Long-term restoration of deficits in bone mineral density is inadequate inpremenopausal women with prior menstrual irregularity

Citation
Lk. Micklesfield et al., Long-term restoration of deficits in bone mineral density is inadequate inpremenopausal women with prior menstrual irregularity, CLIN J SPOR, 8(3), 1998, pp. 155-163
Citations number
34
Categorie Soggetti
Ortopedics, Rehabilitation & Sport Medicine
Journal title
CLINICAL JOURNAL OF SPORT MEDICINE
ISSN journal
1050642X → ACNP
Volume
8
Issue
3
Year of publication
1998
Pages
155 - 163
Database
ISI
SICI code
1050-642X(199807)8:3<155:LRODIB>2.0.ZU;2-Z
Abstract
Objective: To investigate change in bone mineral density (BMD) in premenopa usal women (age, 29-46 years), some of whom were marathon runners with a hi story of menstrual irregularity. Design: Longitudinal follow-up. Setting: University medical school. Participants: We investigated 8 sedenta ry controls (SC) and 19 marathon runners (12 with regular menses (R) and 7 with a history of irregularity (OA) 11.7 +/- 7.9 years before follow-up). Main Outcome Measures: BMD (g/cm(2)) of lumbar spine (LS) and proximal femu r were determined at baseline and follow-up (3-5 years later). We calculate d a menstrual history index (MHI) (estimated periods/year since age 13). Results: Body mass, age at menarche, and femoral BMD were not statistically different. Follow-up LS BMD (g/cm(2)) was lower (p < 0.01) in OA (0.936 +/ - 0.060) than in R (1.043 +/- 0.103) and SC (1.094 +/- 0.077), even when co varying for age or both age and mass. No group changed BMD significantly wi th time. Current MHI was lower (p < 0.001) in OA (9.7 +/- 1.4) than in R (1 1.3 +/- 0.5) and SC (11.8 +/- 0.4). MHI for the teenage years was lower in OA than in SC but not in R. OA had significantly lower MHI than did R and S C for the third and fourth decades. Only MHI during the third decade correl ated significantly with LS BMD for all subjects. Conclusions: Restoration of LS BMD deficit in women with prior menstrual ir regularity aged over 30 is slow and may never reach the same level as age-r elated controls, secondly, this may be the result of both bone loss in the third decade of life and reduced acquisition during adolescence.