Exercise for Bone Health

Rationale and Prescription

Pascale Schwab; Kenneth Scalapino


Curr Opin Rheumatol. 2011;23(2):137-141. 

In This Article

Bone Adaptation to Mechanical Load

The skeleton allows locomotion, provides protection to vital organs, and maintains calcium homeostasis.[4] In order to fulfill these functions throughout life, bone undergoes constant remodeling through a series of bone resorption and bone formation steps that repair bone microtrauma, enhance bone strength in regions of high load, and buffers fluxes in serum calcium level.[2] The rise in osteoporotic fractures with age is known to reflect reduced bone quantity and quality, a problem that is accelerated by the impact of inactivity and reduced muscle mass on bone signaling. In general, disuse and unloading of the skeleton promotes reduced bone mass, whereas loading promotes increased bone mass.[4] Extreme examples of this include prolonged bed rest and space flight that both result in accelerated bone loss.[5] The positive impact of exercise on bone mass varies at different stages of life, with exercise during the prepubertal skeletal growth period preferentially favoring greater bone mass gains, whereas exercise later in life promotes less gain, but reduces expected age-related losses.[6] Recovery of bone mass later in life is difficult in part due to a reduction in mesenchymal stem cells and a low potential for musculoskeletal regeneration.[7•] Laboratory studies of limb loading in animals show that although mechanical stress results in very small gains in total bone, these increments occur at skeletal surfaces subjected to the highest strain wherein they are most needed to resist fracture. Experiments utilizing such models have demonstrated that to optimize bone formation, mechanical loading must be dynamic rather than static,[8] and must be cyclical including rest periods to avoid desensitization of the osteocytes.[9] This pattern of loading results in a greater than 100 fold increase in fatigue resistance[10] despite a much smaller absolute gain in bone mass. Recent interest has focused on the possibility that mechanical signals may increase the mesenchymal stem cell pool and drive differentiation of cells away from adipogenesis toward osteoblastogenesis[7•,11] by stimulating expression of the canonical wnt proteins.[12•] This exercise-induced expansion in mesenchymal stem cells could partially offset their age-associated reduction and further support a unique mechanism by which exercise promotes bone health.

Muscle Forces or Gravity

Total bone mineral content is more strongly associated with muscle mass than with fat mass or total body mass, supporting that muscle forces are closely interrelated with bone mass.[13] As muscle forces are generated during impact or nonimpact exercise, it is difficult to separate the effects of gravity alone from muscle forces[14•] on bone mass. Whether gravitational forces or muscle forces provide the dominant signal promoting bone mass and strength is a matter of debate. It is clear that these forces are not mutually exclusive and there is evidence that the relative impact of each varies based on the skeletal location. Experiments have demonstrated that the majority of the forces generated within the femur during walking are the result of muscle forces and much less the result of weight bearing.[14•,15] Laboratory experiments using a jumping rat model support the idea that contracting musculature alone, without the landing impact, can stimulate osteogenesis.[16] On the other hand, critical weight bearing skeletal sites including the femoral neck appear to be highly sensitive to impact loading and may require ground reaction forces to maintain bone mineral content and structure.[17] As an example, competitive male cyclists generate very high leg muscle forces, but their bone density at all measured skeletal sites including the femoral neck is lower than that of nonathletes.[18,19]

Tensile versus Shear Stress

Bone cells are embedded in the bone matrix within a network of canaliculi bathing in viscous extracellular fluid. With daily activity mechanical forces on the bone matrix are microscopic and insufficient to stretch bone cells. Instead these forces predominantly cause fluid to be pushed back and forth generating shear stress on osteocyte cell membranes and promote osteogenesis.[3••,14•] Indeed, in the course of daily activity, the skeleton is subject to very few high-strain, low-frequency events that could potentially stretch bone matrix placing osteocytes in tensile loading. The skeleton is subject to numerous very low strain (<5 microstrain), high-frequency events (10–50 Hz) that generate shear stresses that are anabolic to bone.[11] Accordingly, oscillatory vibrations that induce cyclical low-level, high-frequency strains increase trabecular bone formation in animal models.[20] Promising results in studies examining the effect of oscillatory vibratory treatments to increase bone mass have been reviewed elsewhere and deserve further investigations.[21]

Osteocyte, the Mechanosensor within Bone

Osteocytes, the predominant cells in bone, are connected to each other through a dense network of cytoplasmic extensions within fluid filled canaliculi and play a critical role in mechanotransduction.[3••] Targeted ablation of osteocytes in a mouse model results in a porous skeleton with proliferative adipose tissue not unlike the aging skeleton. Interestingly, osteocyte-deficient mice are resistant to the bone loss induced by unloading, pointing to the osteocyte as the mechanosensor responsible for this phenomenon.[22] Mechanical loading stimulates several physical signals that induce osteocyte activation including tissue strain, fluid shear, and fluid pore pressure.[23] The unique ability to translate mechanical stimulus to biochemical activity may be related to the fact that the osteocyte is the only cell in bone that expresses sclerostin. Sclerostin is a secreted glycoprotein that inhibits the canonical wnt signaling pathway and acts as an inhibitor of osteoblast differentiation and bone formation. Loss of function mutations of the sclerostin gene results in sclerosteosis, targeted deletion of sclerostin in mice results in a high bone mass phenotype,[24] and sclerostin neutralizing antibody treatment increases bone formation and strength.[25] Evidence that osteocytes serve as key mechanosensors, linking loading with bone remodeling, comes from an in-vivo rodent model wherein sclerostin gene expression by osteocytes was downregulated by loading selectively in high-strain regions of the bone and upregulated by unloading[26] indicating that sclerostin osteocyte expression responds to mechanical stimulus and may turn on or turn off osteoblastogenesis. Periostin, a matrix protein secreted by periosteal osteoblasts, has recently been implicated in this process as well. Periostin is upregulated in response to mechanical loading and leads to increased bone formation at periosteal sites by inhibiting sclerostin gene expression by osteocytes. Furthermore, mechanical load in periostin-deficient mice does not stimulate bone formation unless sclerostin is antagonized.[27]


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