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Returning to high\u2010intensity exercise may place bones at risk of failure due to increased porosity caused by bone resorption. We used point\u2010projection X\u2010ray microscopy images of bone slices from highly loaded (metacarpal, tibia) and minimally loaded (rib) bones from 12 racehorses, 6 that died during a period of high\u2010intensity exercise and 6 that had a period of intense exercise followed by at least 35\u2009days of rest prior to death, and measured intracortical canal cross\u2010sectional 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\u2009&gt;0.04\u2009mm<jats:sup>2<\/jats:sup>) were 1.4\u00d7 to 18.7\u00d7 greater in number and area in the third metacarpal bone from rested than exercised animals (<jats:italic>p<\/jats:italic>\u2009=\u20090.005\u20130.008), but were similar in number and area in ribs from rested and exercised animals (<jats:italic>p<\/jats:italic>\u2009=\u20090.575\u20130.688). An intermediate relationship was present in the tibia, and when large canals and smaller canals that result from partial bony infilling (Ca.Ar\u2009&gt;0.002\u2009mm<jats:sup>2<\/jats:sup>) were considered together. The mechanostat may override targeted remodelling during periods of high mechanical load by enhancing bone formation, reducing resorption and suppressing turnover. 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