FROST, H. M. Muscle, bone, and the Utah paradigm: A 1999 overview. Med. Sci. Sports Exerc., Vol. 32, No. 5, pp. 911–917, 2000. The still-evolving Utah paradigm of skeletal physiology supplements former ideas about the control of postnatal bone strength and “mass” in health and disease, on earth and in orbit, and as functions of physical activities including sports. In its view, peak muscle forces on bone dominate control of the biologic mechanisms that control changes in our postnatal whole-bone strength and mass. This contrasts with former ideas that chiefly nonmechanical factors dominate that control and mechanical factors have little influence on it. The newer view begs the question of how such a bone-muscle relationship would work, and the Utah paradigm offers plausible explanations for that. Whereas many biomechanicians, orthopedists, and sports medicine experts might find the newer view sensible, some people in other disciplines may not. This article summarizes some evidence that support the Utah paradigm and the above-stated view and explores some of the paradigm’s features and implications.
In a 1960 paradigm of bone physiology (39,52,55), chiefly nonmechanical influences (Table 1) on bone’s “effector cells” (osteoblasts and osteoclasts but not their precursor or other cells) determined the strength of whole bones. Osteoblasts added bone, osteoclasts removed it, they functioned independently of each other, and mechanical influences had little effect on bone strength and “mass”. In other words, stimulus → effector cell → health/disease.
Intensive research directed by those ideas (2,8) overlooked tissue- and organ-level features that were found after 1960. Aided by Hard Tissue Workshop participants, those features led to the Utah paradigm of skeletal physiology (4,17,23,29,31,38,47,53) and two basic propositions.