This study examined the hypothesis that exercise-induced changes in circula
ting testosterone would be centrally mediated via hypothalamic-pituitary re
lease of luteinizing hormone (LH). We tested this hypothesis by examining o
vernight LH, total and free testosterone (TT and FT), and cortisol (C) conc
entrations in 10 young healthy men (21 +/- 1 yr) during two experimental se
ssions: a control and an acute heavy-resistance exercise bout (50 total set
s consisting of squats, bench press, leg press, and latissimus dorsi pull-d
own). Exercise was performed from 1500 to 1700, and blood sampling began at
1700 and continued until 0600 the next morning. Blood was sampled every 10
min for LH and every hour for TT, FT, and C. Hormonal concentrations were
determined via RIA, and the secretion characteristics of LH were analyzed w
ith deconvolution analysis. When overnight postexercise concentrations were
compared with control concentrations, no statistically significant (P less
than or equal to 0.05) differences were observed for LH half-life, LH puls
e frequency, interpulse interval, pulse amplitude, or pulse mass. Significa
nt differences were observed for LH production rate (13.6 +/- 4 and 17.9 +/
- 5 IU.l distribution volume(-1).day(-1) for exercise and control, respecti
vely, a 24% reduction). For the ANOVA marginal main effect means due to con
dition, C was significantly elevated (5.9 +/- 0.7 vs. 4.0 +/- 0.4 mug/dl),
while TT (464 +/- 23 vs. 529 +/- 32 ng/dl) and FT (15.6 +/- 0.7 vs. 18.3 +/
- 0.9 pg/ml) were significantly decreased for the exercise condition. These
data demonstrate that the decline in overnight testosterone concentrations
after acute heavy-resistance exercise is accompanied by a blunted LH produ
ction rate and elevated C concentrations.