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Glucose transporter number, function, and subcellular distribution in rat skeletal muscle after exercise training
L J Goodyear1, M F Hirshman, P M Valyou
1Department of Medicine, University of Vermont, Burlington 05405.
Diabetes
|September 1, 1992
Summary
Endurance exercise training boosts skeletal muscle glucose transporters, maintaining elevated glucose uptake even after training stops. This suggests sustained benefits of exercise for glucose regulation.
Area of Science:
- Exercise Physiology
- Molecular Biology
- Metabolic Research
Background:
- Endurance exercise enhances insulin-stimulated glucose uptake in skeletal muscle.
- This beneficial effect can diminish rapidly after exercise cessation.
Purpose of the Study:
- To investigate the mechanisms behind changes in skeletal muscle glucose transport after exercise cessation.
- To examine the impact of detraining on glucose transporter protein levels and activity.
Main Methods:
- Studied female rats undergoing 6 weeks of exercise training versus untrained controls.
- Assessed plasma membrane and homogenate glucose transporter (GLUT4 and R0) levels and glucose transport rates.
- Evaluated changes immediately after training and at 2 and 5 days post-cessation, with and without insulin stimulation.
Main Results:
- Exercise-trained rats showed higher plasma-membrane glucose transporter numbers (R0) and GLUT4 protein levels immediately post-training.
- These elevated levels were sustained for 5 days after training cessation.
- Insulin stimulated glucose transporter translocation and increased carrier turnover in both trained and untrained rats.
Conclusions:
- Skeletal muscle adaptations to endurance exercise, including increased glucose transporters, persist for at least 5 days after training cessation.
- These sustained changes contribute to maintained glucose uptake capacity following detraining.
- Exercise training enhances the capacity for insulin-mediated glucose transporter translocation.