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Fourteen young women with normal menses participated in an endurance running program to investigate the effects of physical training on menstrual function, plasma PRL, and body composition. Body composition, measured by hydrostatic weighing, and PRL (basal and TRH-stimulated ) were determined initially and after each subject had increased her weekly mileage by 30 miles (delta 30) and 50 miles (delta 50). Mean (+/- SEM) total body weight did not change, but the subjects became significantly leaner (relative fat, 25.5 +/- 1.3% at baseline vs. 22.4 +/- 0.9% at delta 50; P less than 0.02). Thirteen women developed menstrual changes (mainly oligomenorrhea), but not amenorrhea. Mean (+/- SEM) unstimulated PRL levels were 16.8 +/- 3.1%, 16.9 +/- 2.4, and 11.5 +/- 2.1 ng/ml at baseline, delta 30, and delta 50, respectively (P less than 0.03 at delta 50 compared to baseline and delta 30). Mean ( +/- SEM) integrated TRH-stimulated PRL responses increased from 5002 +/- 462 ng/ml.min at baseline to 5748 +/- 609 mg/ml.min at delta 30 and 6535 +/- 552 ng/ml.min at delta 50, and were significantly different from one another (F = 4.01; P less than 0.04). Endurance training, without total body weight loss or extreme leanness, results in frequent menstrual dysfunction. Other authors have shown that young female athletes have an increased PRL response to acute exercise compared to nonathletes. One mechanism responsible for menstrual dysfunction in endurance-trained women may be frequent and exaggerated PRL responses to exercise and other stimuli.

The effects of endurance training on body composition and the pituitary-thyroid axis were studied in 29 healthy, young (mean age, 28.7 yr), regularly menstruating women. Women who were initially jogging a mean of 13.5 miles/week were selected for this study to minimize dropouts. Body composition, measured by hydrostatic weighing, and nonfasting plasma concentrations of T4, T3, rT3, TSH, and TRH-stimulated TSH, measured by RIA, were examined initially and after each subject's weekly mileage had increased to 30 miles ( delta 30) for at least 2 consecutive weeks. Two subjects were found to have compensated primary hypothyroidism and were not included in the subsequent data analysis. At delta 30, mean body weight did not change, mean fat weight decreased (- 1.02 kg; P less than 0.005), and mean lean weight increased (+0.75 kg; P less than 0.05). T4 and unstimulated TSH did not change. However, mean (+/-SE) T3 decreased from 107.2 +/- 4.4 to 97.9 +/- 3.4 ng/dl (P less than 0.025), and mean rT3 decreased from 170.9 +/- 13.9 to 154.6 +/- 13.2 pg/ml (P less than 0.025). The decreases in T3 and rT3 were accompanied by significantly greater TSH responses to TRH stimulation [mean (+/-SE) area under TSH curve, 1381.4 +/- 123 vs. 1712.8 +/- 202 micron IU/ml.min; P less than 0.01]. These results indicate that physically active women who undergo additional endurance training 1) become more lean without a change in total weight, and 2) have changes in T3, rT3, and TRH-stimulated TSH indicative of mild thyroidal impairment.