Interaction of aerobic exercise training and clenbuterol: effects on insulin-resistant muscle

1993 ◽  
Vol 75 (4) ◽  
pp. 1471-1476 ◽  
Author(s):  
C. E. Torgan ◽  
G. J. Etgen ◽  
J. T. Brozinick ◽  
R. E. Wilcox ◽  
J. L. Ivy

The effects of aerobic exercise training, chronic administration of the selective beta 2-adrenergic agonist clenbuterol, and the combination of these two treatments on muscle insulin resistance were compared in female obese (fa/fa) Zucker rats. Rats were randomly assigned to trained, clenbuterol, clenbuterol-trained, or control groups. Training consisted of treadmill running for 2 h/day at 18 m/min up an 8% grade. Clenbuterol was administered by intubation (0.4–0.8 mg.kg body wt-1 x day-1) approximately 30 min before the rats ran each day. After 8 wk of treatment, muscle insulin resistance was assessed via hindlimb perfusion in the presence of 8 mM glucose and a submaximal (500 microU/ml) insulin concentration. Training increased citrate synthase activity (mumol.g wet wt-1 x min-1) by 32–74% and insulin-stimulated glucose uptake by 45%. Clenbuterol ingestion induced a 17–29% increase in muscle mass but decreased citrate synthase activity by 34–42% and had no effect on muscle glucose uptake. Administration of clenbuterol to rats that exercise trained prevented the training-induced improvement in insulin-stimulated glucose uptake and attenuated the increases in citrate synthase activity. In addition, both clenbuterol-treated groups displayed a 42% decrease in beta-adrenergic receptor density. The results indicate that clenbuterol administration, possibly through beta-adrenergic receptor downregulation, attenuated a cellular reaction essential for the exercise training-induced increase in citrate synthase activity and improvement in skeletal muscle insulin resistance of the obese Zucker rat.

2008 ◽  
Vol 88 (11) ◽  
pp. 1279-1296 ◽  
Author(s):  
Lorraine P Turcotte ◽  
Jonathan S Fisher

The purpose of this review is to provide information about the role of exercise in the prevention of skeletal muscle insulin resistance, that is, the inability of insulin to properly cause glucose uptake into skeletal muscle. Insulin resistance is associated with high levels of stored lipids in skeletal muscle cells. Aerobic exercise training decreases the amounts of these lipid products and increases the lipid oxidative capacity of muscle cells. Thus, aerobic exercise training may prevent insulin resistance by correcting a mismatch between fatty acid uptake and fatty acid oxidation in skeletal muscle. Additionally, a single session of aerobic exercise increases glucose uptake by muscle during exercise, increases the ability of insulin to promote glucose uptake, and increases glycogen accumulation after exercise, all of which are important to blood glucose control. There also is some indication that resistance exercise may be effective in preventing insulin resistance. The information provided is intended to help clinicians understand and explain the roles of exercise in reducing insulin resistance.


1993 ◽  
Vol 264 (3) ◽  
pp. E373-E379 ◽  
Author(s):  
C. E. Torgan ◽  
J. T. Brozinick ◽  
E. A. Banks ◽  
M. Y. Cortez ◽  
R. E. Wilcox ◽  
...  

This study compared the effects of aerobic exercise training and chronic administration of the selective beta 2-adrenergic agonist clenbuterol on whole body and skeletal muscle insulin resistance in obese (fa/fa) Zucker rats. Obese rats were randomly assigned to training, clenbuterol, or sedentary control groups. Lean littermates served as a second control group. After 4-5 wk of treatment, an oral glucose tolerance test was performed, followed 1 wk later by hindlimb perfusion, during which time the rates of glucose uptake and 3-O-methyl-D-glucose (3-MG) transport were assessed in the presence of a submaximal (500 microU/ml) insulin concentration. Training resulted in a significant increase in citrate synthase and cytochrome oxidase activity in the recruited muscles. Clenbuterol induced a large increase in muscle mass but provoked a significant decrease in oxidative enzyme activity and beta-adrenergic receptor density. Both treatments increased glucose tolerance and reduced the postglucose insulin response, with the improvements being more pronounced in the clenbuterol group. However, only exercise training improved insulin-stimulated hindlimb muscle glucose uptake (11.37 +/- 0.65, 8.73 +/- 0.77, and 8.27 +/- 0.41 mumol.g-1.h-1 for trained, clenbuterol, and sedentary control groups, respectively) and 3-MG transport. These results suggest that aerobic exercise training attenuated the insulin-resistant condition in the obese Zucker rat by a mechanism other than or in addition to beta 2-adrenergic receptor activation.


2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Fabiana S. Evangelista ◽  
Bruno Vecchiatto ◽  
Anna Laura V. Américo ◽  
Luiz Felipe Martucci ◽  
Marilia M. Ferreira ◽  
...  

2010 ◽  
Vol 20 (4) ◽  
pp. 275-281 ◽  
Author(s):  
Kyu-Jin Lee ◽  
Yun-A. Shin ◽  
Kyoung-Young Lee ◽  
Tae-Won Jun ◽  
Wook Song

The purpose of this study was to assess differences in the levels of plasma visfatin among female adolescents and changes in plasma visfatin and insulin resistance in obese female adolescents after 12 wk of aerobic exercise training. Twenty normal-weight female students (body-mass index [BMI] <22.9 kg/m2 and body fat ≤29.9) and 18 obese female students (BMI ≥25 kg/m2 and body fat ≥30%) participated in this study. Eleven obese students were assigned to an exercise group and completed a 12-wk aerobic exercise-training program that included four 40- to 50-min sessions per wk with an energy expenditure of 300–400 kcal/d. Seven obese students were assigned to a control group that received no exercise sessions or dietary restriction. The plasma visfatin levels of obese female adolescents were significantly higher (p < .05) than those of the normal-weight female adolescents. The plasma visfatin levels (294.00 ± 124.74 ng/ml to 185.55 ± 67.30 ng/ml, p < .01) and insulin resistance (p < .05) were significantly reduced after 12 wk of aerobic exercise. The results suggest that aerobic exercise resulting in an energy expenditure of 1,200–1,600 kcal/wk for 12 wk decreases plasma visfatin and insulin resistance in obese female adolescents.


2019 ◽  
Author(s):  
Matheus Santos de Sousa Fernandes ◽  
Lucas de Lucena Simões e Silva ◽  
Márcia Saldanha Kubrusly ◽  
Talitta Ricarlly Lopes de Arruda Lima ◽  
Cynthia Rodrigues Muller ◽  
...  

Abstract Non-alcoholic fatty liver disease (NAFLD) is one of the most common forms of liver disease. Lifestyle modifications, such as a reduction in body weight (BW) and aerobic exercise training (AET), are effective treatments for NAFLD. The aim of the present study was to evaluate the effect of AET on hepatic oxidative metabolism in ob/ob mice. Male ob/ob mice were separated into two groups: the sedentary group (S), n=7, and the trained group (T), n=7. The T mice were submitted to an 8-week protocol of AET at 60% of the maximum velocity achieved in the running test. Before AET, no difference was observed in running capacity between the groups (S=10.4 ± 0.7 min vs. T= 13 ± 0.47 min). However, after AET, the running capacity was increased in the T group (12.8 ± 0.87 min) compared to the S group (7.2±0.63 min). Skeletal muscle in the T group (26.91±1.12 U/mg of protein) showed higher citrate synthase activity compared with the S group (19.28±0.88 U/mg of protein) (p =0.004) . BW and food consumption were significantly reduced in the T group compared to the S group (p=0.008 and p=0.001, respectively). The analysis of hepatic gene expression showed an increase in PGC-1a levels (p=0.002) and a reduction in CPT-1a levels (p=0.03). The levels of TBARs and carbonyls, as well as SOD, CAT and GST, were not different between the groups. In the nonenzymatic antioxidant system, we found that the T group had higher sulfhydryl (p = 0.02), GSH (p=0.001) and GSH/GSSG (p=0.02) activity. The activity of the metabolic enzymes citrate synthase (p=0.004) and β-HAD (p=0.01) was also increased in the T group. Besides improve in metabolism, no differences were observed in the histological analyses. In conclusion, our data demonstrate that AET improves BW control, mitochondrial functionality and oxidative metabolism in ob/ob mice.


Nutrients ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 2174
Author(s):  
Guilherme da Silva Ferreira ◽  
Ana Paula Garcia Bochi ◽  
Paula Ramos Pinto ◽  
Vanessa Del Bianco ◽  
Letícia Gomes Rodrigues ◽  
...  

Background: A low-sodium (LS) diet reduces blood pressure, contributing to the prevention of cardiovascular diseases. However, intense dietary sodium restriction impairs insulin sensitivity and worsens lipid profile. Considering the benefits of aerobic exercise training (AET), the effect of LS diet and AET in hepatic lipid content and gene expression was investigated in LDL receptor knockout (LDLr-KO) mice. Methods: Twelve-week-old male LDLr-KO mice fed a normal sodium (NS) or LS diet were kept sedentary (S) or trained (T) for 90 days. Body mass, plasma lipids, insulin tolerance testing, hepatic triglyceride (TG) content, gene expression, and citrate synthase (CS) activity were determined. Results were compared by 2-way ANOVA and Tukey’s post-test. Results: Compared to NS, LS increased body mass and plasma TG, and impaired insulin sensitivity, which was prevented by AET. The LS-S group, but not the LS-T group, presented greater hepatic TG than the NS-S group. The LS diet increased the expression of genes related to insulin resistance (ApocIII, G6pc, Pck1) and reduced those involved in oxidative capacity (Prkaa1, Prkaa2, Ppara, Lipe) and lipoprotein assembly (Mttp). Conclusion: AET prevented the LS-diet-induced TG accumulation in the liver by improving insulin sensitivity and the expression of insulin-regulated genes and oxidative capacity.


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