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Different Impairment of Muscle Strength in Adults with Childhood-Onset and Acquired GH Deficiency

Istituto Auxologico Italiano IRCCS, Milano, Italy Marco Narici Istituto di Tecnologie Biomediche Avanzate CNR, Milano, Italy Roberto Bottinelli Istituto di Fisiologia Umana Università di Pavia, Italy

We have read with interest the paper by Johansson et al. (1), concerning the positive effects exerted by GH treatment on isometric and isokinetic muscle strength in GH-deficient adults.

Because muscle mass is lower in adults with GH deficiency (GHD), and strength and power are proportional to muscle cross-sectional area (CSA) (2), it is expected that lower "absolute" force values, i.e. not normalized for muscle CSA, are found in GHD patients.

In agreement with previous reports (2, 3, 4), Johannsson et al. (1) actually found reduced isometric muscle strength compared with a group of healthy controls. These authors argue that a large variability in force/CSA exists in the literature, therefore questioning the validity of this parameter. Although it is true that variability in this parameter does exist, it has been shown (5) that these individual variations only exist if CSA is incorrectly measured, muscle voluntary activation is submaximal, and/or force is not measured at the optimum joint angle. In fact, once the CSA is correctly measured (physiological rather than anatomical CSA) and maximum voluntary contractions are truly maximal, the resulting values of force/CSA show good agreement with data on isolated animal muscle or human parallel-fibred muscle, in which the anatomical CSA corresponds to the physiological CSA.

The approach to use "absolute" values of force for comparison between patients and controls, although widely used in clinical studies, can be considered just acceptable in patients with normal body dimensions (i.e. height, weight, and BMI perfectly comparable with those of controls), but it is open to criticism in short-statured adults with childhood-onset GHD.

Once "absolute" quadriceps and hand-grip strengths are normalized for CSA, no differences are found between adults with childhood-onset GH deficiency (GHD) and controls (2, 6), thus suggesting that reduced muscular size and strength are likely attributed to a simple dimensional scaling.

Therefore, the discrepancy between our results (2, 6) and those reported by Johannsson et al. (1) is likely the result of the different populations (mixed population, especially acquired GHD in the Swedish study vs. childhood-onset in our works) compared with the use of force values normalized for CSA in our studies, other than to the higher percentage of multiple hormonal defects in their study population.

We believe that differences between childhood-onset and acquired syndrome might be more evident than previously believed; thus separate data analysis between patients with so different clinical histories and duration of GH-IGF-I lack seems essential.

Adults with childhood-onset GHD, lacking GH during the period of maximal growth, might fit better to the lack of GH than adults with acquired GHD. The latter, having normally developed body size with reduced muscle mass and strength, might undergo more dramatic consequences of muscle mass decrease than the former, who have a proportional decrease in body size, muscle mass and strength.

Patients with childhood-onset and acquired GHD might differ also as far as fiber-type proportion is concerned. In this respect, Rutherford et al. (3) provided some indirect evidence, based on lower half-relaxation time and rightward shift of force-frequency relation of quadriceps muscle, supporting the presence of a higher proportion of fast twitch, type 2 muscle fibers in acquired GHD patients. However, in a recent study in which direct measurements were performed on vastus lateralis biopsy samples, we demonstrated that fiber type distribution (i.e. myosin heavy chain isoform composition) and type 1 and 2A muscle fiber CSA/height² in adults with childhood-onset GHD are not different from controls (7).

Therefore, what seems particularly relevant are the considerable differences between skeletal muscle structural and functional features of patients with childhood-onset and acquired GHD. These differences warrant attention and should be the focus of future investigation.

Footnotes

Received October 21, 1997. Address correspondence to: Alessandro Sartorio, MD, Endocrine Unit, Italian Institute for Auxology, Via Ariosto 13, 20145 Milan, Italy.

References

1. Johannsson G, Grimby G, Sunnerhagen KS, Bengtsson BA. 1997 Two years of growth hormone (GH) treatment increase isometric and isokinetic muscle strength in GH-deficient adults. J Clin Endocrinol Metab. 82:2877–2884.[Abstract/Free Full Text]
2. Sartorio A, Narici M. 1994 Growth hormone (GH) treatment in GH-deficient adults: effects on muscle size, strength, and neural activation. Clin Physiol. 14:527–537.[Medline]
3. Cuneo RC, Salomon F, Wiles CM, Hesp R, Sonksen PH. 1991 Growth hormone treatment in growth hormone-deficient adults. I. Effects on muscle mass and strength. J Appl Physiol. 70:688–694.[Abstract/Free Full Text]
4. Rutherford OM, Beshyah SA, Schott J, Watkins Y, Johnston DG. 1995 Contractile properties of the quadriceps muscle in growth hormone-deficient hypopituitary adults. Clin Sci. 88:67–71.[Medline]
5. Narici M, Landoni L, Minetti AE. 1992 Assessment of human knee extensor muscles stress from in vivo physiological cross-sectional area and strength measurements. Eur J Appl Physiol. 65:438–444.[CrossRef]
6. Sartorio A, Narici M, Conti A, Monzani M, Faglia G. 1995 Quadriceps and hand-grip strength in adults with childhood-onset growth hormone deficiency. Eur J Endocrinol. 132:37–41.[Abstract/Free Full Text]
7. Bottinelli R, Narici M, Pellegrino MA, et al. Contractile properties type distribution of quadriceps muscles in adults with childhood-onset growth hormone deficiency. J Clin Endocrinol Metab. In press.

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