Physical activity, coronary artery calcium, and bone mineral density in elderly men and women: a preliminary investigation.

摘要

The aim of this study was to examine the relationship between cardiorespiratory fitness, coronary artery calcification (CAC), and bone mineral density (BMD) in older adults. Thirteen highly active, endurance-trained "master athletes" (7 male and 6 female) and 12 sedentary (6 male and 6 female) older adults (age 60-78 years) were recruited for this study. All subjects had CAC measured by electron beam computed tomography; BMD assessed by dual-energy X-ray absorptiometry; and plasma mineral regulatory proteins, including matrix Gla protein, fetuin-A, osteocalcin, osteopontin, and osteoprotegerin, measured by enzyme-linked immunosorbent assay. Furthermore, maximal oxygen consumption (VO2max) was measured in each subject to provide an objective measure of cardiorespiratory fitness. As expected, whole-body BMD was elevated in master athletes compared with sedentary adults (1.17 +/- 0.02 vs 1.09 +/- 0.02 g/cm2, P < .05). CAC score did not differ between activity groups, but was 8-fold lower in women comparedwith men (P < .05). The CAC score was not correlated with BMD, and there was no correlation between CAC and VO2max when both sexes were included in the analysis. When the sexes were analyzed separately, several relationships were evident in men only. There was a significant inverse correlation between VO2max and the number of calcified coronary artery lesions (r = -0.596, P < .05), and the correlation between VO2max and logCAC score approached significance (r = -.493, P .08). Furthermore, fetuin-A, a systemic inhibitor of vascular calcification, was positively correlated with VO2max in men (r = 0.679, P < .05). These data provide preliminary evidence that chronic exercise may simultaneously inhibit CAC and increase BMD. The positive correlation between VO2max and plasma fetuin-A levels in men indicates a potential mechanism by which exercise may correlate negatively with CAC. Additional studies with larger sample sizes will be needed to determine if the protective effects of chronic exercise on CAC and BMD are sex specific or mediated through common mechanisms such as changes in circulating levels of mineral regulatory proteins.