Background: Growth hormone (GH) replacement in adult GH-deficient (GHD) patients is reported to have a long-term beneficial effect on muscle mass and function, these effects being greater in young males and in adult-onset compared with those with childhood-onset GHD. To date, more discordant data are reported on the degree of muscle impairment in untreated GHD patients, due to the large heterogeneity of this syndrome.
Methods: Muscle maximum total isotonic strength (ST), lower limb maximum power output (W), maximum aerobic capacity (VO(2)max) and body composition (by tetrapolar bio-impedentiometry) were evaluated in seven short-stature adults with childhood-onset GHD and in seven age-matched normal-stature controls with comparable lifestyle and daily physical activity.
Results: Significant differences were found in body composition between control subjects and GHD patients, who presented higher adiposity (mean BMI+/-SD: GHD, 27.8+/-5.8 kg/m(2); controls, 22.1+/-0.8 kg/m(2); p=0.047), larger fat mass (GHD, 21.8+/-10.7 kg; controls, 8.8+/-3.5 kg; p=0.008), and lower fat-free mass (GHD, 65.8+/-11.4 %; controls, 87.0+/-6.5 %; p=0.002). In absolute terms, GHD patients attained significantly lower values in ST (GHD, 2479+/-493 N; controls, 4578+/-1476 N; p=0.008), W (GHD, 1092+/-452 W; controls, 1910+/-781 W; p=0.035) and VO(2)max (GHD, 1.68+/-0.40 l/min; controls, 2.67+/-0.84 l/min; p=0.035) than those attained by controls. The differences were still evident when the results were normalized by unit body mass, whereas they disappeared when the parameters were expressed per unit fat-free mass, suggesting for these patients the presence of an intrinsic muscle function in the same range as that of control subjects.
Conclusions: Middle-aged and short-stature adults with childhood-onset GHD, who received discontinuous pit-GH substitution therapy only during childhood and have uncorrected long-lasting GHD, still retain a normal intrinsic muscle capability in attaining isotonic strength, generating anaerobic power as well as accomplishing oxidative processes. Nonetheless, it is not known which age-dependent evolution in motor dysfunction could be expected in this subgroup of GHD patients, when ageing processes add up to hormonal deficiencies.