Abstract
We tested the hypothesis that increased muscle mass augments increases in bone strength normally observed with exercise. Myostatin-deficient mice, which show increased muscle mass, were exercised along with wildtype mice. Results indicate that increases in bone strength with exercise are greater in myostatin-deficient mice than in wildtype mice, suggesting that the combination of increased muscle mass and physical activity has a greater effect on boEe strength than either increased muscle mass or intense exercise alone. Introduction: Muscle (lean) mass is known to be a significant predictor of peak BMD in young people, and exercise is also found to increase bone mass in growing humans and laboratory animals. We sought to determine if increased muscle mass resulting from myostatin deficiency would enhance gains in bone strength that usually accompany exercise. Materials and Methods: Male mice lacking myostatin (GDF-8) were used as an animal model showing increased muscle mass. Wildtype and myostatin-deficient mice (n = 10-12 per genotype) were exercised on a treadmill for 30 minutes/day, 5 days/week, for 4 weeks starting at 12 weeks of age. Caged wildtype and myostatin-deficient mice (n = 10-12 per genotype) were included as sedentary controls. Structural and biomechanical parameters were measured from the radius. Results: Ultimate force (Fu), displacement (D u), toughness (energy-to-fracture; U), and ultimate strain (εu) increased significantly with exercise in myostatin-deficient mice but not in normal mice. When Fu is normalized by body mass, exercised myostatin-deficient mice show an increase in relative bone strength of 30% compared with caged controls, whereas exercised wildtype mice do not show a significant increase in ultimate force relative to caged controls. Relative to body weight, the radii of exercised myostatin-deficient mice are >25% stronger than those of exercised normal mice. Conclusions: Increased muscle mass resulting from inhibition of myostatin function improves the positive effects of exercise on bone strength.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 477-483 |
| Number of pages | 7 |
| Journal | Journal of Bone and Mineral Research |
| Volume | 21 |
| Issue number | 3 |
| DOIs | |
| State | Published - Mar 1 2006 |
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Keywords
- Bone material properties
- Bone mechanical properties
- GDF-8
- Mechanical loading
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Orthopedics and Sports Medicine
Cite this
Increased muscle mass with myostatin deficiency improves gains in bone strength with exercise. / Hamrick, Mark W.; Samaddar, Ted; Pennington, Catherine; McCormick, John.
In: Journal of Bone and Mineral Research, Vol. 21, No. 3, 01.03.2006, p. 477-483.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Increased muscle mass with myostatin deficiency improves gains in bone strength with exercise
AU - Hamrick, Mark W.
AU - Samaddar, Ted
AU - Pennington, Catherine
AU - McCormick, John
PY - 2006/3/1
Y1 - 2006/3/1
N2 - We tested the hypothesis that increased muscle mass augments increases in bone strength normally observed with exercise. Myostatin-deficient mice, which show increased muscle mass, were exercised along with wildtype mice. Results indicate that increases in bone strength with exercise are greater in myostatin-deficient mice than in wildtype mice, suggesting that the combination of increased muscle mass and physical activity has a greater effect on boEe strength than either increased muscle mass or intense exercise alone. Introduction: Muscle (lean) mass is known to be a significant predictor of peak BMD in young people, and exercise is also found to increase bone mass in growing humans and laboratory animals. We sought to determine if increased muscle mass resulting from myostatin deficiency would enhance gains in bone strength that usually accompany exercise. Materials and Methods: Male mice lacking myostatin (GDF-8) were used as an animal model showing increased muscle mass. Wildtype and myostatin-deficient mice (n = 10-12 per genotype) were exercised on a treadmill for 30 minutes/day, 5 days/week, for 4 weeks starting at 12 weeks of age. Caged wildtype and myostatin-deficient mice (n = 10-12 per genotype) were included as sedentary controls. Structural and biomechanical parameters were measured from the radius. Results: Ultimate force (Fu), displacement (D u), toughness (energy-to-fracture; U), and ultimate strain (εu) increased significantly with exercise in myostatin-deficient mice but not in normal mice. When Fu is normalized by body mass, exercised myostatin-deficient mice show an increase in relative bone strength of 30% compared with caged controls, whereas exercised wildtype mice do not show a significant increase in ultimate force relative to caged controls. Relative to body weight, the radii of exercised myostatin-deficient mice are >25% stronger than those of exercised normal mice. Conclusions: Increased muscle mass resulting from inhibition of myostatin function improves the positive effects of exercise on bone strength.
AB - We tested the hypothesis that increased muscle mass augments increases in bone strength normally observed with exercise. Myostatin-deficient mice, which show increased muscle mass, were exercised along with wildtype mice. Results indicate that increases in bone strength with exercise are greater in myostatin-deficient mice than in wildtype mice, suggesting that the combination of increased muscle mass and physical activity has a greater effect on boEe strength than either increased muscle mass or intense exercise alone. Introduction: Muscle (lean) mass is known to be a significant predictor of peak BMD in young people, and exercise is also found to increase bone mass in growing humans and laboratory animals. We sought to determine if increased muscle mass resulting from myostatin deficiency would enhance gains in bone strength that usually accompany exercise. Materials and Methods: Male mice lacking myostatin (GDF-8) were used as an animal model showing increased muscle mass. Wildtype and myostatin-deficient mice (n = 10-12 per genotype) were exercised on a treadmill for 30 minutes/day, 5 days/week, for 4 weeks starting at 12 weeks of age. Caged wildtype and myostatin-deficient mice (n = 10-12 per genotype) were included as sedentary controls. Structural and biomechanical parameters were measured from the radius. Results: Ultimate force (Fu), displacement (D u), toughness (energy-to-fracture; U), and ultimate strain (εu) increased significantly with exercise in myostatin-deficient mice but not in normal mice. When Fu is normalized by body mass, exercised myostatin-deficient mice show an increase in relative bone strength of 30% compared with caged controls, whereas exercised wildtype mice do not show a significant increase in ultimate force relative to caged controls. Relative to body weight, the radii of exercised myostatin-deficient mice are >25% stronger than those of exercised normal mice. Conclusions: Increased muscle mass resulting from inhibition of myostatin function improves the positive effects of exercise on bone strength.
KW - Bone material properties
KW - Bone mechanical properties
KW - GDF-8
KW - Mechanical loading
UR - http://www.scopus.com/inward/record.url?scp=33644530668&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33644530668&partnerID=8YFLogxK
U2 - 10.1359/JBMR.051203
DO - 10.1359/JBMR.051203
M3 - Article
C2 - 16491296
AN - SCOPUS:33644530668
VL - 21
SP - 477
EP - 483
JO - Journal of Bone and Mineral Research
JF - Journal of Bone and Mineral Research
SN - 0884-0431
IS - 3
ER -