Abstract
Exercise has long-lasting benefits to bone health that may help prevent fractures by increasing bone mass, bone strength, and tissue quality. Long-term exercise of 6–12 weeks in rodents increases bone mass and bone strength. However, in growing mice, a short-term exercise program of 3 weeks can limit increases in bone mass and structural strength, compared to non-exercised controls. Short-term exercise can, however, increase tissue strength, suggesting that exercise may create competition for minerals that favors initially improving tissue-level properties over structural-level properties. It was therefore hypothesized that adding calcium and phosphorus supplements to the diet may prevent decreases in bone mass and structural strength during a short-term exercise program, while leading to greater bone mass and structural strength than exercise alone after a long-term exercise program. A short-term exercise experiment was done for 3 weeks, and a long-term exercise experiment was done for 8 weeks. For each experiment, male 16-week old C57BL/6 mice were assigned to 4 weight-matched groups–exercise and non-exercise groups fed a control or mineral-supplemented diet. Exercise consisted of treadmill running at 12 m/min, 30 min/day for 7 days/week. After 3 weeks, exercised mice fed the supplemented diet had significantly increased tibial tissue mineral content (TMC) and cross-sectional area over exercised mice fed the control diet. After 8 weeks, tibial TMC, cross-sectional area, yield force, and ultimate force were greater from the combined treatments than from either exercise or supplemented diet alone. Serum markers of bone formation (PINP) and resorption (CTX) were both decreased by exercise on day 2. In exercised mice, day 2 PINP was significantly positively correlated with day 2 serum Ca, a correlation that was weaker and negative in non-exercised mice. Increasing dietary mineral consumption during an exercise program increases bone mass after 3 weeks and increases structural strength after 8 weeks, making bones best able to resist fracture.
Highlights
Bone fragility fractures are common and costly injuries affecting more than 1.5 million people and costing $12-$18 billion in direct care each year [1]
The control diet consisted of an AIN93G diet (TestDiet1, Richmond, IN) modified by adding digestable dicalcium phosphate to contain standard concentrations of minerals– 0.5% Ca and 0.5% P
Exercise had no effect on tibial cortical tissue mineral content (TMC), vTMD, cross-sectional area, and moment of inertia about the anterior-posterior axis, but there was a significant effect of diet on TMC (p < 0.001, Two-way ANOVA, Fig 1) and cross-sectional area (p < 0.01, Two-way ANOVA, Fig 1)
Summary
Bone fragility fractures are common and costly injuries affecting more than 1.5 million people and costing $12-$18 billion in direct care each year [1]. These fractures are often attributed to reduced bone mass. Bone mass (cross-sectional area, bone mineral content) and structural-level strength (yield force, ultimate force) increase in rodents after long-term exercise programs of sixtwelve weeks [7,8,9,10]. Bone seems to favor increasing tissue quality over increasing bone mass and structural-level strength in a short-term exercise program. The limits on bone adaptation seen in short-term exercise suggest that standard dietary amounts of mineral may be insufficient for optimal adaptation of bone in response to exercise
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