Effect of short-term exercise training on insulin-stimulated PI 3-kinase activity in human skeletal muscle

1999 ◽  
Vol 277 (6) ◽  
pp. E1055-E1060 ◽  
Author(s):  
Joseph A. Houmard ◽  
Christopher D. Shaw ◽  
Matthew S. Hickey ◽  
Charles J. Tanner
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Exercise Training ◽  
Kinase Activity ◽  
Vastus Lateralis ◽  
Maximal Oxygen Consumption ◽  
Exercise Bout ◽  
Phosphatidylinositol 3 Kinase ◽  
Insulin Signal Transduction ◽  
Before And After

The purpose of this study was to determine if the improvement in insulin sensitivity with exercise training is associated with enhanced phosphatidylinositol 3-kinase (PI 3-kinase) activity. Nine sedentary men were studied before and after 7 days of exercise training (1 h/day, ≈75% maximal oxygen consumption). Insulin sensitivity was determined with a euglycemic-hyperinsulinemic glucose clamp in the sedentary state and 15–17 h after the final exercise bout. PI 3-kinase activity was determined from samples (vastus lateralis) obtained in the fasted condition and after 60 min of submaximal insulin stimulation during the clamp. After exercise, glucose infusion rate increased ( P < 0.05) significantly (means ± SE, 7.8 ± 0.5 vs. 9.8 ± 0.8 mg ⋅ kg−1 ⋅ min−1), indicating improved insulin sensitivity. Insulin-stimulated (insulin stimulated/fasting) phosphotyrosine immunoprecipitable PI 3-kinase activity also increased significantly ( P < 0.05) with exercise (3.1 ± 0.8-fold) compared with the sedentary condition (1.3 ± 0.1-fold). There was no change in fasting PI 3-kinase activity. These data suggest that an enhancement of insulin signal transduction in skeletal muscle may contribute to the improvement in insulin action with exercise.

Exercise training and calorie restriction increase SREBP-1 expression and intramuscular triglyceride in skeletal muscle

2006 ◽  
Vol 291 (1) ◽  
pp. E90-E98 ◽  
Author(s):  
Kristen J. Nadeau ◽  
Lindsay B. Ehlers ◽  
Lina E. Aguirre ◽  
Russell L. Moore ◽  
Korinne N. Jew ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Exercise Training ◽  
Calorie Restriction ◽  
Fatty Acid Synthase ◽  
Regulatory Element ◽  
Vastus Lateralis ◽  
Vastus Lateralis Muscle ◽  
Sprague Dawley ◽  
Intramuscular Triglyceride

Intramuscular triglyceride (IMTG) deposition in skeletal muscle is associated with obesity and type 2 diabetes (T2DM) and is thought to be related to insulin resistance (IR). Curiously, despite enhanced skeletal muscle insulin sensitivity, highly trained athletes and calorie-restricted (CR) monkeys also have increased IMTG. Sterol regulatory element-binding proteins (SREBPs) are transcription factors that regulate the biosynthesis of cholesterol and fatty acids. SREBP-1 is increased by insulin in skeletal muscle in vitro and in skeletal muscle of IR subjects, but SREBP-1 expression has not been examined in exercise training or calorie restriction. We examined the relationship between IMTG and SREBP-1 expression in animal models of exercise and calorie restriction. Gastrocnemius and soleus muscle biopsies were obtained from 38 Sprague-Dawley rats (18 control and 20 exercise trained). Triglyceride content was higher in the gastrocnemius and soleus muscles of the trained rats. SREBP-1c mRNA, SREBP-1 precursor and mature proteins, and fatty acid synthase (FAS) protein were increased with exercise training. Monkeys ( Macaca mulatta) were CR for a mean of 10.4 years, preventing weight gain and IR. Vastus lateralis muscle was obtained from 12 monkeys (6 CR and 6 controls). SREBP-1 precursor and mature proteins and FAS protein were higher in the CR monkeys. In addition, phosphorylation of ERK1/ERK2 was increased in skeletal muscle of CR animals. In summary, SREBP-1 protein and SREBP-1c mRNA are increased in interventions that increase IMTG despite enhanced insulin sensitivity. CR and exercise-induced augmentation of SREBP-1 expression may be responsible for the increased IMTG seen in skeletal muscle of highly conditioned athletes.

Elevated skeletal muscle glucose transporter levels in exercise-trained middle-aged men

1991 ◽  
Vol 261 (4) ◽  
pp. E437-E443 ◽  
Author(s):  
J. A. Houmard ◽  
P. C. Egan ◽  
P. D. Neufer ◽  
J. E. Friedman ◽  
W. S. Wheeler ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Exercise Training ◽  
Glucose Transporter ◽  
Exercise Bout ◽  
Tolerance Test ◽  
Whole Body ◽  
Oral Glucose ◽  
Middle Aged ◽  
Glut 4

Exercise training has been proposed to improve whole body insulin sensitivity through a postreceptor adaptation in skeletal muscle. This study examined if levels of the insulin-responsive muscle glucose transporter protein (GLUT-4) were associated with improved insulin sensitivity in trained vs. sedentary middle-aged individuals. Muscle GLUT-4 levels and oral glucose tolerance test (OGTT) responses were obtained in age-matched trained and sedentary men (n = 11). Plasma insulin levels during the OGTT were significantly lower (P less than 0.01) in the trained men, whereas no differences were seen in plasma glucose responses. GLUT-4 protein content was approximately twofold higher in the trained men (2.41 +/- 0.17 vs. 1.36 +/- 0.11 micrograms standard, P less than 0.001). OGTT responses and GLUT-4 levels were not altered 15-18 h after a standard exercise bout in six representative sedentary subjects. These data suggest that GLUT-4 levels are increased in conjunction with insulin sensitivity in chronically exercise-trained middle-aged men. This finding suggests a possible mechanism for the improved insulin sensitivity observed with exercise training in humans.

124 Skeletal muscle RNA and insulin sensitivity during insufficient sleep

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A50-A51
Author(s):  
Sarah Morton ◽  
Julia Sharp ◽  
Kenneth Wright ◽  
Josiane Broussard
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Vastus Lateralis ◽  
Statistical Significance ◽  
Whole Body ◽  
P Value ◽  
Insufficient Sleep ◽  
Before And After ◽  
Study Participants ◽  
Laboratory Protocol

Abstract Introduction Insufficient sleep is associated with a down-regulation of genes involved in glycolysis, in conjunction with an upregulation of genes involved in lipid metabolism in skeletal muscle. However, whether changes in RNA are associated with impairments in insulin sensitivity is unclear. We therefore tested the hypothesis that insufficient sleep will induce alterations in skeletal muscle RNA that correlate with changes in insulin sensitivity. Methods As part of an ongoing study, sixteen sedentary, healthy, lean adults (24.9±3.4y; 22.6±1.7kg/m2; 6F; mean±SD) participated in a controlled 6-day in-laboratory protocol with 9h in bed (habitual sleep) followed by 4 nights of 5h in bed (insufficient sleep), achieved by delaying bedtime by 4 hours. For one week prior to the study, participants maintained a 9h sleep schedule based on their habitual bed and wake times. Participants consumed energy-balanced diets 3 days prior to and throughout the laboratory protocol. Whole body insulin sensitivity was assessed using glucose infusion rate from a hyperinsulinemic euglycemic clamp before and after 4 nights of insufficient sleep. Skeletal muscle biopsies of the vastus lateralis were taken immediately before each clamp. In a subset of subjects (n=12), RNA sequencing was performed (Novogene Co., Ltd). Generalized linear model likelihood ratio tests were completed using the DESeq2/EdgeR R packages with a false discovery rate (FDR) cut-off of 5%. P-values were adjusted for multiple comparisons using the Benjamini-Hochberg method and a corrected p-value of 0.05 and log2 fold-change of 0 were set as the threshold for statistical significance. Results Insulin sensitivity was impaired by 6% following insufficient sleep (10.1±1.4 vs 9.1±1.1mg/kg/min, p&lt;0.05, mean±SEM). Preliminary results from skeletal muscle RNAseq analyses suggest approximately 25 genes were down-regulated and 60 genes were up-regulated. Down-regulated genes were involved in insulin-like growth factor binding and signal transduction (p=8.4e-11), while up-regulated genes were involved in glycolysis and ATP binding (p=1.1e-9). While there were trends for associations between changes in gene expression and insulin sensitivity, these relationships did not reach statistical significance. Conclusion Preliminary findings suggest insufficient sleep alters skeletal muscle RNA. Changes in these aforementioned pathways may contribute to metabolic dysregulation during insufficient sleep. Support (if any) NIH K01DK110138, R03 DK118309, UL1 TR002535, and GCRC RR-00036

Effect of training on insulin binding to rat skeletal muscle sarcolemmal vesicles

1986 ◽  
Vol 250 (5) ◽  
pp. E570-E575
Author(s):  
G. K. Grimditch ◽  
R. J. Barnard ◽  
S. A. Kaplan ◽  
E. Sternlicht
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Exercise Training ◽  
Insulin Binding ◽  
Whole Body ◽  
Rat Skeletal Muscle ◽  
Binding Studies ◽  
Muscle Enzyme ◽  
Intravenous Glucose ◽  
High Affinity

We examined the hypothesis that the exercise training-induced increase in skeletal muscle insulin sensitivity is mediated by adaptations in insulin binding to sarcolemmal (SL) insulin receptors. Insulin binding studies were performed on rat skeletal muscle SL isolated from control and trained rats. No significant differences were noted between groups in body weight or fat. An intravenous glucose tolerance test showed an increase in whole-body insulin sensitivity with training, and specific D-glucose transport studies on isolated SL vesicles indicated that this was due in part to adaptations in skeletal muscle. Enzyme marker analyses revealed no differences in yield, purity, or contamination of SL membranes between the two groups. Scatchard analyses indicated no significant differences in the number of insulin binding sites per milligram SL protein on the high-affinity (15.0 +/- 4.1 vs. 18.1 +/- 6.4 X 10(9)) or on the low-affinity portions (925 +/- 80 vs. 884 +/- 106 X 10(9)) of the curves. The association constants of the high-affinity (0.764 +/- 0.154 vs. 0.685 +/- 0.264 X 10(9) M-1) and of the low affinity sites (0.0096 +/- 0.0012 vs. 0.0102 +/- 0.0012 X 10(9) M-1) also were similar. These results do not support the hypothesis that the increased sensitivity to insulin after exercise training is due to changes in SL insulin receptor binding.

Exercise training prevents maturation-induced decrease in insulin sensitivity

1996 ◽  
Vol 80 (6) ◽  
pp. 1963-1967 ◽  
Author(s):  
N. Nakai ◽  
Y. Shimomura ◽  
N. Ohsaki ◽  
J. Sato ◽  
Y. Oshida ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Insulin Sensitivity ◽  
Exercise Training ◽  
Infusion Rate ◽  
Glucose Transporter ◽  
Euglycemic Clamp ◽  
Glut 4 ◽  
Hindlimb Muscle ◽  
Female Wistar Rats ◽  
Sensitivity Improvement

We examined the effects of exercise training initiated before maturation or after maturation on insulin sensitivity and glucose transporter GLUT-4 content in membrane fractions of skeletal muscle. Female Wistar rats (4 wk of age) were divided into sedentary and exercise-trained groups. At 12 wk of age, a subset of the trained animals (Tr) was killed along with a subset of sedentary controls (Sed). One-half of the remaining sedentary animals remained sedentary (Sed-Sed) while the other half began exercise training (Sed-Tr). The remaining rats in the original trained group continued to train (Tr-Tr). Euglycemic clamp (insulin infusion rate at 6 mU.kg body wt-1. min-1) was performed at 4, 12, and 27 wk. After euglycemic clamp in all animals except the 4-wk-old, hindlimb (gastrocnemius and part of quadriceps) muscles were removed for preparation of membrane fractions. In sedentary rats, glucose infusion rate (GIR) during euglycemic clamp was decreased from 15.9 mg.kg-1.min-1 at 4 wk of age to 9.8 mg.kg-1.min-1 at 12 wk of age and 9.1 mg.kg-1.min-1 at 27 wk of age. In exercise-trained rats, the GIR was not significantly decreased by maturation (at 12 wk) and further aging (at 27 wk). Initiation of exercise after maturation restored the GIR at 27 wk of age to the same levels as these for the corresponding exercise-trained rats. GLUT-4 content in plasma and intracellular membrane fractions of hindlimb muscle obtained just after euglycemic clamp showed the same trend as the results of GIR. These results suggest that exercise training prevented the maturation-induced decrease in insulin sensitivity. Improvement of insulin sensitivity caused by exercise training was attributed, at least in part, to the increase in insulin-sensitive GLUT-4 on the plasma membrane in skeletal muscle.

Effect of a single bout of exercise and chronic exercise training on insulin sensitivity in racing sled dogs

2014 ◽  
Vol 10 (3) ◽  
pp. 167-172 ◽  
Author(s):  
S.E. Pratt-Phillips ◽  
R.J. Geor ◽  
M. Buser ◽  
A. Zirkle ◽  
A. Moore ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Exercise Training ◽  
Exercise Bout ◽  
Post Exercise ◽  
Exercise Challenge ◽  
Sled Dogs ◽  
Significant Difference ◽  
Single Bout ◽  
Three Stages

Two experiments were designed to investigate the role of exercise on insulin sensitivity (IS) in Alaskan racing sled dogs. In both experiments, IS was quantified with an isoglycemic-hyperinsulinemic clamp (IHC), whereby IS was defined as the glucose infusion rate (GIR) divided by the mean insulin concentration during the clamp. In Experiment 1, IS was quantified in 12 racing sled dogs during three stages of exercise training: unexercised for 4 months over the summer (deconditioned), and after two and four months of exercise conditioning. At each stage IS was assessed in unexercised dogs (n=6) and 60 h following a standard exercise challenge (n=6) consisting of a 35.4 km run completed in 2.5 h. In Experiment 2, IS was assessed in deconditioned dogs (n=6) and in well-conditioned dogs that had either completed a 708 km race 5-days prior (n=3) or were unraced for the previous month (n=3). In Experiment 1, there were no significant differences (Pã0.05) in GIR or IS between the three levels of conditioning, nor were there any effects of the exercise bout 60 h prior to the IHC. In Experiment 2 there was no significant difference in IS between well-conditioned dogs and untrained dogs (Pã0.05). However, dogs that completed a 708 km race 5-days prior to the IHC had a significantly higher IS than dogs that were deconditioned and those that were conditioned but unraced. These results suggest that the workload of an exercise challenge is a factor in post-exercise changes in IS but that exercise conditioning has little impact on IS in Alaskan sled dogs.

Muscle glycogen availability and temperature regulation in humans

1989 ◽  
Vol 66 (1) ◽  
pp. 72-78 ◽  
Author(s):  
L. Martineau ◽  
I. Jacobs
Keyword(s):  
Skeletal Muscle ◽  
Muscle Glycogen ◽  
Temperature Regulation ◽  
Vastus Lateralis ◽  
Water Immersion ◽  
Vastus Lateralis Muscle ◽  
Glycogen Concentration ◽  
Exercise Regimen ◽  
Before And After ◽  
Muscle Groups

The effects of intramuscular glycogen availability on human temperature regulation were studied in eight seminude subjects immersed in 18 degrees C water for 90 min or until rectal temperature (Tre) decreased to 35.5 degrees C. Each subject was immersed three times over a 3-wk period. Each immersion followed 2.5 days of a specific dietary and/or exercise regimen designed to elicit low (L), normal (N), or high (H) glycogen levels in large skeletal muscle groups. Muscle glycogen concentration was determined in biopsies taken from the vastus lateralis muscle before and after each immersion. Intramuscular glycogen concentration before the immersion was significantly different among the L, N, and H trials (P less than 0.01), averaging 247 +/- 15, 406 +/- 23, and 548 +/- 42 (SE) mmol glucose units.kg dry muscle-1, respectively. The calculated metabolic heat production during the first 30 min of immersion was significantly lower during L compared with N or H (P less than 0.05). The rate at which Tre decreased was more rapid during the L immersion than either N or H (P less than 0.05), and the time during the immersion at which Tre first began to decrease also appeared sooner during L than N or H. The results suggest that low skeletal muscle glycogen levels are associated with more rapid body cooling during water immersion in humans. Higher than normal muscle glycogen levels, however, do not increase cold tolerance.

Effects of an acute exercise bout in hypoxia on extracellular vesicle release in healthy and prediabetic subjects

2021 ◽  
Author(s):  
Geoffrey Warnier ◽  
Estelle De Groote ◽  
Florian A. Britto ◽  
Ophélie Delcorte ◽  
Joshua P. Nederveen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Acute Exercise ◽  
Vastus Lateralis ◽  
Venous Blood ◽  
Plasma Concentrations ◽  
Exercise Bout ◽  
Multivesicular Body ◽  
International Standards ◽  
Size Exclusion ◽  
Number Of Particles

Purpose: To investigate exosome-like vesicle (ELV) plasma concentrations and markers of multivesicular body (MVB) biogenesis in skeletal muscle in response to acute exercise. Methods: Seventeen healthy (BMI: 23.5±0.5kg·m-2) and fifteen prediabetic (BMI: 27.3±1.2kg·m-2) men were randomly assigned to two groups performing an acute cycling bout in normoxia or hypoxia (FiO2 14.0%). Venous blood samples were taken before (T0), during (T30) and after (T60) exercise and biopsies from m. vastus lateralis were collected before and after exercise. Plasma ELVs were isolated by size exclusion chromatography, counted by nanoparticle tracking analysis (NTA), and characterized according to international standards, followed by expression analyses of canonical ELV markers in skeletal muscle. Results: In the healthy normoxic group, the total number of particles in the plasma increased during exercise from T0 to T30 (+313%) followed by a decrease from T30 to T60 (-53%). In the same group, an increase in TSG101, CD81 and HSP60 protein expression was measured after exercise in plasma ELVs; however, in the prediabetic group, the total number of particles in the plasma was not affected by exercise. The mRNA content of TSG101, ALIX and CD9 were upregulated in skeletal muscle after exercise in normoxia; whereas, CD9 and CD81 were downregulated in hypoxia. Conclusions: ELV plasma abundance increased in response to acute aerobic exercise in healthy subjects in normoxia, but not in prediabetic subjects, nor in hypoxia. Skeletal muscle analyses suggested that this tissue did not likely play a major role of the exercise-induced increase in circulating ELVs.

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