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Journal of Clinical Endocrinology & Metabolism, Vol 62, 551-556, Copyright © 1986 by Endocrine Society
ARTICLES |
FE Chang, WG Dodds, M Sullivan, MH Kim and WB Malarkey
Acute exercise may stimulate PRL secretion, which, in turn, may contribute to exercise-associated menstrual dysfunction. We compared the response of PRL secretion in sedentary women and women runners with normal and abnormal menstrual cycles. We also studied the GH response to acute exercise, as GH may bind to lactogenic receptors. Five nonrunning women, 5 eumenorrheic running women, four oligomenorrheic running women, and six amenorrheic running women were studied on 2 consecutive days. On day 1, the women cycled on a bicycle ergometer against an increasing workload until total exhaustion. Serum PRL and GH increased several-fold in response to acute exercise in all three groups of running women. On day 2, the women simulated a daily training run by enduring a designed submaximal exercise regimen. In response to submaximal exercise, no group had a significant elevation of PRL or GH. Therefore, a threshold of exercise intensity exists that must be achieved before a significant increase in PRL or GH secretion occurs in women runners; serum PRL and GH in the nonrunning group did not increase significantly even in response to acute maximal exercise. The transient elevations in PRL and GH in women runners probably do not contribute to their menstrual dysfunction unless individual hypersensitivity of the hypothalamic-pituitary-ovarian axis to such intermittent elevations is present.
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