To test the hypothesis that the appearance of disulfide-linked growth hormone (GH) aggregates during and after an acute resistance exercise test (ARET) in men could be influenced by chronic physical training.
Fourteen men (28 ± 1 yr) underwent two different 8-wk physical training programs designed to improve military performance. Before and after chronic training, subjects performed an ARET (six sets of 10 repetition-maximum squat) and had venous blood drawn pre-, mid-, and post-ARET (0, 15, and 30 min postexercise). To determine whether GH molecules were disulfide-linked, serum samples were chemically reduced via glutathione (GSH). Serum immunoreactive GH (IRGH) and immunofunctional GH (IFGH) concentrations were determined using two specific immunoassays, in nonreduced (−GSH) and reduced (+GSH) states. Data were analyzed using repeated-measures ANOVA.
No differences were observed in the GH responses of the two training programs; therefore, training group data were combined for analysis. GSH reduction increased the mean GH signal (−GSH: 1.4 ± 0.3 μg·L−1 vs +GSH: 1.7 ± 0.3 μg·L−1; P < 0.01) only when quantifying IRGH. Post hoc testing indicated that serum contained IRGH disulfide-linked GH aggregates at the mid, 0-, 15-, and 30-min posttime points of the ARET (P < 0.01), whereas GSH reduction did not affect IFGH concentrations. Chronic physical training had no effect on the ARET-induced GH response.
Acute resistance exercise leads to the appearance of disulfide-linked IRGH aggregates, and this response does not appear to be affected by 8 wk of chronic physical training. The physiological significance of increased proportions of disulfide-linked GH aggregates postexercise remains uncertain; however, structural alterations in GH moieties after acute exercise may represent important regulatory steps in mediating GH biological activity at selected target tissues.
Military Performance Division, US Army Research Institute of Environmental Medicine, Natick, MA
Address for correspondence: Bradley C. Nindl, Ph.D., 15 Kansas St., Building42, Natick, MA 01760; E-mail: email@example.com.
Submitted for publication March 2008.
Accepted for publication September 2008.