Exercise during growth may contribute to the prevention of osteoporosis by increasing peak bone mineral density (BMD). However, exercise during puberty may be associated with primary amenorrhea and low peak BMD, while exercise after puberty may be associated with secondary amenorrhea and bone loss. As growth before puberty is relatively sex hormone independent, are the prepubertal years the time during which exercise results in higher BMD? Are any benefits retained in adulthood? We measured areal BMD (g/cm 2 ) by dual-energy X-ray absorptiometry in 45 active prepubertal female gymnasts aged 10.4 ؎ 0.3 years (mean ؎ SEM), 36 retired female gymnasts aged 25.0 ؎ 0.9 years, and 50 controls. The results were expressed as a standardized deviation (SD) or Z score adjusted for bone age in prepubertal gymnasts and chronological age in retired gymnasts. In the cross-sectional analyses, areal BMD in the active prepubertal gymnasts was 0.7-1.9 SD higher at the weightbearing sites than the predicted mean in controls (p < 0.01). The Z scores increased as the duration of training increased (r ‫؍‬ 0.32-0.48, p ranging between <0.04 and <0.002). During 12 months, the increase in areal BMD (g/cm 2 /year) of the total body, spine, and legs in the active prepubertal gymnasts was 30 -85% greater than in prepubertal controls (all p < 0.05). In the retired gymnasts, the areal BMD was 0.5-1.5 SD higher than the predicted mean in controls at all sites, except the skull (p ranging between <0.06 and <0.0001). There was no diminution across the 20 years since retirement (mean 8 ؎ 1 years), despite the lower frequency and intensity of exercise. The prepubertal years are likely to be an opportune time for exercise to increase bone density. As residual benefits are maintained into adulthood, exercise before puberty may reduce fracture risk after menopause. (J Bone Miner Res 1998;13:500-507)

Figure 6Serum bone specific alkaline phosphatase, osteocalcin, collagen propeptide of type I collagen (PICP), and urinary type I C-telopeptide breakdown products (CrossLaps) versus bone age. Prepubertal (filled circles), peripubertal (open circles), and postpubertal (crosses).

Cross-sectional studies of elite athletes suggest that growth is an opportune time for exercise to increase areal bone mineral density (BMD). However, as the exercise undertaken by athletes is beyond the reach of most individuals, these studies provide little basis for making recommendations regarding the role of exercise in musculoskeletal health in the community. To determine whether moderate exercise increases bone mass, size, areal, and volumetric BMD, two socioeconomically equivalent schools were randomly allocated to be the source of an exercise group or controls. Twenty boys (mean age 10.4 years, range 8.4 -11.8) allocated to 8 months of 30-minute sessions of weight-bearing physical education lessons three times weekly were compared with 20 controls matched for age, standing and sitting height, weight, and baseline areal BMD. Areal BMD, measured using dual-energy X-ray absorptiometry, increased in both groups at all sites, except at the head and arms. The increase in areal BMD in the exercise group was twice that in controls; lumbar spine (0.61 ؎ 0.11 vs. 0.26 ؎ 0.09%/month), legs (0.76 ؎ 0.07 vs. 0.34 ؎ 0.08%/month), and total body (0.32 ؎ 0.04 vs. 0.17 ؎ 0.06%/month) (all p < 0.05). In the exercise group, femoral midshaft cortical thickness increased by 0.97 ؎ 0.32%/month due to a 0.93 ؎ 0.33%/month decrease in endocortical (medullary) diameter (both p < 0.05). There was no periosteal expansion so that volumetric BMD increased by 1. 14 ؎ 0.33%/month, ( p < 0.05). Cortical thickness and volumetric BMD did not change in controls. Femoral midshaft section modulus increased by 2.34 ؎ 2.35 cm 3 in the exercise group, and 3.04 ؎ 1.14 cm 3 in controls ( p < 0.05). The growing skeleton is sensitive to exercise. Moderate and readily accessible weight-bearing exercise undertaken before puberty may increase femoral volumetric BMD by increasing cortical thickness. Although endocortical apposition may be a less effective means of increasing bone strength than periosteal apposition, both mechanisms will result in higher cortical thickness that is likely to offset bone fragility conferred by menopause-related and age-related endocortical bone resorption. (J Bone Miner Res 1998;13:1814-1821)

Cross-sectional studies of elite athletes suggest that growth is an opportune time for exercise to increase areal bone mineral density (BMD). However, as the exercise undertaken by athletes is beyond the reach of most individuals, these studies provide little basis for making recommendations regarding the role of exercise in musculoskeletal health in the community. To determine whether moderate exercise increases bone mass, size, areal, and volumetric BMD, two socioeconomically equivalent schools were randomly allocated to be the source of an exercise group or controls. Twenty boys (mean age 10.4 years, range 8.4 -11.8) allocated to 8 months of 30-minute sessions of weight-bearing physical education lessons three times weekly were compared with 20 controls matched for age, standing and sitting height, weight, and baseline areal BMD. Areal BMD, measured using dual-energy X-ray absorptiometry, increased in both groups at all sites, except at the head and arms. The increase in areal BMD in the exercise group was twice that in controls; lumbar spine (0.61 ؎ 0.11 vs. 0.26 ؎ 0.09%/month), legs (0.76 ؎ 0.07 vs. 0.34 ؎ 0.08%/month), and total body (0.32 ؎ 0.04 vs. 0.17 ؎ 0.06%/month) (all p < 0.05). In the exercise group, femoral midshaft cortical thickness increased by 0.97 ؎ 0.32%/month due to a 0.93 ؎ 0.33%/month decrease in endocortical (medullary) diameter (both p < 0.05). There was no periosteal expansion so that volumetric BMD increased by 1.14 ؎ 0.33%/month, ( p < 0.05). Cortical thickness and volumetric BMD did not change in controls. Femoral midshaft section modulus increased by 2.34 ؎ 2.35 cm 3 in the exercise group, and 3.04 ؎ 1.14 cm 3 in controls ( p < 0.05). The growing skeleton is sensitive to exercise. Moderate and readily accessible weight-bearing exercise undertaken before puberty may increase femoral volumetric BMD by increasing cortical thickness. Although endocortical apposition may be a less effective means of increasing bone strength than periosteal apposition, both mechanisms will result in higher cortical thickness that is likely to offset bone fragility conferred by menopause-related and age-related endocortical bone

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Lack of consistent information concerning the pathophysiology of corticosteroid-related bone loss may be due to coexisting independent factors that influence bone mineral density (BMD). For example, the disease being treated may increase bone turnover and cause bone loss, and its severity may influence the dose of corticosteroids chosen. Similarly, disease remission due to the treatment or disease progression despite treatment may influence bone turnover and the rate of bone loss. The hormonal changes purportedly responsible for reduced bone formation or increased bone resorption may be the result of the disease, not the corticosteroids. To determine the pathophysiology of corticosteroid-related bone loss, we conducted a controlled, prospective study in men with no systemic illness treated with corticosteroids to reduce antisperm antibodies. We measured BMD using dual x-ray absorptiometry and circulating biochemical and hormonal determinants of bone turnover in 9 men before and during prednisolone treatment and in 10 age-matched controls. The results were expressed as the mean +/- SEM. There were no differences in BMD between the two groups at baseline. The patients received 50 mg prednisolone daily for 3.7 +/- 0.6 months (range, 1-6). BMD decreased by 4.6 +/- 0.8% at the lumbar spine (P = 0.0007), by 2.6 +/- 0.6% at the trochanter (P = 0.004), and by 4.8 +/- 1.9% at the Ward's triangle (P < 0.04). The decrease in lumbar spine BMD correlated with the cumulative dose of corticosteroids (r = -0.49; P = 0.03). Serum osteocalcin and skeletal alkaline phosphatase decreased by 28.5 +/- 15.5% (P = 0.08) and 24.2 +/- 8.6% (P < 0.03), respectively. The decrease in lumbar spine BMD correlated with the decrease in osteocalcin (r = -0.48; P < 0.02). Serum testosterone and sex hormone-binding globulin decreased by 28.6 +/- 4.4% (P < 0.003) and 28.5 +/- 8.3% (P < 0.007), respectively. The testosterone/sex hormone-binding globulin ratio did not change. The decrease in total testosterone correlated with the decrease in osteocalcin (r = -0.40; P = 0.05). There were no detectable changes in urinary C-telopeptide, serum PTH, or serum calcium. Estradiol decreased by 23.5 +/- 11.4% (P < 0.003). Corticosteroid therapy results in rapid bone loss, probably due to reduced bone formation. Neither increased bone resorption nor secondary hyperparathyroidism appears to contribute to the rapid bone loss. Whether the reduction in bone formation may be partly mediated by changes in sex steroids remains unclear.