Wj. Inder et al., ELEVATED BASAL ADRENOCORTICOTROPIN AND EVIDENCE FOR INCREASED CENTRALOPIOID TONE IN HIGHLY TRAINED MALE-ATHLETES, The Journal of clinical endocrinology and metabolism, 80(1), 1995, pp. 244-248
Basal cortisol and ACTH levels have previously been shown to be elevat
ed in highly trained athletes, whereas the AGTH response to ovine CRH
has been reported to be diminished compared to that in nonathletic con
trols. Naloxone, a nonselective opioid receptor antagonist, is known t
o stimulate ACTH and cortisol secretion. The mechanism of this respons
e is thought to be via increased hypothalamic CRH secretion. The aim o
f this study was to examine basal and naloxone-stimulated levels of hy
pothalamic-pituitary-adrenal axis hormones in male athletes. Ten highl
y trained male athletes and 10 nonathletic controls took part in the s
tudy. Peripheral venous blood was sampled for cortisol, ACTH, CRH, and
arginine vasopressin (AVP) for 2 h before the administration of 20 mg
naloxone, iv, and 15, 30, 45, 60, 90, and 120 min after naloxone trea
tment. Body mass index was significantly lower in the athletes (P < 0.
001). Basal (prenaloxone) ACTH levels were higher in the athletes (P <
0.05), whereas levels of cortisol, CRH, and AVP were similar in both
groups. After naloxone treatment, there was a significantly greater ri
se in ACTH in the athletes (P < 0.02). There was also a trend for the
cortisol response to be greater, which was not statistically significa
nt (P < 0.07). Although in both groups, peripheral CRH rose after nalo
xone treatment (P < 0.005), a rise of similar magnitude occurred over
the 2-h period before naloxone (P < 0.0001). Plasma AVP did not change
significantly after naloxone treatment. Neither the plasma cortisol l
evel at baseline nor the body mass index correlated significantly with
the ACTH or cortisol response to naloxone. The presence of an enhance
d ACTH response to naloxone is evidence that central opioid tone may b
e increased in highly trained athletes. However, there is no associate
d suppression of the hypothalamic-pituitary-adrenal axis, and basal AC
TH levels are raised, without any detectable change in peripheral plas
ma CRH or AVP. An additional factor (other than CRH) that stimulates A
CTH secretion may be released after naloxone administration.