Intracortical remodelling increases in highly-loaded bone after exercise cessation
Resorption within cortices of long bones removes excess mass and damaged tissue, and increases during periods of reduced mechanical loading. Returning to high-intensity exercise may place bones at risk of failure due to increased porosity caused by bone resorption. We used microradiographs of bone slices from highly-loaded (metacarpal, tibia) and minimally-loaded (rib) bones from 12 racehorses, 6 that died during a period of high-intensity exercise and 6 that had a period of intense exercise followed by at least 35 days of rest prior to death, and measured intracortical canal cross-sectional area (Ca.Ar) and number (N.Ca) to infer remodelling activity across sites and exercise groups. Large canals that are the consequence of bone resorption (Ca.Ar > 0.04 mm2) were 1.4x to 18.7x greater in number and area in the third metacarpal bone from rested than exercised animals (p = 0.005- 0.008), but were similar in number and area in ribs from rested and exercised animals (p = 0.575-0.688). An intermediate relationship was present in the tibia, and when large canals and smaller canals that result from partial bony infilling (Ca.Ar > 0.002 mm2) were considered together. The mechanostat may override targeted remodelling during periods of high mechanical load by enhancing bone formation, reducing resorption and suppressing turnover. Both systems may work synergistically in rest periods to remove excess and damaged tissue.