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Does Lower-Body BMD Develop at the Expense of Upper-Body BMD in Female Runners?


Medicine & Science in Sports & Exercise: October 2003 - Volume 35 - Issue 10 - pp 1733-1739
APPLIED SCIENCES: Physical Fitness and Performance

NEVILL, A. M., M. BURROWS, R. L. HOLDER, S. BIRD, and D. SIMPSON. Does Lower-Body BMD Develop at the Expense of Upper-Body BMD in Female Runners? Med. Sci. Sports Exerc., Vol. 35, No. 10, pp. 1733–1739, 2003.

Purpose: Evidence suggests that exercise plays an important role in stimulating site-specific bone mineral density (BMD). However, what is less well understood is how these benefits dissipate throughout the body. Hence, the purpose of the present study was to compare the levels of, and the correlation between, BMD recorded at 10 sites in female endurance runners, and to investigate possible determinants responsible for any inter-site differences observed.

Methods: Repeated measures ANOVA was used to compare the BMD between sites and factor analysis was used to describe the pattern of intersite correlations. Allometric ANCOVA was used to identify the primary determinants of bone mass and how these varied between sites.

Results: The ANOVA and factor analysis identified systematic differences in BMD between sites, with the greatest BMD being observed in the lower-body sites, in particular the legs. An investigation into the possible mechanisms responsible for these differences revealed “distances run” (km·wk−1) as a positive, and “years of training” as a negative determinant of bone mass (P < 0.001). However, the effect of a number of determinants varied between sites (P < 0.05). Specifically, the ANCOVA identified that running further distances resulted in higher bone mass in the arms and legs. In contrast, training for additional years appeared to result in lower bone mass in the arms and lumber spine. Calcium intake was also found to be positively associated with bone mass in the legs but negatively associated at all other sites.

Conclusions: A combination of running exercise and calcium intake would appear to stimulate the bone mass of women endurance runners at lower-body sites but at the expense of bone mass at upper-body sites.

Osteoporosis is a bone disease associated with low bone mineral density (BMD) that increases the risk of debilitating bone fractures. Therefore, it is important to find effective intervention strategies for building bone and for preventing bone loss. The osteogenic stimulus provided by load-bearing exercise indicates it is an important lifestyle factor that could be used for the prevention of bone loss (23,26). However, the specific role of physical activity in the maintenance or enhancement of bone mass or architecture remains elusive despite considerable research attention, with results inconsistent and inconclusive due to numerous methodological variations and limitations (30).

Physical activity has been shown to increase BMD in animals and human females by 0.9% per year in those limbs exercised (30). Indeed, strains on bone greater than needed for steady state remodeling will cause a modeling response that increases bone mass to meet the increasing load requirement (11). Various studies have concentrated on researching the effects of impact loading regimes across different sports on BMD and bone mineral content (BMC), and have suggested that the higher the impact load, the higher the BMD and BMC seen (2,8,17,22,24). However, several studies have demonstrated that extremely high training loads can have a detrimental effect on bone (6) often via hormonal mechanisms (10,12), whereas other studies have failed to demonstrate a relationship between training patterns and osteoporosis (18). These differences could be due to the fact that a minimum effective strain stimulus of mechanical loading is required to evoke an increase in the level of BMD, thus suggesting that high strain rates, distributed in unusual patterns, and short in duration and of sufficient frequency should be used to strengthen the bone (11).

It has also been suggested that this adaptive response to impact occurs only at the site of loading, indicating the site-specific nature of the bone remodeling response (1,28). However, the majority of studies have only looked at BMD and BMC at a few bone sites, i.e., lumbar spine, hip, and radius (9), leaving incomplete the understanding of the effect of physical activity on bone health at skeletal sites throughout the body. In a recent study by Jorgensen et al. (14), it was concluded that there are significant differences in the classification of osteoporosis and osteopenia depending on the bone site measured. Moreover, McCarthy et al. (19) and Platen et al. (24) stated that the heterogeneity of response in the skeleton means that it is difficult to predict overall bone loss from measurements at one particular site. Indeed, Kanis (15) warns of discrepancies and misclassifications that can occur when diagnosing osteoporosis due to highly variable coefficients of variation (3) and inadequate level of correlation between BMD recorded at different skeletal sites throughout the body.

Given the site-specific nature of the bone remodeling response together with this evidence of inadequate correlations between skeletal sites, there would appear to be a lack of understanding of how the benefits of exercise at the loaded site dissipates to other sites throughout the body. Hence, the purpose of the present study was to compare the levels of, and the degree of correlation between, BMD recorded at 10 skeletal sites throughout the body in a group of female endurance runners. If significant and systematic differences in BMD are observed between sites, a proportional allometric regression model, originally proposed by Nevill et al. (20), will be used to identify the important determinants of bone mass and whether these determinants varied between skeletal sites, thus providing possible insight into the mechanisms for the observed differences in BMD between sites.

1University of Wolverhampton, School of Sport, Performing Arts, and Leisure, UNITED KINGDOM;

2University of Exeter, School of Sport and Health Science, Exeter, UNITED KINGDOM;

3University of Birmingham, Edgbaston, Birmingham, UNITED KINGDOM;

4Centre for Population Health, Sunshine Hospital and Melbourne University, Victoria, AUSTRALIA; and

5Kent and Canterbury Hospital, Canterbury, UNITED KINGDOM

Address for correspondence: Professor Alan M. Nevill, University of Wolverhampton, School of Sport, Performing Arts and Leisure, Walsall Campus, Gorway Road, Walsall, WS1 3BD, United Kingdom; E-mail:

Submitted for publication February 2003.

Accepted for publication June 2003.

©2003The American College of Sports Medicine