Bone mineral density and menstrual irregularities. A comparative study on cortical and trabecular bone structures in runners with alleged normal eating behavior.
Bone mineral density (BMD), and associated biochemical and endocrine markers were compared in a group of runners with menstrual dysfunction (IR, n=13), and a group of performance matched eumenorrheic runners (R, n=15). All subjects claimed to have normal eating habits. Body height and weight, body mass index, and amount of body fat were similar. The IR group consisted of 5 presently oligomenorrheic (O) and 8 presently amenorrheic (A) runners. The BMD values of the athletes were additionally compared with corresponding values in a reference group (C) of healthy age matched controls (n=54). BMD values were significantly lower in IR compared with R on all measuring sites: Total body (-9%, p=0.03), femoral neck (-11%, p=0.01), lumbar spine (-12%, p=0.001), lower leg (-6.5%, p=0.03) and arms (-7%, p=0.01). In addition, IR athletes had lower total body (-5%, p=0.01), and lumbar spine BMD (-10%, p=0.001) than C. No differences were observed in serum IGF-1, SHBG, testosterone and cortisol, or in the biochemical marker of bone formation (osteocalcin) and bone resorption (1 CTP). Values of serum E2, FSH and LH were low in IR and normal in R. TSH was in the normal range in both groups, but f-T4 was significantly lower in IR than in R. The athletes were furthermore grouped according to past and present menstrual dysfunction severity. At all measuring sites, with the exception of the lower leg, increasing menstrual dysfunction severity was linearly associated with declining BMD values (p<0.05). In conclusion, even highly conditioned cortical bone tissue seems to be negatively related to menstrual disorders, which may serve to explain the high incidence of stress fractures in athletes with menstrual disorders. Single measurements of biochemical markers of bone resorption and formation may not reflect the current bone status.
Tomten
S E
SE
The Norwegian University of Sport and Physical Education, Oslo.
Falch
J A
JA
Birkeland
K I
KI
Hemmersbach
P
P
Høstmark
A T
AT
D000273:Adipose Tissue / Q000033:anatomy & histology; D000328:Adult; D000568:Amenorrhea / Q000209:etiology; D015415:Biomarkers / Q000097:blood; D001827:Body Height; D015992:Body Mass Index; D001835:Body Weight; D015519:Bone Density; D001842:Bone and Bones / Q000473:pathology*; D001133:Bones of Upper Extremity / Q000473:pathology; D016022:Case-Control Studies; D004958:Estradiol / Q000097:blood; D005247:Feeding Behavior / Q000502:physiology*; D005260:Female; D005272:Femur Neck / Q000473:pathology; D005360:Fibula / Q000473:pathology; D005640:Follicle Stimulating Hormone / Q000097:blood; D015775:Fractures, Stress / Q000209:etiology; D006801:Humans; D006854:Hydrocortisone / Q000097:blood; D007334:Insulin-Like Growth Factor I / Q000032:analysis; D008159:Lumbar Vertebrae / Q000473:pathology; D007986:Luteinizing Hormone / Q000097:blood; D008599:Menstruation Disturbances / Q000150:complications* / Q000473:pathology; D009839:Oligomenorrhea / Q000209:etiology; D015675:Osteocalcin / Q000097:blood; D010446:Peptide Fragments / Q000097:blood; D011347:Procollagen / Q000097:blood; D012420:Running / Q000502:physiology*; D012738:Sex Hormone-Binding Globulin / Q000032:analysis; D013739:Testosterone / Q000097:blood; D013972:Thyrotropin / Q000097:blood; D013974:Thyroxine / Q000097:blood; D013977:Tibia / Q000473:pathology
D015415:Biomarkers; D010446:Peptide Fragments; D011347:Procollagen; D012738:Sex Hormone-Binding Globulin; C042813:procollagen type I carboxy terminal peptide; D015675:Osteocalcin; D013739:Testosterone; D004958:Estradiol; D007334:Insulin-Like Growth Factor I; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D013972:Thyrotropin; D013974:Thyroxine; D006854:Hydrocortisone