A Review of Three Decades of Research Dedicated to Making Equine Bones Stronger: Implications for Horses and Humans

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TL;DR

This literature review summarizes over 30 years of research on preventing skeletal injuries in athletic horses. The key finding is that stall confinement without high-speed exercise causes significant bone loss (disuse osteopenia), while as little as one short sprint (50–82 m) per week dramatically increases bone strength. The clinical significance extends to humans, where a sedentary lifestyle and lack of high-load exercise similarly weaken the skeleton, and proper nutrition alone cannot compensate for inadequate mechanical loading.

Full summary

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**Background:** Skeletal injuries, particularly dorsal metacarpal disease (bucked shins), affect up to 70% of two-year-old Thoroughbreds. Despite decades of research, bone-related injuries remain a major concern in equine athletics. This review compiles findings from over three decades of research by the author and collaborators, beginning in 1990, aimed at understanding how to strengthen equine bone and prevent injuries, with implications for human skeletal health as well.

**Methods:** This is a narrative literature review summarizing a research program that evolved over 30+ years. The initial study was a blinded, placebo-controlled trial of 53 Quarter Horses in race training examining the effects of bioavailable silicon (sodium aluminosilicate, SZA) supplementation. Subsequent studies included: (1) radiographic photodensitometry (RBAE) of the third metacarpus in horses at various stages of training and housing; (2) controlled trials comparing pasture vs. stall housing in Arabian yearlings, weanlings, and mature horses; (3) exercise intervention studies in juvenile bull calves (n=18, n=24), weanling horses (n=18), gestating gilts (n=number not specified), and yearling horses; (4) a study of endurance exercise vs. pasture housing in 11 two-year-old Arabians; (5) pharmaceutical studies examining furosemide (crossover, n=10) and omeprazole effects on calcium balance and bone markers; and (6) studies of bioavailable silicon in yearlings, broodmares, and aged Standardbreds.

**Key Results:** The initial silicon study found that supplemented groups had more horses complete the race program without injury, and the medium and high dosage groups completed greater distances before injury (90 and 83 km, respectively) vs. controls (50 km). The medium treatment group had faster average race time (20.3 s) vs. control (20.7 s) at 320 m. Critically, an incidental finding showed that bone mineral content (RBAE) of the third metacarpus decreased by day 62 of training, remained low through day 104, and most bone injuries occurred between days 60–120 when bone mass was lowest. Subsequent studies confirmed that stall housing caused bone loss: in Arabian yearlings, RBAE decreased by day 28 of stalling and remained low for 140 days, with decreased serum osteocalcin and increased urinary deoxypyridinoline. Mature horses lost bone mass after 12 weeks of stalling despite walking exercise and double the NRC-recommended calcium. Partial pasture turnout (12 h/day) prevented bone loss in weanlings. Exercise studies showed that juvenile calves sprinting only 50 m/day, 5 days/week (cumulative 1500 m over 6 weeks) had increased cortical thickness, decreased medullary cavity area, increased cortical bone density, and a trend for higher fracture force vs. confined controls. Weanling horses sprinting 82 m/day, 5 days/week (cumulative 3280 m over 8 weeks) showed increased bone mineral content vs. confined controls. Critically, one sprint per week (71 m) was sufficient: all exercised calf groups had greater dorsal cortical widths and fracture force vs. controls, with no differences between once, three times, or five times per week groups, and over 20% increase in bone strength from just 426 m cumulative sprinting over 6 weeks. Endurance exercise (up to 60 km/day) in Arabians showed no difference in RBAE vs. pasture controls. Furosemide caused transient negative calcium balance that returned to baseline in 3 days. Omeprazole at preventative dose (1 mg/kg daily for up to 2 months) showed no impairment of bone health.

**Clinical Implications:** The research demonstrates that stall confinement without high-speed exercise is a primary cause of bone loss in athletic horses, and this loss can be prevented by as little as one short sprint per week. Pasture turnout, even partial (12 h/day), prevents bone loss. Endurance exercise without speed does not strengthen bone. Proper nutrition is necessary but insufficient without appropriate exercise. Pharmaceutical caution is warranted, particularly with bisphosphonates that inhibit osteoclasts and may impair bone healing. For humans, the implications are direct: a sedentary lifestyle weakens the skeleton regardless of diet, short bouts of high-load exercise (approximately 20 cycles) can increase bone strength, and achieving high peak bone mass requires loading during youth. The findings emphasize that skeletal injuries often result from bone being ill-prepared for high loads after sedentary periods, rather than from nutritional deficiencies alone.