No prospective randomized study with fracture as end point exists in men. D
ata from retrospective and prospective observational and case control studi
es suggest that activity in men is associated with reduced fracture risk. T
his may be correct, but consistently replicated sampling bias may produce t
he same observation, as these studies are hypothesis generating, never hypo
thesis testing. Higher musculoskeletal mass, better health, coordination, a
nd less tendency to fall may lead to exercise, not the reverse. It would be
extremely difficult to conduct an exercise intervention study with fractur
e as the end point because of the large cohorts needed. However, showing a
positive effect on surrogate end points for fractures as increased bone mas
s or reduced fall frequency would support the notion that exercise has a fr
acture-protective effect. Exercise during growth seems to build a larger an
d stronger skeleton in boys. However, cessation of exercise is its Achilles
heel; biologically important increased peak bone mass or improvement in mu
scle strength achieved by exercise during growth may be eroded in retiremen
t, leaving no biological significant benefits in old age when fractures occ
ur. Exercise during adulthood may prevent bone loss or produce a small incr
ease in BMD of a few percent, probably a non-biologically significant incre
ase in reducing the fracture risk in elderly men. However, exercise in adul
ts seems to increase muscle strength and improve balance, with reduced fall
frequency as the result and maybe reduced frequency of injuries also. The
effects of exercise on bone size, shape, and architecture during growth and
adolescence must be defined as well as the effect of muscle function, fall
frequency, and frequency of injurious falls in elderly men. Also, continue
d low level of exercise may maintain some of the benefit after more vigorou
s activity level during younger years, but dose-response relationships need
to quantified. Additionally, the null hypothesis that exercise has no effe
ct on fracture rates in old age cannot be rejected by any published data. T
he proof rests on demonstration of a reduction in spine and hip fractures i
n well-designed and executed prospective, open-randomized studies, none of
which exist. Our inability to answer these questions should be acknowledged
before recommendations are made at the community level.