Endurance training amplifies the pulsatile release of growth hormone: Effects of training intensity

The effects of intensity of run training on the pulsatile release of growth hormone (GH) were investigated in 21 eumenorrheic untrained women. The O₂ consumption (V̇O₂) at the lactate threshold (LT); fixed blood lactate concentrations (FBLC) of 2.0, 2.5, and 4.0 mM; peak V̇O₂; maximal V̇O₂; body composition; and pulsatile release of GH were measured. Subjects in both the at-lactate threshold (@LT, n = 9) and above-lactate threshold (>LT, n = 7) training groups increased V̇O₂ at LT and FBLC of 2.0, 2.5, and 4.0 mM and V̇O(2 max) after 1 yr of run training. However, the increase observed in the >LT group was greater than that in the @LT group (P < 0.05). No change was observed for the control group (n = 5). No among- or within-group differences were observed for body weight, although trends for reductions in percent body fat (P < 0.06) and fat weight (P < 0.15) were observed in the >LT group, and both training groups significantly increased fat-free weight (P < 0.05). Significant differences (P < 0.05) in the pulsatile release of GH were observed within the >LT group, as a result of 1 yr of run training, for maximal peak height (7.4 μg/l pre vs. 13.1 μg/l post), incremental peak amplitude (6.8 μg/l pre vs. 10.3 μg/l post), peak area (340 μg · l^-1 · min^-1 pre vs. 598 μg · l^-1 · min^-1 post), nadir GH concentration (0.60 μg/l pre vs. 2.2 μg/l post), and integrated (24-h) concentration of GH (4,390 μg · l^-1 · min^-1 pre vs. 7,710 μg · l^-1 · min^-1 post). No changes were observed for these variables within the @LT or control group. Results of the present study indicate that exercise training amplifies the pulsatile release of GH. This effect occurs when some training is above the LT. Our findings may have clinical implications in conditions characterized by impoverished pulsatile secretion of GH.