Georgina Pearce

Exercise Before Puberty May Confer Residual Benefits in Bone Density in Adulthood: Studies in Active Prepubertal and Retired Female Gymnasts

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/cm2) 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 weight‐bearing 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/cm2/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.

Moderate exercise during growth in prepubertal boys: changes in bone mass, size, volumetric density, and bone strength: a controlled prospective study

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 cm3 in the exercise group, and 3.04 ± 1.14 cm3 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.

The differing tempo of growth in bone size, mass, and density in girls is region-specific

The differing tempo and direction of growth of the periosteal and endocortical surfaces, and the differing tempo of growth of the axial and appendicular skeleton, may predispose to regional deficits in bone size, bone mineral content (BMC), and volumetric bone mineral density (vBMD). These traits were measured during 2 years by dual x-ray absorptiometry in 109 girls. By 7 years of age, bone size was approximately 80% of its maturational peak, and BMC was approximately 40% of its peak. Before puberty, the legs grew more rapidly than the trunk. During puberty, the growth spurt was truncal. Between 7 and 17 years, femoral and lumbar spine BMC increased by 50-150% because bone size increased. vBMD increased by 10-30%. Thus, growth builds a bigger, but only moderately denser, skeleton. Regions growing rapidly, or distant from their peak, may be more severely affected by illness than those growing slowly or nearer completion of growth. Depending on the age of exposure to disease, deficits may occur in limb dimensions (prepuberty), spine dimensions (early puberty), or vBMD by interference with mineral accrual (late puberty). As vBMD is independent of age before puberty, the position of an individuals vBMD in the population distribution is established early in life. Bone fragility in old age may have its foundations in growth.

Short stature and delayed puberty in gymnasts: Influence of selection bias on leg length and the duration of training on trunk length☆☆☆★

BACKGROUND Delays in bone age, the onset of puberty, and skeletal growth in gymnasts could be, in part, the reason for an interest in gymnastics, rather than being the result of vigorous exercise. We hypothesized that short stature and delayed bone age are present at the start of gymnastics, and training delays growth, producing short stature, even after retirement. METHODS Sitting height and leg length were measured in 83 active female gymnasts, 42 retired gymnasts, and 154 healthy control subjects. Results were expressed as age-specific SD scores (mean +/- SEM). RESULTS In the cross-sectional data, active gymnasts had delayed bone age (1.3 +/- 0.1 years), reduced height -1.32 +/- 0.08 SD, sitting height -1.24 +/- 0.09 SD, and leg length, -1.25 +/- 0.08 SD (all P <.001). However, in those training for less than 2 years, the deficit was confined to leg length (-0.8 +/- 0.2 SD). During 2 years of follow-up of 21 gymnasts, only the deficit in sitting height worsened (by 0.4 +/- 0.1 SD). In 13 gymnasts followed up in the immediate 12 months after retirement, sitting height accelerated, resulting in a lessening of the deficit in sitting height by 0.46 +/- 0.14 SD (P <.01). Adult gymnasts who had been retired for 8 years had no deficit in sitting height, leg length, or menstrual dysfunction. CONCLUSIONS Short stature in active gymnasts is partly due to selection of individuals with reduced leg length. Reduced sitting height is likely to be acquired but is reversible with cessation of gymnastics. A history of gymnastic training does not appear to result in reduced stature or menstrual dysfunction in adulthood.

Present and future of osteoporosis therapy

In the 50-year “modern” history of osteoporosis, there have been about 17 antifracture studies with sufficient attention to design to allow inference regarding efficacy. Antivertebral fracture efficacy has been reported with etidronate, estrogen patch, calcitonin, and 1,25-dihydroxyvitamin D. Two studies using fluoride were positive, and two were negative. Hip fractures have been neglected. One study showed efficacy of hip protectors, one showed efficacy of vitamin D and calcium in nursing home dwellers. The source of most hip fractures is the community. One community based antihip fracture efficacy study using annual injections of vitamin D was positive. There have been no antivertebral or antihip fracture studies in men, or in corticosteroid-related osteoporosis in men or women. Lack of independently repeated demonstration of efficacy, small fracture numbers, and data pooling in some of these (the best) studies leave great uncertainty. Estrogen and bisphosphonates appear to be the best options at this time. New data suggest that calcium supplementation is likely to reduce the rate of bone loss and perhaps reduce fracture rates. The challenge is to maintain and restore the constituents of bone mineral density (BMD), that is: to promote periosteal and endosteal bone formation; reduce endosteal bone resorption and cortical porosity; and increase trabecular thickness, number, and connectivity. There are many opportunities, for instance, intermittent parathyroid hormone (PTH) increases bone strength and, with estrogen, may increase connectivity. The anabolic effects of PTH may be partly mediated by IGF-1. IGF-1 increases periosteal, endosteal, and trabecular bone formation, cortical and trabecular width, and trabecular and endocortical connectivity. With bisphosphonate, IGF-1 may increase bone area and strength as the bisphosphonate decreases medullary area while IGF-1 increases subperiosteal area. Anabolic effects of fluoride warrant further study provided that the study design addresses the issue of bone strength, the narrow toxic-therapeutic window, and cortical bone loss. Aluminum, a constituent of zeolite, has anabolic effects which may be partly mediated by TGF-β. Prostaglandin E2 increases periosteal and endosteal bone formation but may increase cortical porosity. More data are needed regarding these growth factors, silicon compounds, strontium salts, and flavenoids. The effects of medroxyprogesterone and 19 norprogestins on BMD have not been compared. Raloxifene, a new estrogen agonist free of endometrial hyperplastic effects, is being studied. Most treated individuals with osteoporosis (i.e., low BMD with or without a fracture) will not suffer a fracture so treatment must be safe. Success—absence of fracture—will be measured by the epidemiologist because it is difficult to distinguish efficacy from chance in an individual as the peak incidence of fractures in the community is usually only about 1–4/100 per year.

Does weight-bearing exercise protect against the effects of exercise-induced oligomenorrhea on bone density?

Does weight-bearing exercise offset bone loss associated with oligomenorrhea? If so, bone mineral density (BMD) will be stable at weight bearing sites but decrease at non-weight-bearing sites with increasing duration of oligomenorrhea. To test this hypothesis, BMD (g/cm2), was measured by dual-energy X-ray absorptiometry in 41 oligomenorrheic ballet dancers aged 17.7±0.2 years (mean ± SEM) and 46 age-matched controls with normal menstrual function. BMD correlated negatively with the duration of oligomenorrhea at weight-bearing and non-weight-bearing sites (femoral neck,r=−0.33,p<0.05; Wards triangle,r=−0.29,p=0.06; trochanter, r=−0.33,p<0.05; lumbar spine,r=−0.25,p=0.1; skull,r=−0.29,p=0.06; arms,r=−0.32,p<0.05; ribs,r=−0.30,p=0.06). The slopes of the regression of BMD on duration of oligomenorrhea were greater at the proximal femur (trochanter, −0.28±0.13, femoral neck, −0.24±0.11; Wards triangle, −0.29±0.15) than the skull (−0.15±0.08,p<0.05,p<0.1,p<0.1 respectively). The slopes at the trochanter and femoral neck were also greater than at the ribs (−0.10±0.05; bothp<0.1). In the dancers with oligomenorrhea of less than 40 months duration, BMD was higher than the age-predicted mean at weight-bearing sites (except the lumbar spine), but not at non-weight-bearing sites (femoral neck, 9.1±3.4%; Wards triangle, 10.0±1.7%; trochanter, 9.4±4.1%, allp<0.05; lumbar spine , −2.1±2.7%, NS; skull, −2.5±2.1%, NS; ribs, −3.0±1.6% NS; arms, −3.9±1.6%;p<0.05). In the dancers with greater than 40 months oligomenorrhea, BMD was no higher than the age predicted mean, at the weight bearing sites, and was lower at non-weight bearing sites (femoral neck, 4.3±2.3%, NS; Wards triangle, 3.5±3.2%, NS; trochanter, 2.1±2.7%, NS; lumbar spine, −3.8±2.1%, NS; arms, −7.5±0.8%,p<0.05; skull, −6.2±1.8%,p<0.01; ribs, −5.4±1.1%,p<0.0001). In conclusion, weight-bearing exercise is unlikely to offset the deleterious effects of oligomenorrhea. Bone loss appears to occur at all sites but may begin from a higher level at weight-bearing sites and may proceed more rapidly.

Interaction Between Genetic and Nutritional Factors

Patients with fractures have a deficit in areal bone mineral density (aBMD) relative to age-matched controls. This may be the result of the attainment of a low peak aBMD, bone loss, or both (1). As the variance (or spread) of peak aBMD is large (1 standard deviation is approximately 10% of the mean), an individual’s aBMD at maturity is likely to be a major determinant of aBMD for many years, particularly if aBMD tracks in adulthood. With advancing years, the magnitude of the bone loss contributes increasingly to aBMD, so that combinations of the level of peak aBMD and the rate and duration of bone loss before, during, and following menopause contribute to the deficit in aBMD in old age.