Biomedical Engineering Reference
In-Depth Information
fracture. Bone strength cannot be directly measured in humans, but imaging
techniques (e.g., peripheral quantitative computed tomography (pQCT), magnetic
resonance imaging (MRI), DXA hip structural analysis, QCT-based finite element
analysis) can generate surrogates of strength. A meta-analysis of the few studies
that evaluated the effects of exercise training on estimates of bone strength
concluded that exercise does not significantly increase bone strength in adults [
72
].
However, this should be interpreted cautiously because the studies included in
the meta-analysis did not necessarily find the expected benefits of exercise training
on BMD.
On average, only small increases in BMD of 1-2% can be generated in adults
through exercise training. This magnitude of change is similar to or smaller than the
changes in BMD that occur in response to pharmacologic therapies that have
proven anti-fracture efficacy, including estrogens [
33
], raloxifene [
19
], bisphos-
phonates [
35
], denosumab [
18
], and parathyroid hormone [
69
]. In this context and
in the absence of strong evidence from RCTs for anti-fracture benefits of exercise, it
might be argued that exercise is unlikely to be as effective in preventing osteopo-
rotic fractures as pharmacologic therapy. However, there are two important con-
siderations for why exercise should continue to be avidly promoted for the
prevention and treatment of osteoporosis. First, exercise is effective in reducing risk
for falling [
26
] by improving such factors as balance and strength, which are not
targets of pharmacologic osteoporosis therapies. Second, it is possible that exercise
improves bone strength in a more structurally and functionally appropriate manner
than pharmacologic therapies. Evidence to support this comes from preclinical
studies of laboratory animals, which indicate that bisphosphonates [
63
] and para-
thyroid hormone [
31
] generate relative increases in bone strength that are roughly
proportional to the relative increases in bone mineral content (BMC) and BMD.
For example, bisphosphonate therapy increased BMC and BMD by *15% and
increased ultimate force and energy to failure by 15-20% [
63
]. In contrast,
mechanical loading of the rat forelimb resulted in smaller increases in ulnar whole-
bone BMC and BMD of *6%, but these were associated with disproportionately
large increases in ultimate force and energy to failure of 60-90% [
81
]. This
remarkable improvement in bone strength occurred because mechanical loading led
to a localized increase in bone area and moment of inertia at the site of peak strain.
Thus, mechanical loading can target specific bone regions whereas systemically
administered drugs presumably affect all regions of the skeleton, including non-
load-bearing regions. This suggests that exercise can selectively strengthen skeletal
regions that are susceptible to osteoporotic fracture. However, the extent to which
pre-clinical findings are of clinical relevance remains unclear. The level of strain
that generated the large increases in bone strength in rats was 2,000-3,000 le [
81
].
Based on in vivo measurements of tibial strain, it seems unlikely that strains of this
magnitude are regularly achieved by humans during physical activities [
11
,
66
,
67
].
There in an unmet need to devise exercise protocols that can safely stimulate bone
formation (or diminish bone loss) at sites that are prone to fracture.
Observational studies suggest that muscle power and physical activity are
directly, but modestly, associated with bone strength in older women and men
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