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The Journal of Clinical Endocrinology & Metabolism Vol. 86, No. 4 1839
Copyright © 2001 by The Endocrine Society


Letters to the Editor

Physical Performance in Growth Hormone- Deficient Adults

Alessandro Sartorio, Claudio Lafortuna and Marco V. Narici

Istituto Auxologico Italiano (A.S.), IRCCS, 20145 Milano, Italy; Istituto Tecnologie Biomediche Avanzate (C.L.), CNR, 20090 Milano, Italy; and Department of Exercise and Sport Science (M.V.N.), Metropolitan University of Manchester, Alsager, United Kingdom ST7 2HL

To the editor:

We have read with interest the paper by Woodhouse et al. (1), dealing with the evaluation of submaximal aerobic performance in adults with adult-onset GH deficiency (GHD) before and after recombinant GH (rec-GH) treatment.

The authors point out how the perception of increased fatigue and impaired physical performance experienced by these patients derives from a markedly reduced maximal aerobic capacity (VO2max). Thus, even the execution of ordinary daily activities requires a greater fraction of VO2max, imposing to the patients a discomfort out of proportion to their exercise task.

The study by Woodhouse et al. (1) suggests that these changes may be, in part, related to the lack of GH-insulin-like growth factor I actions on muscle mass, because the rec-GH treatment was associated with a marked increase in skeletal muscle insulin-like growth factor I messenger RNA, improving aerobic capacity indices and self-reported fatigue during low-intensity exercise.

A picture thus emerges, in line with a common view (2, 3), of the adult-onset GH-deficient patient as a poor performer, provided with a below normal amount of contractile elements devoted to locomotor tasks and to cardiorespiratory support of exercise.

Our group reached quite different conclusions in studies of short-statured childhood-onset GH-deficient adults, which seem to have a normally "proportioned" contracting machinery (4, 5, 6). In fact, although absolute values of quadriceps strength and fiber cross-sectional area (CSA) of patients were significantly lower than controls (4), differences disappeared once the absolute values were normalized for quadriceps CSA and the subjects’ height. Normal muscle twitch kinetics and fatiguability in the quadriceps of GH-deficient patients were fully consistent with the lack of a significant shift in fiber type proportion (4).

In another recent study from our group (5), analyzing the anaerobic performance of adults with GH deficiency, we concluded that both lactacid and alactacid maximum anaerobic power were similar in controls and patients when absolute differences (35%) were adequately normalized for body mass. These findings indicate that the GH-deficient patients’ ability to sustain anaerobic power and their rate of fatigue were comparable, in relative terms, with those of healthy controls.

Furthermore, as far as the aspects of mechanics and energetics of locomotion (walking and running) are concerned (6), we have clearly demonstrated that patients and healthy controls moved with the same metabolic cost and efficiency of locomotion, provided that walking and running velocities are expressed as Froude number (which takes into account the scale differences between the two groups). Nevertheless, it is noteworthy that our patients with childhood-onset GHD were actually unable to run at speeds higher than 8 km/h-1 for the time needed to reach a metabolic steady state (6). At this maximally attained speed their specific VO2 was about 25 mL/min-1 · kg-1 and their average heart rate was about 180 beats/min-1, which, from their measured resting and age-estimated maximum heart rate, would correspond to about 90% of the maximum, strongly suggesting a a remarkable reduction in VO2 max also in childhood-onset patients with GHD.

The considerable differences between patients with childhood-onset and adult-onset GHD (related to the duration, age of appearance, degree of the disease) make mandatory for the future to analyze separately the data recorded in so different clinical conditions.

Moreover, the apparent discrepancy between the effects of rec-GH on muscle strength (which remained unchanged) and submaximal aerobic performance (significantly improved), as reported by Woodhouse et al. (1), warrant further attention and should be the focus of future studies investigating the effects of rec-GH on muscle.

References

  1. Woodhouse LJ, Asa SL, Thomas SG, Ezzat S. 1999 Measures of submaximal performance evaluate and predict functional response to growth hormone (GH) treatment in GH-deficient adults. J Clin Endocrinol Metab. 84:4570–4577.[Abstract/Free Full Text]
  2. Cuneo RC, Salomon F, Wiles CM, Hesp R, Sonksen PH. 1991 Growth hormone treatment in growth hormone deficient adults. II. Effects on exercise performance. J Appl Physiol. 70:695–700.[Abstract/Free Full Text]
  3. Nass R, Huber RM, Klauss V, Muller OA, Schopohl J, Strasburger CJ. 1995 Effect of growth hormone (hGH) replacement therapy on physical work capacity and cardiac and pulmonary function in patients with hGH deficiency acquired in the adulthood. J Clin Endocrinol Metab. 80:552–557.[Abstract]
  4. Bottinelli R, Narici M, Pellegrino MA, et al. 1997 Contractile properties and fiber type distribution of quadriceps muscles in adults with childhood-onset growth hormone deficiency. J Clin Endocrinol Metab. 82:4133–4138.[Abstract/Free Full Text]
  5. Narici M, Ferretti G, Susta D, Faglia G, Sartorio A. 1999 Maximum anaerobic performance of childhood-onset GH-deficient adults. Growth Horm IGF Res. 9:228–235.[CrossRef][Medline]
  6. Minetti AE, Ardigò LP, Saibene F, Ferrero S, Sartorio A. 2000 Mechanical and metabolic profile of locomotion in adults with childhood-onset GH deficiency. Eur J Endocrinol. 142:35–41.[Abstract]




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