Why do long-distance runners not have more bone? A vital biomechanical explanation and an estrogen effect

Abstract

Inanimate structures cannot detect and repair their fatigue damage or microdamage, so to minimize it they need more structural material and strength. Living bone handles this matter differently. Bone modeling drifts adapt bone architecture and strength to the loads on bones in ways that tend to keep strains from exceeding a "modeling threshold" range. Strains (or equivalent features) above that threshold switch mechanically controlled modeling ON. Where strains stay below that threshold, this modeling goes OFF. Repeatedly loading-deloading a bone causes microdamage in it, and basic multicellular unit (BMU)-based bone remodeling normally repairs it. Where strains stay below an operational "microdamage threshold," remodeling can repair whatever microdamage happens for as long as it happens. Strains above that threshold can cause too much microdamage to repair completely and lead to fatigue fractures of trabeculae or whole bones. The modeling threshold normally lies comfortably below the microdamage threshold. Since modeling normally adjusts bone architecture to keep strains from exceeding the modeling threshold, this keeps strains below the microdamage threshold, too, and voluntary activities do not cause more microdamage than remodeling can repair. Therefore, long-distance runners do not need more bone mass and strength than nonrunners of comparable age, sex, and body size.