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The Journal of Clinical Endocrinology & Metabolism 86(10):4765– 4770
Copyright © 2001 by The Endocrine Society
GH Is Needed for the Maturation of Muscle Mass and
Strength in Adolescents
LENA HULTHÉN, BENGT-ÅKE BENGTSSON, KATHARINA STIBRANT SUNNERHAGEN,
LEIF HALLBERG, GUNNAR GRIMBY, AND GUDMUNDUR JOHANNSSON
Research Centre for Endocrinology and Metabolism (G.J., B.-Å.B.), Department of Clinical Nutrition (L.Hu., L.Ha.), and
Department of Rehabilitation Medicine (K.S.S., G.G.), Sahlgrenska University Hospital, SE-413 45 Göteborg, Sweden
The postpubertal period and the early years of adulthood may
be of importance for continuing tissue maturation of importance in adulthood and aging. An example of this is the peak
bone mass. This study has evaluated the importance of GH for
lean mass and muscle strength in adolescents and young
adults. GH treatment was discontinued in 40 adolescents aged
16 –21 yr with GH deficiency of childhood onset. Measurements of isometric and isokinetic knee-extensor and flexor
strength, handgrip strength, lean body mass, fat-free mass,
and total body nitrogen were performed annually for 2 yr. Two
hundred fifty healthy adolescents were randomly selected for
prospective measurements of lean mass and handgrip
strength between the ages of 17 and 21 yr. In the adolescents
with continuing GH deficiency, lean body mass decreased,
compared with the patients defined as having sufficient endogenous GH. The isometric strength in knee flexors in-
D
URING PUBERTY, LEVELS of sex steroids and GH
increase markedly and interact in a complex manner
(1). During this period longitudinal bone and tissue growth
reaches its peak (2, 3). Whether the influence of GH and sex
steroids can explain all features of the pubertal development
is not known.
The postpubertal period and the early years of adulthood
may be of importance for tissue maturation with slower
changes than during puberty but of importance for adulthood and aging. The best example of this is the peak bone
mass that occurs sometime between the postpubertal years
and the third to fourth decade of life (2, 4, 5), which is of
importance for the bone density and fracture risk in adults.
That GH may be of importance for the attainment of peak
bone mass is supported by reduced bone mineral density in
young adults with childhood-onset GH deficiency (6).
Cross-sectional studies indicate that peak muscle strength
occurs between 20 and 30 yr of age (7, 8). Indirect evidence
that GH may be of importance in this development is the
reduced muscle mass and strength found in young adults
with GH deficiency (9). Moreover, there is an association
between the increase in lean body mass and bone mass in
children (10). Both the continuing consolidation of bone and
maturation of muscle in young adults are therefore of importance in the decision of whether to continue GH replacement during the transition between childhood and adulthood in adolescents with GH deficiency.
Abbreviations: DXA, Dual-energy x-ray absorptiometry; GHD, GH
deficiency; GHS, GH sufficiency.
creased in the sufficient endogenous GH group and was unchanged in the GH deficiency group during the 2 yr off GH
treatment (between group, P < 0.05). The mean and peak
handgrip strength increased on average by 9 –15% in the group
with sufficient endogenous GH and was unchanged in those
with GH deficiency (P < 0.05). Lean body mass and handgrip
strength (both, P < 0.001) increased in both the healthy boys
and girls who were followed for 4 yr with a more marked
increase in the boys. The mean increase in handgrip between
the age of 17 and 21 yr was 7–9%. The increased lean mass and
improved muscle performance seen in healthy adolescents
did not occur in adolescents with GH deficiency. These findings suggest that GH is of importance for the maturation of
lean mass and muscle strength in adolescents and young
adults. (J Clin Endocrinol Metab 86: 4765– 4770, 2001)
The aim of this prospective trial was to study the longitudinal development of muscle strength and lean tissue in
adolescents and the impact of GH on these measurements.
Adolescents discontinuing GH treatment since childhood
were followed for 2 yr, and a large cohort of healthy control
adolescents was followed annually for 4 yr.
Subjects and Methods
Patients
Forty adolescent patients on GH-promoting treatment were recruited
for the study as previously described (11). In short, the criteria for
inclusion were GH deficiency of childhood onset. They should have
received GH treatment for the past three consecutive years and were
otherwise being considered to end treatment. Most subjects had idiopathic and isolated GH deficiency and 12 subjects had organic hypothalamic/pituitary disease (Table 1). Patients with other anterior pituitary hormone deficiencies received, when required, stable replacement
therapy with glucocorticoids (7), thyroid hormone (12), and gonadal
steroids (10). The mean daily dose of cortisone acetate and T4 was 21 mg
(range 15–20) and 0.12 mg (range 0.05– 0.2), respectively. All other hormone replacement was kept stable 3 months before entering the study
and throughout the study period. There was no patient in the hypopituitary group that had visual impairment or a physical disability that
could impair on daily physical activity.
During a stabilizing period of 3 months, all the patients received a
standardized GH dose of 0.03 mg/kg per day. After a baseline visit at
which all the physical, laboratory, and body composition examinations
were performed, GH treatment was discontinued. The patients were
then reexamined with the same protocol once a year for 2 yr. The studies
included measurement of knee-extensor and flexor strength for isometric and isokinetic contractions, handgrip strength, and dual-energy x-ray
absorptiometry (DXA). The metabolic aspects have been presented elsewhere (11).
On the basis of the results of the GH secretion assessments, the
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J Clin Endocrinol Metab, October 2001, 86(10):4765– 4770
Hulthén et al. • Muscle Strength and GH in Adolescents
TABLE 1. Clinical characteristics of the 40 GHD and GHS adolescents who discontinued GH treatment
Variable
All patients
GHD
GHS
Gender (men/women)
Age (yr)
Age at GH start (yr)
Body height (m)
Cause of pituitary deficiency
Idiopathic
Acute lymphatic leukemia
Brain tumor
Other
31/9
19 (16 –21)
11 (2–16)
1.72 (1.54 –1.85)
17/4
19 (16 –21)
11 (6 –15)
1.74 (1.61–1.83)
15/4
19 (17–21)
12 (2–16)
1.70 (1.54 –1.85)
28
3
5
4
Values are means, with ranges in parentheses.
subjects were retrospectively classified into two groups as previously
described (11): a GH-deficient (GHD) group in which continued severe
adult GHD was identified, and a GH-sufficient (GHS) group. Thus, 21
patients were classified as GHD and 19 as GHS. These two patient
groups were similar in terms of the average daily dose of GH during the
past 2 yr before entering the study. The period of GH treatment was,
however, longer in the GHD group (9 yr; range 4 –15 vs. 7 yr; range 3–16
yr; P ⫽ 0.04) and the prospective evaluation of age at onset of puberty
was somewhat lower in the GHD group (13 vs. 14 yr).
Healthy population
A cohort study of a representative group of 1244 adolescents, 620 boys
and 624 girls, was performed in 1994 in Göteborg, Sweden. Data were
originally collected to gather baseline information on iron status in
Swedish adolescents before the general iron fortification of white wheat
flour was removed. Adolescents, 15–16 yr old in different socioeconomic
areas in Göteborg, were selected to be representative for the population
according to a socioeconomic index. Information about food habits and
health status in this population will be presented elsewhere.
From the original study group of 1244 adolescents, a subgroup of 250
boys and girls was randomly selected for further measurements. Out of
this subgroup, 237 (95%) adolescents (137 girls and 100 boys) agreed to
participate (12). This group was followed annually for 4 yr between the
age of 17 and 21 yr with measurements of DXA and handgrip strength.
Methods
Muscle function. Knee-extensor and flexor strength for isometric contraction at a knee angle of 60 degrees (␲ g/3 rad), for isokinetic concentric
muscle action at angular velocities of 180 degrees/sec (␲ g rad/sec) and
local muscle endurance in quadriceps was measured using a Kin-Com
dynamometer (Chattecx Co., Chattanooga, TN) as previously described
(13). The methodological error for duplicate measurements for isometric
muscle strength, isokinetic muscle strength at an angular velocity of
180 degrees/sec, and local muscle endurance was 9%, 8%, and 1.4%,
respectively (14).
Right and left handgrip strength was measured using an electronic
grip force measurement instrument (Grippit, AB Detector, Göteborg,
Sweden), which measures the maximum momentary force and the mean
force over a set period of 10 sec in Newton using the same method and
set-up as previously described (15). The methodological error between
duplicate determinations has been shown to be 4.4 –9.1% (16). Verbal
instructions were given to encourage maximal force production. All
measurements in patients (M.H.) and controls (S.L.) were performed by
the same study technician.
Body composition. Body weight was measured in the morning to the
nearest 0.1 kg with the subject wearing indoor clothing, and body height
was measured barefoot to the nearest 0.01 m.
Lean body mass was determined using DXA. The Lunar Corp.-DPX-L
(Lunar Corp., Madison, WI) was used in the patients and the 2000 Plus
(Hologic, Inc., Waltham, MA) in the controls. Precision error (1 sd) on
the Lunar Corp.-DPX-L as determined from double examinations of 10
healthy subjects was 0.7% for lean body mass.
Total body potassium was measured by counting the emission of 1.46
MeV ␥ radiation from the naturally occurring 40K isotope in a highsensitive 3ğ whole-body counter with a coefficient of variation of 2.2%.
Body cell mass was calculated on the assumption that there is a constant
intracellular potassium/nitrogen ratio of 3 mmol of potassium per gram
of nitrogen and a protein content equal to 25% of the body cell mass.
Total body nitrogen was measured by in vivo neutron activation. This
method is based on the capture of low-energy (thermal) neutrons by N
nuclei. A Cf source was used to produce the neutrons. The patients were
irradiated from below by a 15 cm ⫻ 50 cm rectangular neutron field. The
measurement error is approximately ⫾4%.
Ethics
Informed consent was obtained from all patients. The Ethics Committee at the Faculty of Medicine, Göteborg University, approved the
study.
Statistical analysis
All descriptive statistical results are presented as the mean and sem
or the mean and a 95% confidence interval. A two-stage method was
used for statistical analysis (17), which means that the repeated measurements from each patient were reduced to one summary variable,
reflecting the within-individual change with time. In the present study,
the coefficient of the slope (␤) for the estimated individual regression line
was chosen as the summary variable, using each effect variable as a
dependent and time as an independent variable. A t test was used to test
effect of treatment and differences among subgroups of patients. Correlations were sought by calculating Pearson’s linear correlation coefficient. Significance was obtained if the two-tailed P value was 0.05 or
less.
Results
Four patients were not followed for 2 yr. One man was not
interested in further investigations after the baseline visit,
and two women and one man with severe GHD withdrew
from the study as a result of psychological symptoms. Fifteen
healthy controls with only one baseline measurement at the
age of 16 yr were excluded from the analysis.
Patients discontinuing GH
Body weight increased in the GHS patient group from
64.7 ⫾ 2.7 at baseline to 68.1 ⫾ 3.5 kg after 2 yr (P ⬍ 0.01) and
not in the patients with continuing GHD into adulthood. This
increase was associated with unchanged fat-free mass, lean
body mass (Fig. 1A) and total body nitrogen in the GHS
group. In the GHD group, however, fat-free mass decreased
from 56.2 ⫾ 2.3 at baseline to 51.6 ⫾ 2.2 kg (P ⫽ 0.009) at 2
yr, lean body mass decreased from 50.7 ⫾ 1.9 to 46.9 ⫾ 1.7
kg (P ⫽ 0.002) (Fig. 1A), and total body nitrogen decreased
from 1.95 ⫾ 0.10 to 1.64 ⫾ 0.06 kg (P ⫽ 0.009). The mean
individual time response in these measurements were different between the two patient groups (fat-free mass, P ⫽
Hulthén et al. • Muscle Strength and GH in Adolescents
J Clin Endocrinol Metab, October 2001, 86(10):4765– 4770 4767
fatigue index tended to deteriorate in both groups during the
period of observation.
The mean right and left peak (data not shown) and mean
handgrip strength over a period of 10 sec demonstrated a
between-group difference with time (Fig. 1B). Thus, the mean
and peak handgrip increased on average by 9 –15% in the
GHS group and was unchanged in the adolescents with
continuing GHD.
In the GHD group, the change in lean body mass correlated with the changes in isometric knee extensor strength
(r ⫽ 0.66; P ⫽ 0.003), isokinetic knee extension (r ⫽ 0.86; P ⬍
0.001), and flexion strength (r ⫽ 0.62; P ⫽ 0.006). Similar
correlations were observed in the GHS group with an additional correlation between the change in lean body mass
and isometric knee extensor strength (r ⫽ 0.70; P ⬍ 0.001). A
correlation between the changes in lean body mass and handgrip strength was seen in the GHD subjects (r ⫽ 0.62 to 0.65;
P ⬍ 0.01) and not in the GHS group.
Healthy adolescents
FIG. 1. Box plot demonstrating mean (⫾ SEM and ⫾ SD) individual
change in lean body mass (LBM) (A) and peak handgrip strength (B)
in 21 adolescents with continuing GHD into adulthood, 19 adolescents
defined as having GHS and 223 adolescent controls followed for 2 and
4 yr, respectively. ␤ is the estimated mean within individual change
with time. *, P ⱕ 0.05; ***, P ⬍ 0.001, compared with the GHD group.
0.04; lean body mass, P ⫽ 0.03, and total body nitrogen, P ⫽
0.009).
Muscle performance (Table 2)
In the GHD adolescents, the isometric strength in knee
extensors and knee flexors did not change during the 2-yr
period after GH treatment was discontinued. The concentric
muscle strength during knee flexion at an angular velocity of
180 degrees/sec decreased and a similar tendency for concentric knee extension at an angular velocity of 180 degrees/
sec was found. The GHS adolescents increased their isometric knee flexor strength during the 2-yr period with a similar
tendency for the isometric knee extensors. A between-group
difference in the mean individual change with time was
observed in isometric knee flexors and a similar tendency
was observed in concentric knee flexion strength at an angular velocity of 180 degrees/sec (P ⫽ 0.08) demonstrating
improved muscle strength in the GHS group, compared with
the GHD group. The local muscle endurance expressed as the
The healthy group of adolescents was followed over a
period of 4 yr (Table 3). During that period of time, the body
weight increased. This increase was partly explained by an
increase in lean mass (Fig. 1A). Moreover, the handgrip
strength, both measured as peak torque (Fig. 1B) and mean
torque over a period of 10 sec, increased. The mean increase
between the age of 17 and 21 yr was 7–9%. Similar results
were found whether analyzing the changes between 19 and
21 yr or when the entire period was included.
Both girls and boys between the age of 17 and 21 yr demonstrated this increase. The boys, however, demonstrated a
more marked increase in body weight, lean mass, and handgrip strength (Fig. 2). No correlation was seen between the
increase in lean body mass and the increase in handgrip
strength in the girls, whereas positive correlations were observed in the boys (r ⫽ 0.25– 0.33; P ⬍ 0.05).
Discussion
Adolescents with childhood-onset GHD and continued
severe GHD into adulthood lost body nitrogen and lean body
mass with unchanged muscle strength when GH replacement was discontinued. Prospective data from a large group
of randomly selected healthy adolescents at similar ages as
the patients demonstrated, however, increased lean body
mass and muscle strength. The expected improvement in
muscle performance with time therefore did not occur in
adolescents with GHD.
The highest daily GH production rate is seen in late puberty, and after the age of 18 –25 yr, there is an exponential
fall in the mean 24-h GH secretion continuing into middle
years of life with an accompanying fall in serum IGF-I levels
(18). This fall in GH levels has been postulated to be of
importance for the sarcopenia of aging (19). This has, however, been questioned because short-term GH treatment of
healthy aging volunteers has not been able to restore muscle
function (20, 21). This trial has addressed the question of
whether GH is of importance for muscle mass and function
in early adulthood.
This is the first prospective long-term study of muscle
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J Clin Endocrinol Metab, October 2001, 86(10):4765– 4770
Hulthén et al. • Muscle Strength and GH in Adolescents
TABLE 2. Measurements of isometric (knee angle of 60 degrees) and isokinetic peak torque (Nm) at angular velocity of 180 degrees/sec
for knee extension and flexion, fatigue index, and handgrip strength (N) in 21 adolescent GHD and 19 GHS patients discontinuing GH
treatment at final height
Variable
Knee extension
Isometric
GHD
GHS
Concentric 180°/sec
GHD
GHS
Knee flexion
Isometric
GHD
GHS
Concentric 180°/sec
GHD
GHS
Fatigue index
GHD
GHS
Handgrip, right
Peak
GHD
GHS
Average 10 sec
GHD
GHS
␤ (95% CI)a
Baseline
1 yr
2 yr
P
202 ⫾ 12
199 ⫾ 9
196 ⫾ 13
207 ⫾ 13
199 ⫾ 15
209 ⫾ 13
⫺1.78 (⫺4.9 –1.34)
5.08 (1.16 –9.0)
0.6
0.2
120 ⫾ 7
125 ⫾ 7
113 ⫾ 8
124 ⫾ 8
113 ⫾ 8
124 ⫾ 8
⫺3.56 (⫺5.47–⫺1.65)
⫺0.17 (⫺2.43–2.09)
0.08
0.9
95 ⫾ 7
81 ⫾ 5
86 ⫾ 5
86 ⫾ 5
90 ⫾ 6b
89 ⫾ 6
⫺2.52 (⫺4.69 –⫺0.35)b
4.06 (2.48 –5.64)
0.3
0.02
67 ⫾ 4
61 ⫾ 5
62 ⫾ 3
60 ⫾ 4
59 ⫾ 3
61 ⫾ 4
⫺3.67 (⫺5.18 –⫺2.16)
⫺0.11 (⫺1.36 –1.14)
0.03
0.9
33 ⫾ 3
37 ⫾ 3
34 ⫾ 3
35 ⫾ 2
36 ⫾ 3
41 ⫾ 2
1.75 (⫺0.14 –3.64)
2.08 (1.06 –3.1)
0.08
0.06
410 ⫾ 27
392 ⫾ 24
412 ⫾ 25
414 ⫾ 27
411 ⫾ 23
445 ⫾ 29
0.56 (⫺6.89 –7.5)b
26.3 (20.3–32.3)
367 ⫾ 26
331 ⫾ 22
358 ⫾ 22
350 ⫾ 22
360 ⫾ 22
380 ⫾ 25
⫺3.22 (⫺9.67–3.23)b
24.5 (18.2–30.8)
0.9
⬍0.001
0.6
0.001
Values are means ⫾ SEM. ␤ is the estimated coefficient of the slope for the individual regression line reflecting individual time response.
The P value represents the overall within group change.
a
CI, 95% confidence interval for SEM.
b
P ⬍ 0.05, compared with overall change in the GHS group.
TABLE 3. Body weight and lean body mass measured using DXA and measurements of handgrip strength (Newton; N) in randomly
selected 100 male and 122 female adolescents between the ages of 17 and 21 years
Variable
Age 17
Age 18
Age 19
Age 21
Mean ␤ (95% CI)a
P
Body weight (kg)
Lean body mass (kg)
Handgrip strength, right
Peak
Average during 10 sec
Handgrip strength, left
Peak
Average during 10 sec
63.9 ⫾ 0.8
45.4 ⫾ 0.7
66.0 ⫾ 0.8
46.6 ⫾ 0.7
67.0 ⫾ 0.8
46.8 ⫾ 0.7
68.7 ⫾ 0.9
47.3 ⫾ 0.7
1.37 (1.25–1.49)
0.55 (0.49 – 0.61)
⬍0.001
⬍0.001
399 ⫾ 8
358 ⫾ 8
399 ⫾ 8
359 ⫾ 8
412 ⫾ 8
370 ⫾ 8
427 ⫾ 9
387 ⫾ 9
8.6 (7.4 –9.8)
8.5 (7.4 –9.6)
⬍0.001
⬍0.001
358 ⫾ 7
319 ⫾ 7
366 ⫾ 8
327 ⫾ 8
379 ⫾ 8
335 ⫾ 8
390 ⫾ 9
347 ⫾ 8
10.4 (9.1–11.7)
8.8 (7.5–10.1)
⬍0.001
⬍0.001
Values are means ⫾ SEM. ␤ is the estimated coefficient of the slope for the individual regression line reflecting individual time response.
The P value represents the overall within group change.
a
CI, 95% confidence interval for SEM.
strength in young adulthood. It demonstrates continuing
increase in handgrip strength in both boys and girls between
19 and 21 yr of age, which is in agreement with previous
cross-sectional studies, which suggested that peak isometric
and dynamic muscle strength occurs in the ages between 20
and 30 yr (7, 8). In boys there is a marked increase in muscle
strength through the years of puberty, whereas girls experience an almost linear increase in muscular strength with
chronological age, until about 15 yr of age (3, 22) despite a
marked increase in the GH secretion during puberty. Our
data suggest that there is a further slow increase into the
second decade of life in both females and males. This increase
did not occur in the adolescents who continued to lack GH
into adulthood, which indicates that GH is of importance for
the continuing increase in muscle mass and muscle strength
after puberty. That the increase in lean body mass and handgrip strength was more marked in the young men than in the
women suggests that sex steroids or the interplay between
sex steroids and GH is still of importance in early adulthood.
The peak gain in muscle mass and the peak gain in muscle
strength occur within 1 yr of peak height velocity, supporting
the role of sex steroids and GH on development of muscle
mass and function (3). In a cross-sectional study of children
and young adults aged 4 –26 yr, lean body mass increased
until the age of 16.6 and 13.4 yr in males and females, respectively (23). This is in contrast with this longitudinal
study that shows a continuing increase of lean body mass in
both healthy boys and girls between 19 and 21 yr of age.
Muscle strength is closely associated with muscle mass (24)
although neural activation, contractile properties, and force
transmission is also of importance for the individual variation in muscle strength. These properties are, however, not
affected by puberty (25). In our study a close correlation was
found between the increase in lean body mass and the in-
Hulthén et al. • Muscle Strength and GH in Adolescents
FIG. 2. Box plot demonstrating mean (⫾ SEM and ⫾ SD) individual
change in lean body mass (LBM) (A) and peak handgrip strength (B)
in 100 male and 122 female randomly selected adolescents followed
for 4 yr between the age of 17 and 21 yr. ␤ is the estimated mean within
individual change with time. ***, P ⬍ 0.001, compared with the female
adolescents.
crease in muscle strength, suggesting in the analogy with the
changes in muscle mass and strength in puberty that peak
muscle mass and peak muscle strength are achieved at a
similar age.
The loss of lean body mass in the GHD group was expected
and in accordance with two previous smaller trials also demonstrating unchanged isometric quadriceps strength 12
months (26) and 2 yr (27) after GH treatment was discontinued in young adults with GH deficiency. In our study,
both the large control group and the patients defined as
having sufficient GH secretion demonstrated a small longitudinal increase in lean body mass and muscle strength that
may be of importance for the attainment of peak muscle
strength. Such changes did not occur in the GHD group
suggesting that the presence of GH is needed for normal
maturation of muscle mass and muscle function in the postpubertal years and in early adulthood.
Bone mass is associated with muscle mass both in children
(10) and adults (28). The increase in muscle mass and muscle
strength may therefore be of importance in the attainment of
J Clin Endocrinol Metab, October 2001, 86(10):4765– 4770 4769
peak bone mass, which in turn affects the fracture risk in
adults. Adequate levels of GH during puberty and the years
thereafter may therefore influence peak bone mass, both
through direct actions on bone and indirect through muscle
mass and muscle strength.
Similar results were obtained for isometric and isokinetic
muscle strength during knee extension and knee flexion although not as clear as for handgrip strength. Some data
indicate that muscle groups may mature differently. For
example, no clear adolescent spurt occurs in trunk strength
and abdominal muscle endurance whereas this is observed
in upper and lower body strength (3). Other plausible explanations are that the methodological error in the measurement of handgrip strength is lower and that handgrip is less
influenced by environment and physical activity than lower
body muscle strength.
We cannot exclude the possibility that the changes seen in
lean body mass and muscle strength were indirect through
different changes in physical activity among the study
groups. A study of 1,069,556 18-yr-old boys from the Military
Service Conscription Registry in Sweden demonstrated increased body weight and decreased physical performance
between the years 1969 and 1994 (Hulthén, L., personal communication) that does not support increased physical activity
in the GH sufficient group and healthy controls. Also, the
tendency for increased fatigue index in both patient groups
suggests that different physical activity in the patients group
is not responsible for the findings in this study. We know,
however, that GHD affects well-being (29) and may cause a
more sedentary lifestyle (30).
This study demonstrates that young adults/adolescents
with GHD lose lean body mass and do not gain muscle
strength, compared with healthy subjects in the same age,
when their GH treatment is discontinued. This clearly suggests that GH in adolescence and in young adulthood is of
importance for the maturation of muscle mass and muscle
strength, which in turn may be of importance for the attainment of peak muscle strength and peak bone mass. Whether
reduced GH secretion may explain the loss of bone mass and
lean mass in aging remains to be proven. Our observation is
of importance for adolescents with continuing GHD into
adulthood whom usually discontinue GH treatment at final
height.
Acknowledgments
We are indebted to Sigrid Lindstrand at the Research Center for
Endocrinology and Metabolism for invaluable contribution during the
testing of the healthy adolescents and to Marita Hedberg of the Department of Rehabilitation Medicine for excellent assistance during the
muscle tests of the patients. We also acknowledge the important contribution of Ingrid Hansson, Lena Wirén, and Anne Rosén and of the
Research Center for Endocrinology and Metabolism.
The Swedish Study Group for Growth Hormone Treatment in Children was responsible for referring the GH-treated children into this
study. This group consists of: Kerstin Albertsson-Wikland, Jan Alm,
Stefan Aronson, Jan Gustafsson, Lars Hagenäs, Anders Häger, Sten
Ivarsson, Berit Kriström, Claude Marcus, Christian Moëll, Karl-Olof,
Nilsson, Martin Ritzén, Torsten Tuvemo, Ulf Westgren, Otto Westphal,
and Jan Åman.
4770
J Clin Endocrinol Metab, October 2001, 86(10):4765– 4770
Received March 26, 2001. Accepted June 18, 2001.
Address all correspondence and requests for reprints to: Gudmundur
Johannsson, M.D., Ph.D., Research Center for Endocrinology and Metabolism, Sahlgrenska University Hospital, se-413 45 Göteborg, Sweden.
E-mail: [email protected].
This work was supported by grants from the Swedish Medical Research Council (Project No. 11621).
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