insulin

1985 ◽  
Vol 248 (5) ◽  
pp. E546-E552 ◽  
Author(s):  
A. Zorzano ◽  
T. W. Balon ◽  
L. P. Garetto ◽  
M. N. Goodman ◽  
N. B. Ruderman
Keyword(s):  
Skeletal Muscle ◽  
Glucose Transport ◽  
Glucose Utilization ◽  
Glycogen Synthesis ◽  
Common Factor ◽  
Insulin Binding ◽  
Moderate Intensity ◽  
Insulin Effect ◽  
Aminoisobutyric Acid ◽  
Prior Exercise

After exercise the ability of insulin to stimulate glucose transport and glycogen synthesis in rat skeletal muscle is markedly enhanced (25). The present study was designed to determine whether prior exercise augments the stimulation of other processes by insulin and, if so, whether this can be attributed to an increase in insulin binding to its receptor. Toward this end rats were run on a treadmill for 45 min at moderate intensity and the uptake of alpha-aminoisobutyric acid (AIB) by muscle was then assessed using the isolated perfused hindquarter preparation. Approximately 30 min after the cessation of exercise, both the sensitivity and responsiveness of insulin-stimulated AIB uptake were significantly enhanced in the soleus and the red portion of the gastrocnemius. As previously shown for glucose transport and glycogen synthesis, only small effects were observed in the white portion of the gastrocnemius, which unlike the other muscles was not depleted of glycogen during the run. Insulin-stimulated glucose utilization was also enhanced in the incubated soleus muscle of exercised rats; however, insulin binding to the soleus was not altered. These studies indicate that the ability of insulin to stimulate processes other than glucose transport and glycogen synthesis is enhanced in skeletal muscle after exercise and that this is not due to an alteration in insulin binding. The changes in insulin-stimulated AIB uptake and glucose metabolism after exercise are the reverse of those found in denervated and immobilized muscle and in both situations insulin binding is not altered. This suggests that a common factor(s) modulates the increase in insulin effect after exercise and the insulin resistance of disuse.

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.

Additive effects of prior exercise and insulin on glucose and AIB uptake by rat muscle

1986 ◽  
Vol 251 (1) ◽  
pp. E21-E26 ◽  
Author(s):  
A. Zorzano ◽  
T. W. Balon ◽  
M. N. Goodman ◽  
N. B. Ruderman
Keyword(s):  
Glucose Uptake ◽  
Moderate Intensity ◽  
Additive Effects ◽  
Absolute Rate ◽  
Intense Exercise ◽  
Rat Muscle ◽  
Prior Exercise ◽  
Ad Libitum ◽  
Insulin Responsiveness ◽  
Parallel Fashion

After exercise of moderate intensity the ability of insulin to stimulate the uptake of glucose and alpha-aminoisobutyric acid (AIB) in perfused rat muscle is enhanced in a parallel fashion. The present study was designed to examine the effect of intense exercise on the subsequent uptake of these substrates. For this purpose, rats fed ad libitum were run on a treadmill for 50 min at high intensity and glucose and AIB uptake by muscle were then assessed in the isolated perfused hindquarter preparation. In confirmation of previous studies, 30 min after such exercise the absolute rate of glucose uptake in the presence of 20,000 microU/ml of insulin was greater due to additive effects of insulin and prior exercise. A novel finding was that 150 min postexercise the rate of glucose uptake was still increased in the presence of a supramaximal concentration of insulin, but entirely due to an increase in insulin responsiveness. The uptake of AIB and its response to insulin in general paralleled that of glucose. The results indicate that both glucose and AIB uptake by skeletal muscle in the presence of a supramaximal concentration of insulin are increased after intense exercise. They suggest that this is initially due to an additive effect of insulin and exercise and later due to an increase in insulin responsiveness. The findings are compatible with the notion that after exercise insulin is able to recruit or activate glucose (and possibly AIB) transporters in muscle, that it does not affect in the resting state.

Are the reductions in triacylglycerol and insulin levels after exercise related?

2002 ◽  
Vol 102 (2) ◽  
pp. 223-231 ◽  
Author(s):  
Jason M.R. GILL ◽  
Sara L. HERD ◽  
Natassa V. TSETSONIS ◽  
Adrianne E. HARDMAN
Keyword(s):  
Insulin Sensitivity ◽  
Insulin Response ◽  
Insulin Concentration ◽  
Moderate Intensity ◽  
Fasting Insulin ◽  
Prior Exercise ◽  
Exercise Induced ◽  
Induced Changes ◽  
Postprandial Insulin Response ◽  
Postprandial Insulin

Moderate exercise improves insulin sensitivity and reduces triacylglycerol (triglyceride; TG) concentrations. We hypothesized that changes in insulin sensitivity are an important determinant of exercise-induced changes in postprandial TG concentrations. Altogether, 38 men and 43 women, all of whom were normotriglyceridaemic and normoglycaemic, each underwent two oral fat tolerance tests with different pre-conditions: control (no exercise) and prior exercise (90min of exercise at 60% of maximal O2 uptake the day before). Venous blood samples were obtained in the fasting state and for 6h after a high-fat mixed meal. In the control trial there were significant correlations between log fasting TG concentration and log fasting insulin concentration (r = 0.42, P < 0.0005) and between log postprandial TG response (area under the curve) and log postprandial insulin response (r = 0.48, P < 0.0005). Prior exercise reduced the fasting TG concentration by 18.2±2.2% (mean±S.E.M.) (P < 0.0005), the postprandial TG response by 21.5±1.9% (P < 0.0005), the fasting insulin concentration by 3.8±3.1% (P < 0.01) and the postprandial insulin response by 11.9±2.5% (P < 0.0005). However, there was no relationship between the exercise-induced changes in log fasting TG and log fasting insulin (r = 0.08, P = 0.50), nor between the exercise-induced changes in log postprandial TG response and log postprandial insulin response (r = 0.04, P = 0.70). These data suggest that the reductions in fasting and postprandial TG levels elicited by a session of moderate-intensity exercise are not mediated by an increase in insulin sensitivity.

Exercise and improved insulin sensitivity in older women: evidence of the enduring benefits of higher intensity training

2006 ◽  
Vol 100 (1) ◽  
pp. 142-149 ◽  
Author(s):  
Loretta DiPietro ◽  
James Dziura ◽  
Catherine W. Yeckel ◽  
P. Darrell Neufer
Keyword(s):  
Insulin Sensitivity ◽  
Exercise Training ◽  
Glucose Utilization ◽  
Aerobic Training ◽  
Insulin Dose ◽  
Moderate Intensity ◽  
Placebo Control ◽  
Transient Effects ◽  
Euglycemic Hyperinsulinemic Clamp ◽  
Low Intensity

Few studies have compared the relative benefits of moderate- vs. higher intensity exercise training on improving insulin sensitivity in older people while holding exercise volume constant. Healthy older (73 ± 10 yr) women ( N = 25) who were inactive, but not obese, were randomized into one of three training programs (9-mo duration): 1) high-intensity [80% peak aerobic capacity (V̇o2 peak); TH] aerobic training; 2) moderate-intensity (65% V̇o2 peak; TM) aerobic training; or 3) low-intensity (stretching) placebo control (50% V̇o2 peak; CTB). Importantly, exercise volume (300 kcal/session) was held constant for subjects in both the TH and the TM groups. V̇o2 peak was determined by using a graded exercise challenge on a treadmill. Total body fat and lean mass were determined with dual-energy X-ray absorptiometry. The rate of insulin-stimulated glucose utilization as well as the suppression of lipolysis were determined ∼72 h after the final exercise bout by using a two-step euglycemic-hyperinsulinemic clamp. We observed improved glucose utilization at the higher insulin dose with training, but these improvements were statistically significant only in the TH (21%; P = 0.02) compared with the TM (16%; P = 0.17) and CTB (8%; P = 0.37) groups and were observed without changes in either body composition or V̇o2 peak. Likewise in the TH group, we detected a significant improvement in insulin-stimulated suppression (%) of adipose tissue lipolysis at the low-insulin dose (38–55%, P < 0.05). Our findings suggest that long-term higher intensity exercise training provides more enduring benefits to insulin action compared with moderate- or low-intensity exercise, likely due to greater transient effects.

Pressor and subpressor doses of angiotensin II increase insulin sensitivity in NIDDM. Dissociation of metabolic and blood pressure effects

Diabetes ◽  
1994 ◽  
Vol 43 (12) ◽  
pp. 1445-1449 ◽  
Author(s):  
A. D. Morris ◽  
J. R. Petrie ◽  
S. Ueda ◽  
J. M. Connell ◽  
H. L. Elliott ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Insulin Sensitivity ◽  
Angiotensin Ii ◽  
Pressure Effects ◽  
Increase Insulin Sensitivity ◽  
Blood Pressure Effects

scholarly journals Carbohydrate Restriction with or without Exercise Training Improves Blood Pressure and Insulin Sensitivity in Overweight Women

Healthcare ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 637
Author(s):  
Shengyan Sun ◽  
Zhaowei Kong ◽  
Qingde Shi ◽  
Haifeng Zhang ◽  
On-Kei Lei ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Insulin Sensitivity ◽  
Exercise Training ◽  
Fasting Glucose ◽  
Training Group ◽  
Moderate Intensity ◽  
Cardiometabolic Health ◽  
Carbohydrate Restriction ◽  
Obese Women ◽  
Low Carbohydrate Diet

Objective: The purpose of this study was to evaluate the effects of a 4-week low-carbohydrate diet (LC) with or without exercise training on cardiometabolic health-related profiles in overweight/obese women. Methods: Fifty overweight/obese Chinese women (age: 22.2 ± 3.3 years, body mass index (BMI): 25.1 ± 3.1 kg·m−2) were randomized to either a LC control group (LC-CON, n = 16), a LC and high-intensity interval training group (LC-HIIT, n = 17), or a LC and moderate-intensity continuous training group (LC-MICT, n = 17). All groups consumed LC for 4 weeks, while the LC-HIIT and LC-MICT groups followed an additional five sessions of HIIT (10 × 6 s cycling sprints and 9 s rest intervals, 2.5 min in total) or MICT (cycling continuously at 50–60% of peak oxygen uptake (VO2peak) for 30 min) weekly. Blood pressure, fasting glucose, insulin sensitivity, and several metabolic or appetite regulating hormones were measured before and after intervention. Results: Significant reductions in body weight (− ~2.5 kg, p < 0.001, η2 = 0.772) and BMI (− ~1 unit, p < 0.001, η2 = 0.782) were found in all groups. Systolic blood pressure was reduced by 5–6 mmHg (p < 0.001, η2 = 0.370); fasting insulin, leptin, and ghrelin levels were also significantly decreased (p < 0.05), while insulin sensitivity was improved. However, there were no significant changes in fasting glucose, glucagon, and gastric inhibitory peptide levels. Furthermore, no group differences were found among the three groups, suggesting that extra training (i.e., LC-HIIT and LC-MICT) failed to trigger additional effects on these cardiometabolic profiles. Conclusions: The short-term carbohydrate restriction diet caused significant weight loss and improved blood pressure and insulin sensitivity in the overweight/obese women, although the combination with exercise training had no additional benefits on the examined cardiometabolic profiles. Moreover, the long-term safety and effectiveness of LC needs further study.

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