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Increased muscle fatigability in GLUT-4-deficient mice
M Gorselink1, M R Drost, K F J de Brouwer
1Department of Physiology, University of Maastricht, 6200 MD Maastricht, The Netherlands.
American Journal of Physiology. Endocrinology and Metabolism
|January 15, 2002
Summary
Mice lacking GLUT-4 (glucose transporter type 4) show reduced muscle power and increased fatigue. This is linked to lower glycogen stores and fiber type changes, indicating GLUT-4 is crucial for muscle energy.
Area of Science:
- Exercise Physiology
- Molecular Biology
- Muscle Metabolism
Background:
- Glucose transporter type 4 (GLUT-4) is vital for glucose uptake in muscles, especially during contraction.
- Understanding GLUT-4's role is key to comprehending muscle function and energy metabolism.
Purpose of the Study:
- To investigate the impact of GLUT-4 gene disruption on muscle contractile performance in mice.
- To determine if GLUT-4 deficiency enhances muscle fatigability.
Main Methods:
- In situ analysis of isometric and shortening contractile performance in GLUT-4-deficient (GLUT-4(-/-)) and wild-type (WT) mice.
- Assessment of muscle mass, peak power, fiber-type composition, resting glycogen content, and fatigue susceptibility.
Main Results:
- No significant difference in isometric performance per muscle mass between GLUT-4(-/-) and WT mice.
- Shortening contractions showed a 1.4-fold decrease in peak power per unit mass in GLUT-4(-/-) mice, associated with a shift from IIB to IIA fibers.
- GLUT-4(-/-) mice exhibited lower resting glycogen content (34%) and enhanced fatigue susceptibility.
Conclusions:
- GLUT-4 deficiency impairs muscle shortening performance and increases fatigability, likely due to reduced glycogen stores and fiber-type alterations.
- Alternative energy pathways do not fully compensate for the absence of GLUT-4 during sustained muscle activity.