Does exercise reduce the burden of fractures? A review.
The null hypothesis that exercise has no effect on fracture rates in old age cannot be rejected on the basis of any published, randomized, prospective data. The view that exercise reduces the number of fractures is based on prospective and retrospective, observational cohort studies and case-control studies, all hypothesis-generating, not hypothesis-testing. Consistently replicated sampling bias may confirm the finding when evaluating other than randomized prospective studies. Better health, better muscle function, more muscle mass, better coordination may lead to exercise. The causal relationship could be between better health and exercise and better health and fewer fractures, not exercise and fewer fractures. The hypothesis should be tested in prospective, randomized studies evaluating hip, spine and other fragility fractures separately. Blinded studies assessing the effects of exercise can obviously not be done, but open trials can and should be undertaken to increase the level of evidence within the evidence-based system. There are firm data supporting the view that exercise during growth builds a stronger skeleton. Exercise during growth seems to result in high peak BMD and high muscle strength. However, the Achilles heel of exercise is its cessation. Are the skeletal and muscular benefits attained during growth retained after the cessation of exercise and can any residual benefits be found in old age, the period when fragility fractures rise exponentially? Does exercise during adulthood produce any biologically important reduction in surrogate end-points for fractures other than BMD, since BMD can be influenced only marginally by exercise after completion of growth? Recommendations for exercise should be based on evidence, not on opinion. Can continued recreational exercise maintain some of the benefits in BMD and muscle function achieved in youth? What level of recreational exercise is needed to retain these benefits, if not fully, then at least to some extent? Dose-response relationships should be quantified. Furthermore, the effect of exercise on independent, surrogate end-points for fractures, such as bone size, shape, architecture, muscle function, fall frequency and frequency of injurious falls during defined periods in the life cycle must be determined. Absence of evidence is not evidence of absence of effect, but if we recommend exercise then should this be to children, adults, elderly, men and women with fractures, all persons? What type of exercise? For how long? Lifelong? If exercise could be implemented for most persons in society, would this reduce the number of fractures? Would the increased costs associated with the efforts to increase the activity level be lower than the reduced costs associated with any reduction in fractures? Our inability to answer these questions must be acknowledged before recommendations are made at the community level.
Karlsson
Magnus
M
Department of Orthopedics, Malmö University Hospital, SE-205 02, Malmö, Sweden. magnus.karlsson@orto.mas.lu.se
D000058:Accidental Falls / Q000517:prevention & control*; D000293:Adolescent; D000328:Adult; D000367:Age Factors; D000368:Aged; D000369:Aged, 80 and over; D001823:Body Composition / Q000502:physiology; D015519:Bone Density / Q000502:physiology; D017281:Cost of Illness; D015444:Exercise / Q000502:physiology*; D005260:Female; D050723:Fractures, Bone / Q000209:etiology / Q000503:physiopathology* / Q000517:prevention & control*; D006801:Humans; D008297:Male; D008875:Middle Aged; D018482:Muscle, Skeletal / Q000502:physiology; D012307:Risk Factors; D012737:Sex Factors