Abstract and Introduction
This Perspectives provides a back-to-basics rationale for the ideal exercise prescription for osteoporosis. The relevance of fundamental principles of mechanical loading and bone adaptation determined from early animal studies is revisited. The application to human trials is presented, including recent advances. A model of broadscale implementation is described, and areas for further investigation are identified.
One of the most spectacular accomplishments of the human body is the capacity of the skeleton to adapt to changes in habitual mechanical loading to maintain structural integrity. The ability to detect damage and repair itself is equally physiologically impressive. The failure of bone due to loss of mass and structural integrity toward the end of life, the condition commonly referred to as osteoporosis, undermines the suggestion that bone has a self-sustaining mechanoadaptive response. A closer look, however, reveals that age-related bone loss is a manifestation of the principle. Bone loss across the lifespan parallels age-related sedentarianism. That is, most people progressively unload their skeleton as they age by becoming considerably less active. In fact, individuals who maintain young adult levels of exercise throughout life tend to maintain their bone mass[1–3] and are therefore at reduced risk of low trauma fracture in their later years. For those diagnosed with osteoporosis — defined as low bone mineral density (BMD) (≤−2.5 T-score from dual-energy x-ray absorptiometry DXA) or presence of fragility fracture(s) or both — in older age, however, this knowledge is small comfort.
Primarily a condition of later life, the trend of aging populations will increase the already substantial global personal and financial burden of osteoporosis. In 2010, there were an estimated 137 million women and 21 million men over the age of 50 at high risk of osteoporotic fracture, and this number is expected to double by 2040. Although the global economic cost of osteoporotic fractures is difficult to estimate, in the United States alone in 2018, the total annual cost of osteoporotic fractures was $57 billion and estimated to increase to $95 billion by 2040. Traditionally, first-line treatment for osteoporosis is medication; however, compliance is notoriously poor and efficacy is far from universal. Adverse events, although relatively rare, can be serious, and discontinuation of certain medication is associated with rapid bone loss and increased risk of fracture.[7,8] Harnessing the natural capacity of bone to optimize its strength through exercise, a therapy with few nonresponders or side effects, is an obvious alternative strategy to manage osteoporosis. The fact that exercise will simultaneously prevent the falls that cause fracture enhances its appeal as a therapeutic agent (Figure 1).
Intuitively, fractures occur when trauma exceeds the intrinsic ability of bone to resist the forces on it. Osteoporotic fractures occur when the material or structural properties of a bone are compromised to the extent that only minimal trauma is required to cause a break. A number of medications enhance bone mineral density (BMD) and bone structure, thereby reducing the propensity to fracture. Nevertheless, the trauma associated with a fall is the most common cause of osteoporotic hip fracture, ergo risk factors for falling are indirect, but powerful, factors of risk for fracture unaffected by medications. This schematic illustrates the comparative predominance of influence of exercise (vs drugs) on risk factors for osteoporotic fracture — acting both directly on bone and indirectly on risk of falling (9–14).
Determining the best exercise prescription for individuals who have already lost substantial amounts of bone has been a problematic endeavor. Loading a fragile skeleton seems counter to the medical tenet of primum non nocere — first, do no harm. The following Perspective will provide the evidence, rationale, and current status of safe and effective exercise prescription for osteoporosis.
Exerc Sport Sci Rev. 2022;50(2):57-64. © 2022 American College of Sports Medicine