CLINICAL STUDY Mechanical and metabolic profile of locomotion in adults with childhood-onset GH deficiency Alberto E Minetti 1,2,3 , Luca P Ardigo ` 2 , Franco Saibene 3 , Simona Ferrero 4 and Alessandro Sartorio 4,5 1 Exercise and Sport Science, Manchester Metropolitan University, Alsager, UK, 2 CSAM-Ergonomia, Fondazione S Maugeri, IRCCS, Pavia, Italy, 3 Reparto di Fisiologia, ITBA, CNR, Segrate (MI), Italy, 4 Centro per i Disordini della Crescita, LSRE, Istituto Auxologico Italiano, IRCCS, Milan, Italy, and 5 Divisione Malattie Metaboliche, Istituto Auxologico Italiano, IRCCS, Piancavallo (VB), Italy (Correspondence should be addressed to A Sartorio, Laboratorio Sperimentale di Ricerche Endocrinologiche (LSRE), Istituto Auxologico Italiano, IRCCS, Via Ariosto 13–20145 Milan, Italy; Email: sartorio@auxologico.it) Abstract Objective: The aim of the present study was to evaluate the energy cost and the mechanical work of locomotion in a group of adults with childhood-onset GH deficiency (GHD). Subjects: Eight males with childhood-onset GHD (mean age S.D.: 31.7 3.6 years; mean height: 145.1 6.7 cm) and six age-, sex- and exercise-matched normal subjects were studied. Design: GHD patients and healthy controls were requested to walk and run in the speed range of 2–11 km h ¹1 . For each condition, simultaneous mechanical and metabolic measurements were taken. Methods: Oxygen consumption, and mechanical internal and external work of locomotion were evaluated with standard open-circuit respirometryand three-dimensional motion analysis respectively. Results: External work was not significantly different between GHD patients and healthy controls, while internal work was higher for patients at all speeds. In walking, the relationships between both the mechanical energy recovery and the metabolic cost with speed were shifted towards lower speeds in patients. As a consequence, the optimal speed of walking, i.e. the speed at which the cost of locomotion is minimum, was lower for GHD patients. Stride frequency was significantly higher (11.2–11.3%) for GHD patients at all speeds of walking and running. GHD patients were unable to run at speeds higher than 8 km h ¹1 for the time needed to reach a metabolic steady state. Conclusion: It appears that both the mechanics and energetics of locomotion in short-statured adults with childhood-onset GHD are not strikingly different from those of healthy controls, thus demonstrating a substantial ‘normality’ in this group of GHD patients at metabolically attainable speeds. The ‘harmonic’ body structure and the adherence to allometric transformations in these patients do not exclude the possibility of a different metabolic role of GH in normally statured adults with childhood-onset GHD and in those with acquired GHD, taking into account the well recognized heterogeneity of the adult GHD syndrome. European Journal of Endocrinology 142 35–41 Introduction Several studies reported that growth hormone (GH) deficiency (GHD) in adults is associated with reduced maximal isometric muscle strength, muscle size and muscle fibre area (1–6), thereby indicating the impor- tance of GH in adults for the maintenance of muscle mass and strength. The majority of clinical studies, recruiting ‘mixed’ study groups (childhood- and adult-onset GHD), used ‘absolute’ values of strength and power for comparison between controls and patients. Although this choice can be considered acceptable in patients with adult- onset GHD who usually have normal body dimensions (their height, weight and body mass index (BMI) are perfectly matched with those of healthy controls), it appears highly questionable in short-statured adults with childhood-onset GHD. In our experience, once actual quadriceps and hand- grip strengths were normalized for cross sectional area (CSA), no differences were found between adults with childhood-onset GHD and controls (3, 5), thus suggest- ing that reduced muscular size and strength are probably related to a simple dimensional down-scaling rather than to a real impairment of muscle function. Taking into account this statement, differences between childhood- and adult-onset GHD syndrome might be more evident than previously believed; thus, separate data analysis between patients with very different clinical histories and duration of lack of GH–insulin-like growth factor (IGF)-I seems essential. Adults with adult-onset GHD, having normally developed body size with reduced muscle mass and strength, might undergo more dramatic consequences of muscle mass decrease than adults with childhood- onset GHD who, lacking GH during the period of European Journal of Endocrinology (2000) 142 35–41 ISSN 0804-4643 2000 Society of the European Journal of Endocrinology Online version via http://www.eje.org Downloaded from Bioscientifica.com at 08/04/2019 05:15:17PM via free access