Exercise Maintains Bone Mass, but Do People Maintain Exercise?
Exercise Maintains Bone Mass, but Do People Maintain Exercise?
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运动可以维持骨量,但人们会坚持运动吗?
DOI:
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发表时间:
2001
影响因子:
6.2
通讯作者:
M. Bouxsein
中科院分区:
文献类型:
--
作者:
D. Nelson;M. Bouxsein
IT HAS long been recognized that increased mechanical loading of the skeleton results in bone gain, whereas unloading the skeleton leads to bone loss. This relationship between loading and bone is implicit in the writings of Julius Wolff, who proposed that bone structure, including the distribution and amount of mineral, reflect the customary loading patterns that the bone is subjected to. It follows that an increase in weight-bearing physical activity would increase bone mass and present a seemingly simple preventative strategy for prevention and treatment of osteoporosis. This seemingly simple strategy has proven difficult to achieve in practice, because most exercise interventions in adults have led to increases in bone mass that are relatively small. However, even if the ideal bone-promoting ex ercise regimen was known, one would still be faced with the tremendous challenge of motivating individuals to exercise for their health, whether skeletal or otherwise. In this issue of the Journal, the article by Kontulainen et al. offers some hope for the maintenance of bone gained through intensive exercise training, even when the level of training is subsequently reduced. The subjects in this observational study initially self-selected to participate in rigorous racquet sports (tennis or squash) for an average of four to five times per week. The authors previously reported that those women who started training before menarche had a greater skeletal benefit, assessed as the difference in bone mineral content (BMC) between the playing and nonplaying arm, than those who started after menarche. (7) During the 5-year follow-up period, the subjects voluntarily reduced their playing time to just once or twice each week. Results from the current study suggest that both “young starters” and “old starters” maintained this skeletal benefit despite a reduced training schedule. After the reduction in training, the difference in BMC of the nondominant versus dominant humeral shaft was 22% in the young starters, 10% in the old starters, and 3.5% in control subjects. Although this is good news for the athletically inclined members of our society, the critical issue is whether controlled interventions will result in similar benefits and, ultimately, translate to a reduction in the risk of osteoporosis and related fractures. To understand the relationships more thoroughly among mechanical loading, growth, and bone it is essential to distinguish between effects on bone size and bone density. Kontulainen and colleagues represent skeletal benefit in terms of side-to-side differences in humeral BMC. This limits the possible interpretations of their findings, because BMC measurements reflect both bone size as well as bone density. Before skeletal maturity, the effects of exercise on the skeleton may be mediated primarily by alterations in bone size and shape. (8) Apparent skeletal benefits resulting from alterations in skeletal geometry may be more resistant to subsequent reductions in mechanical loading than skeletal benefits solely because of increased bone density. The precise relationships between skeletal loading, in the form of exercise and skeletal status have yet to be defined. Studies of the effects of physical activity on bone vary with respect to the exercise regimen used, skeletal site assessed, study population enrolled, and bone densitometry technique used. As such, it is difficult to generalize about the public health benefits of exercise interventions for the prevention of osteoporosis, although there is general agreement that weight-bearing exercise confers a positive effect on the skeleton. Growing evidence indicates that impact loading may provide the greatest osteogenic stimulus for the keleton. (9–11) However, despite the potentially positive ef fects of impact loading on bone mass and density, some
影响因子:
158.5
作者:
CUMMINGS, SR;NEVITT, MC;VOGT, TM
通讯作者:
VOGT, TM
影响因子:
39.2
作者:
DALSKY, GP;STOCKE, KS;BIRGE, SJ
通讯作者:
BIRGE, SJ
影响因子:
4.1
作者:
Hamrick, MW;McPherron, AC;Hudson, J
通讯作者:
Hudson, J