The anabolic actions of GH in GH-deficient adults and children are well documented. Replacement with GH in such individuals promotes protein synthesis and reduces irreversible loss of protein through oxidation. Although GH is known to be self-administered by athletes, its protein metabolic effects in this context are unknown. This study was designed to determine whether 4 wk of high dose recombinant human GH (r-hGH) administration altered whole body leucine kinetics in endurance-trained athletes at rest and during and after 30 min of exercise at 60% of maximal oxygen uptake. Eleven endurance-trained male athletes were studied, six randomized to receive r-hGH ( mg/), and five to receive placebo. Whole body leucine turnover was measured at rest and during and after exercise, using a 5-h primed constant infusion of 1-[(13)C]leucine, from which rates of leucine appearance (an index of protein breakdown), leucine oxidation, and nonoxidative leucine disposal (an index of protein synthesis) were estimated. Under resting conditions, r-hGH administration increased rate of leucine appearance and nonoxidative leucine disposal, and reduced leucine oxidation (P < ). This effect was apparent after 1 wk, and was accentuated after 4 wk, of r-hGH administration (P < ). During and after exercise, GH attenuated the exercise-induced increase in leucine oxidation (P < ). There were no changes observed in placebo-treated subjects compared with the baseline study. We conclude that GH administration to endurance-trained male athletes has a net anabolic effect on whole body protein metabolism at rest and during and after exercise.
The recent appearance of teriparatide (TRPT) for the anabolic treatment of severe osteoporosis reopens the need to explain some points in relatinship with its use associated with antirresorptive drugs. Osteoporotic women treated with alendronate (ALN) or raloxifene (RLX) maintain their capacity to respond to treatment with TRPT, although those pretreated with RLX have BMD gains similar to those expected in women without previous treatment, while the response of those pre-treated with ALN is more delayed and limited, although not abolished. Combined treatment with ALN and PTH (in women) or TRPT (in men) does not have any synergic effect, although the response on the lumbar BMD is greater than that of ALN alone. On the femoral neck, the combined use of ALN reduces the apparent loss of BMD evaluated by DXA. On the contrary, the combined use of ALN lessens the effect of anabolic treatment on the remodeling markers and volumetric BMD. In men previously treated with TRPT for 18 months, discontinuation of treatment causes loss of lumbar BMD close to 4% in one year, while immediate treatment with ALN induces an additional gain of 5% in the same period. In osteoporotic women treated with PTH for one year, later and immediate treatment with daily ALN causes an important additional gain of BMD that almost doubles that obtained with PTH. One way or the other, absence of data on fractures makes it impossible to clarify definitively the doubts regarding the efficacy of the association of antiresorptive and anabolic treatments.