Decreased Hypothalamic Gonadotropin-Releasing Hormone Secretion in Male Marathon Runners

Abstract

Hypogonadotropic hypogonadism due to a deficiency in hypothalamic gonadotropin-releasing hormone is common in female athletes ("hypothalamic amenorrhea"). It is not known, however, whether a similar phenomenon occurs in male athletes. We investigated the integrity of the hypothalamic-pituitary-gonadal axis in six highly trained male marathon runners (who were running 125 to 200 km per week). The mean (+/- SEM) frequency of spontaneous luteinizing hormone pulses was diminished in the runners, as compared with healthy controls (2.2 +/- 0.48 vs. 3.6 +/- 0.24 pulses per eight hours, P less than 0.05). The amplitude of the pulses was also low in the runners (0.9 +/- 0.24 vs. 1.6 +/- 0.15 mlU per milliliter; P less than 0.05), and the responses of luteinizing hormone to gradually increasing doses of exogenous gonadotropin-releasing hormone were decreased. Plasma testosterone levels were similar in the two groups and increased equally in response to an intramuscular injection of 2000 units of human chorionic gonadotropin. During short-term intense physical exercise (a treadmill run at 72 percent of maximal oxygen consumption for two hours), the plasma gonadotropin levels in the athletes remained stable, but significant elevations in plasma levels of cortisol, prolactin, and testosterone occurred. We conclude that highly trained male athletes, like their female counterparts, may have a deficiency of hypothalamic gonadotropin-releasing hormone. This condition may be caused by the prolonged, repetitive elevations of gonadal steroids and other hormones known to suppress gonadotropin-releasing hormone secretion that are elicited by their daily exercise.

Testosterone Is Significantly Reduced in Endurance Athletes without Impact on Bone Mineral Density

“…However, although low, the values of TT and FT have always been within the normal range [18, 19, 20, 21, 22, 31]. Other authors [23, 24, 27], and Lucia et al [25]especially, have found normal T levels in male endurance athlete groups composed of marathon runners, professional CY and elite TR. Lucia et al [25]suggested that the professional status of the athletes could explain the contradictory results obtained in other studies [18, 20, 21, 22, 31].…”

“…In male athletes, circulating total T (TT) and free T (FT) concentrations are influenced by the intensity, duration and type of physical activity [14]. Although the increase in T during short-term resistance or endurance exercise seems to be unequivocal [15, 16, 17], studies on the effect of endurance exercise training on the hypothalamic-pituitary-gonadal (HPG) axis, as evaluated in subjects at rest, have shown conflicting results [18, 19, 20, 21, 22, 23, 24, 25]. The major subclinical alterations in the male reproductive endocrine system reported in endurance athletes include a reduction in circulating levels of TT and FT [18, 19, 20, 21, 22].…”

Stress, the Stress System and the Role of Glucocorticoids

“…CRH inhibits the secretion of GnRH from the hypothalamus [52,53], while glucocorticoids suppress the activity of the reproductive axis by decreasing secretion of GnRH, follicle-stimulating hormone/luteinizing hormone and gonadal steroids [52,53,54,55]. Representative examples of stress-mediated suppression of the gonadal axis are highly trained runners and ballet dancers, who may present with suppression of gonadal function due to chronic activation of the HPA axis [56,57]. …”

Basal testicular testosterone production in endurance-trained men is suppressed

“…This collective evidence (along with the findings in amenorrheic athletic women of central adaptations in the hypothalamic-pituitary-ovarian axis; (see review, Hackney 1996), has led some investigators to conclude that the peripheral aspects of the H-P-T axis (i.e., the testicles) function normally in endurance-trained men (Hackney et al 1990;MacConnie et al 1986). Procedural and methodological limitations of the studies cited above, however, may make this assumption suspect concerning only a central mechanistic adaptation.…”

“…In this aforementioned study (Hackney et al 1990), testicular testosterone responsiveness of the endurance-trained men to the LH response of the GnRH stimuli seemed normal and appropriate. In a similar fashion, MacConnie et al (1986) used human chorionic gonadotropin (hCG, a LH-like agent) to stimulate testicular testosterone production in endurance-trained men and they saw normal responses. Both Hackney et al (1990) and MacConnie et al (1986) concluded from their data that the peripheral aspects of the H-P-T axis were intact and responsive in endurance-trained men.…”