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Published on: November 16, 2011
Myostatin dysfunction is associated with lower physical activity and reduced improvements in glucose tolerance in
Mindaugas Kvedaras1, Petras Minderis1, Raulas Krusnauskas1
1Institute of Sport Science and Innovations, Lithuanian Sports University, Kaunas, Lithuania.
Abstract:
Myostatin is an inhibitor of skeletal muscle growth and might be involved in adaptations to caloric restriction (CR). We compared responses to 12-week 30% CR in male mice of Berlin high strain with myostatin dysfunction (BEH) and wild-type myostatin (BEH+/+). BEH mice were heavier than BEH+/+ mice (58.8 ± 2.0 versus 53.1 ± 2.7 g, p < 0.001), had 1.8-fold greater hind limb muscle mass and were less (p < 0.05) physically active when fed ad libitum. After CR, BEH and BEH+/+ strains experienced similar weight loss (24.7 ± 5.7 versus 20.6 ± 6.5%, p > 0.05, respectively) and decreases (p < 0.001) in plasma IGF-1 and total cholesterol, but loss of hind limb muscle mass was greater (p < 0.001) in BEH mice than BEH+/+ mice. BEH mice had better (p < 0.001) glucose tolerance and showed smaller (p < 0.05) improvements of it than BEH+/+ mice after CR (1038.2 ± 174.7 versus 744.4 ± 95.8 glucose mM× 120 min, p < 0.01 for BEH; 1365.8 ± 218.5 versus 831.5 ± 134.4 glucose mM ×120 min, p < 0.001, for BEH+/+, respectively). In summary, myostatin dysfunction is associated with muscle hypertrophy and high glucose tolerance, but greater muscle wasting and smaller improvements in glucose tolerance in response to CR.
Insights
Myostatin dysfunction causes muscle growth but leads to greater muscle loss during caloric restriction (CR). Mice with myostatin dysfunction showed higher initial glucose tolerance but less improvement after CR compared to controls.
Area of Science:
- Muscle physiology
- Metabolic adaptation
- Genetics
Background:
- Myostatin inhibits skeletal muscle growth.
- Myostatin may play a role in adaptations to caloric restriction (CR).
- Understanding myostatin's role in CR is crucial for metabolic and muscle health research.
Purpose of the Study:
- To compare the effects of 12-week 30% CR on mice with myostatin dysfunction (BEH) versus wild-type controls (BEH+/+).
- To investigate the impact of myostatin dysfunction on muscle mass, physical activity, and glucose metabolism during CR.
Main Methods:
- A 12-week, 30% caloric restriction (CR) protocol was applied to male Berlin high (BEH) mice with myostatin dysfunction and wild-type (BEH+/+) controls.
- Measurements included body weight, hind limb muscle mass, physical activity, plasma IGF-1, total cholesterol, and glucose tolerance.
Main Results:
- BEH mice exhibited greater baseline muscle mass and higher glucose tolerance but less physical activity than BEH+/+ mice.
- Both groups lost similar weight and showed decreased plasma IGF-1 and cholesterol after CR.
- BEH mice experienced greater hind limb muscle mass loss and smaller improvements in glucose tolerance following CR compared to BEH+/+ mice.
Conclusions:
- Myostatin dysfunction is linked to muscle hypertrophy and enhanced baseline glucose tolerance.
- However, myostatin dysfunction exacerbates muscle wasting and blunts glucose tolerance improvements during caloric restriction.
- These findings highlight a complex role for myostatin in metabolic and muscle adaptations to energy deficit.
