ISSN 0362-1197, Human Physiology, 2019, Vol. 45, No. 4, pp. 452–460. © Pleiades Publishing, Inc., 2019.

Russian Text © The Author(s), 2019, published in Fiziologiya Cheloveka, 2019, Vol. 45, No. 4, pp. 127–136.

REVIEWS

Effect of Growth Hormone Administration on the Mass

and Strength of Muscles in Healthy Young Adults:
A Systematic Review and Meta-Analysis
K. V. Sergeevaa, *, A. B. Miroshnikova, and A. V. Smolenskya
aRussian State University of Physical Training, Sports, Youth and Tourism, Moscow, Russia
*e-mail: sergeeva_xenia@mail.ru
Received September 21, 2018; revised October 10, 2018; accepted December 20, 2018

Abstract—The growth hormone (GH) is prohibited for use by athletes, while its anabolic effect on muscle tis-
sue is still debated. The review provides a systematic evaluation of the GH effects on the body composition
and strength parameters in well-trained healthy young subjects. A meta-analysis of published data from ran-
domized controlled trials (RCTs) was performed in accordance with the Preferred Reporting Items for Sys-
tematic Reviews and Meta-Analyses (PRISMA) guidelines. Pooled results of 11 RCTs showed that GH
administration significantly increases the lean body mass (2.72, 95% CI: 2.02; 3.38, p < 0.01), total water con-
tent (1.10, 95% CI: 0.54; 1.66, p < 0.01), and extracellular water (1.78, 95% CI: 1.04; 2.52, p < 0.01) and
reduces the fat mass (–0.67, 95% CI: –0.93; –0.40, p < 0.01) without changing the muscle protein synthesis
rate (0.00, 95% CI: –0.01; 0.02, p = 0.70) and muscle strength (–0.02, 95% CI: –0.05; 0.02, p = 0.36) as com-
pared with placebo. A conclusion was made that GH administration can improve the body composition in
healthy young subject by exerting a significant lipolytic effect without causing hypertrophy of muscle fibers.
The increase in lean body mass is due to an accumulation of extracellular water.

Keywords: growth hormone, meta-analysis

DOI: 10.1134/S0362119719030162

The growth hormone (GH) was broadly used in
sports from the 1980s. In 1989, Olimpic Committee
officially prohibited its use in athletes, but sales of
GH-based drugs have increased several folds over the
past years. Illegal use of GH in elite and recreational
athletes [1] is explained by its ability to increase the
muscle mass and to decrease the fat mass. The idea is
questionable because data on the anabolic effect of
GH originate mostly from studies evaluating replace-
ment therapy with GH-based drugs in patients with
various forms of short stature and GH deficiency [2–
5]. In fact, there is no reliable data to support an ana-
bolic effect of GH in healthy adults. The scientific and
medical communities accept the assumption that GH
is an anabolic hormone without any criticism and
ignore the fact that exogenous GH administration
does not increase the muscle strength in healthy adults
according to the majority of studies, while the muscle
mass increases apparently because water is retained in
large amounts in the body [6]. GH replacement ther-
apy fails to delay senescence, to improve the physical
condition, and to increase the muscle mass and
strength in middle-aged and elderly healthy males
with GH deficiency [7–15]. Moreover, GH is
100 times higher than normal in patients with acro-
megaly, which is due to excess GH production by pitu-
itary tumors, but, in terms of sports parameters, acro-
megalic patients have a low tolerance for training [16],
display mild true muscle hypertrophy, and suffer from
myopathy and atrophy of type II muscle [6]. The
problem is pressing because GH treatment may pres-
ent a severe health hazard and involves risks of danger-
ous side effects, such as hypertension, cancer, and
insulin resistance [17].
The objective of this review is to systematically
evaluate the effects of GH administration on the mus-
cle strength, body composition, and resistance train-
ing-induced muscle hypertrophy in well-trained
healthy young adults.
METHODS
Searching strategy. A systematic search for relevant
trials was performed using MEDLINE, EMBASE,
the Cochrane Database of Systematic Reviews, and
the Cochrane Controlled Register of Trials; covered
the periods from the creation dates of the databases to
August 2018; and included no limitation with respect
to the language or data of publication. Our searching
strategy included the use of a validated filter to identify
randomized trials and a contextual search procedure.
“Growth hormone” and “randomized controlled

452
 EFFECT OF GROWTH HORMONE ADMINISTRATION ON THE MASS AND STRENGTH
trial” were used as queries. In addition, lists of refer-
ences were examined in all original articles and reviews
found. Two independent experts revised the search
results (the titles and abstracts of publications). All
potentially relevant articles were selected and
inspected in full to determine whether they meet the
inclusion criteria accepted in the study. The same
experts independently extracted the data with the use
of standard forms. Discrepancies in selection results
were reconciled via joint discussions.
The inclusion criteria. The meta-analysis included
the randomized placebo-controlled trials, including
crossover trials, that met the following criteria: (a)
subjects lacked health problems; (2) the sample size
was at least 5 subjects; (3) the subjects’ ages were 18–
45 years; and (4) data were reported for at least one of
the clinical outcomes of interest, including body com-
position (lean body mass, body fat mass, total body
water, and extracellular water), muscle strength
parameters (e.g., strength of the biceps brachii muscle,
strength of the quadriceps femoris muscle, or isomet-
ric back strength), and parameters of muscle protein
synthesis (e.g., fractional rate of muscle protein syn-
thesis). A trial was excluded from the meta-analysis if
(1) the aim was exclusively to evaluate the effect of GH
secretion stimulators, (2) the trial included patients
with combined somatic disorders, or (3) GH was eval-
uated as a means to treat a particular disease (e.g., GH
deficiency or fibromyalgia). When results obtained for
one cohort had been reported in several publications,
the data were only once included in the meta-analysis.
Data abstraction. The following data were
extracted from each trial: sample characteristics (age,
sex, body mass index (BMI), and maximal oxygen
uptake (VO2max), intervention characteristics (drug
dose, injection frequency, and treatment duration),
trial quality (design, randomization, and statistical
method), and clinical outcomes.
Evaluation of trial quality (assessment of risk of
bias). Methodical quality of the trials was evaluated
using the Cochrane Collaboration’s tool for assessing
risk of bias [18]. We assessed the use of the following
strategies, which provide for high trial quality: the
methods to allocate the patients to particular arms and
to blind the allocation; blinding of the investigators,
participants, and experts evaluating the outcomes and
analyzing the data; and selected reporting and other
sources of errors that might affect the results (e.g.,
funding sources). Risk of bias was estimated as low,
high, or unclear in each category. Unclear risk of bias
was established when insufficient details and insuffi-
cient information had been provided or when the study
result was known, but its contribution to risk of bias
was unclear.
Statistical analyses of the data. To evaluate the dif-
ferences in outcome, the weighted mean differences
and the corresponding 95% confidence intervals (CI)
for continuous data were calculated using the DerSi-
HUMAN PHYSIOLOGY Vol. 45 No. 4 2019
453
monian and Laird random-effects model, which
makes it possible to estimate the variance among trials.
The heterogeneity of the data was evaluated using the
χ2 and I2 tests for homogeneity [19]. Testing for overall
effect was performed using Z-statistics; the result was
considered significant at two-sided p < 0.05. For each
result, point and interval (95% CI) estimates were
obtained to evaluate the overall effect of intervention.
A sensitivity analysis was carried out for each individ-
ual trial to evaluate its effect on the summary esti-
mates. Testing for publication bias (a systematic error
due to preferential publication of positive results) was
performed by Egger’s test for funnel plot asymmetry
[20].
When different units of measure had been used to
report the outcomes, the standard mean difference
(SMD) was used for the groups compared and the
final estimates were expressed in standard deviation
units rather than in result scale units. Data analyses
were carried out using the Review Manager (RevMan)
computer program (version 5.3, Copenhagen: The
Nordic Cochrane Centre, The Cochrane Collabora-
tion, 2014).
RESULTS
The initial search of databases yielded a total of
1553 sources (424 in PubMed, 460 in EMBASE, and
669 in the Cochrane database), of which 1020 were
unique without duplication. In the search, 253 abstracts
and 62 articles were used for a full-text analysis, and
51 of them were excluded from further analysis
because they failed to meet the inclusion criteria. Pri-
mary data had been improperly presented in one trial
[21] and were consequently excluded from the meta-
analysis. Eleven RCTs [22–32] met the criteria of
inclusion in this systematic review and determined the
subject number for eight endpoints (Fig. 1).
Subject characteristics. Trial subjects were mostly
males (72%), were well trained (mean VO2max
48.9 mL/kg/min (SD 6.7 mL/kg/min)), and had a
mean age of 27.7 years (SD 3.2 years) and a mean BMI
of 23.9 kg/m2 (SD 1.7 kg/m2). Baseline characteristics
of the trial participants are summarized in Table 1.
Trial characteristics. In total, 271 subjects partici-
pated in the 11 trials. Of all subjects, 139 received GH
treatment. The samples were usually small (mean
sample size 12.3 subjects (SD 8.2 subjects); the drop-
out rate was low (95% of the subjects completed their
trials). The mean treatment duration was 31.2 days
(SD 23.5 days). The treatment period was longer than
30 days only in four trials [22, 23, 29, 32], and none of
the trials lasted longer than 3 months. The mean daily
GH dose was 41.1 μg/kg/day (SD 16 μg/kg/day). GH
was administered subcutaneously in all trials (Table 1).
Trial quality. The trials varied in methodical qual-
ity. None of the trials met all quality criteria, but six
trials met six out of the seven criteria [22, 24, 25, 27,
454 SERGEEVA et al.
Potentially relevant sources identified
by searching the databases (n = 1553)
PubMed = 424
EMBASE = 460
Cochrane = 669
Original articles after removing
duplicates (n = 1020)
Abstracts reviewed (n = 253)
Full-text articles retrieved for more
detailed review (n = 62)
Trials included
in meta-analysis (n = 11)
Fig. 1. Scheme of trial selection.
28, 31]. Subject allocation blinding was adequate in
only one trial [29], and randomization sequence gen-
eration was unclear in two trials [23, 32]. The com-
pleteness of final data was inadequate in one trial [23]
and unclear in two trials [29, 32]. Trial staff, investiga-
tors, and result assessment specialists were blinded in
all but one trial [26]. A funnel plot of study distribution
did not display signs of publication bias or other sys-
tematic errors due to the low sample size.
The effect of GH on the body composition. Our
meta-analysis of the eight RCTs [22, 23, 25, 27–29,
31, 32] showed that GH substantially, by 2.72 kg,
increased the lean body mass as compared with pla-
cebo (95% CI: 2.02; 3.38, p < 0.01). The lean body
mass is determined by summing the total water and the
dry lean mass of the body. An increase in lean body
mass was accompanied by an increase in extracellular
water (weighted mean difference 1.78 kg, 95% CI:
1.04; 2.52, p < 0.01). Results from two trials [21, 30]
Articles excluded (n = 185)
Full-text articles excluded
(n = 51)
Irrelevant outcome: 14
Irrelevant population: 16
Treatment duration
< 1 week: 7
No clinical outcome: 12
No placebo control: 2
included only the outcomes measured at the end of the
trial (without initial values) and were not included in
the meta-analysis. These trials additionally showed an
increase in extracellular fluid in the test group com-
pared with the control group. Three trials [25, 30, 32]
showed a significant increase in total water in the test
group (weighted mean difference 1.10 kg, 95% CI:
0.54; 1.66, p < 0.01). Two methodologically well-
designed RCTs [24, 32] evaluated the fractional rate of
protein synthesis; i.e., the protein synthesis rate was
measured as the rate of stable isotope-labeled amino
acid incorporation in muscle tissue. The trials showed
that GH did not affect the protein synthesis
rate (weighted mean difference 0.00% per hour, 95%
CI: –0.01; 0.02, p = 0.70). The fat mass decreased in
the group receiving GH as compared with the placebo
group (weighted mean difference –0.67, 95% CI:
‒0.93; –0.40, p < 0.01) (Fig. 2).
HUMAN PHYSIOLOGY Vol. 45 No. 4 2019
 Table 1. Baseline characteristics of the subjects and interventional treatments

Mean age (SD), Mean VO2max (SD), Subject number n at the

Mean BMI (SD), kg/m2 Interventional treatment
years mL/kg/min start/end of trial
Trial
(reference)
GH treatment GH dose,
GH group control group GH group control group GH group control group GH group control group
duration, days μg/kg/day

HUMAN PHYSIOLOGY
[23] 23.4(2.8)**** 23.4(2.8)**** – – 11/8 11/10 – – 42 30

Vol. 45
[24] 33(2) 33(2) – – 10/10 10/10 – – 14 50

No. 4
[25] 25.6(4.2) 27.0(4.4) 42.8(7.2) 45.2(7.2) 20/20 10/10 23.1(2.6) 23.2(3.9) 30 67

2019
[26] 32(9) 32(11) 41.8(9.8) 44.8(7.9) 24/24 24/24 27.5(3.0) 28.0(3.1) 7 19

[27] 24.0(4.0) 25.0(4.0) 60.1(9.6) 57.8(7.2) 8/8 8/8 22.2(2.0) 21.4(1.6) 14 28*****

[28] 31(–) 33(–) 54.2(–) 53.4(–) 6/6 5/5 24(–) 25(–) 30 67

[29]*** 27.6(5.7) 28.3(5.0) 45.6(9.9) 43.4(9.9) 37/32 33/32 23.3(2.8) 24.5(3.1) 56 28*****

[32] 27(4.2)**** 27(4.2)**** – – 9/7 9/9 23.5(–) 23.5(–) 84 40

[22]** 27.9(3.7) 27.9(3.7) – – 8/8 8/8 – – 42 38*****

[31] 21–29* 21–29* – – 8/8 8/8 22.5–27.0* 22.5–27.0* 10 33

EFFECT OF GROWTH HORMONE ADMINISTRATION ON THE MASS AND STRENGTH

[30]** 26.5(2.7) 26.5(2.7) – – 8/8 8/8 22.8(1.7) 22.8(1.7) 14 52*****

* Data reported as ranges. ** A crossover study. *** Pooled data for males and females. **** Pooled data for the test and control arms. ***** As based on the absolute doses and mean
body weight reported for the trial.
455
456 SERGEEVA et al.
The GH effect on muscle strength. Changes in the
strength characteristics of the biceps brachii and quad-
riceps femoris muscles were evaluated in two trials [23,
32]. The treatment durations was 42 [32] and 84 [23]
days; i.e., the trials were the longest of all trials
included in the meta-analysis. Treatment with GH did
not increase the strength of the biceps brachii muscle
in the one-repetition maximum (1RM) test (–0.24 kg,
95% CI: –1.50; 1.03, p < 0.71) and the strength of the
quadriceps femoris muscle (–1.06 kg, 95% CI: –3.65;
1.54, p = 0.43). Strengths of seven muscle groups were
evaluated in one trial [32]. Significant differences were
not observed between the test and control groups; the
groups displayed comparable strength characteristics
(–0.10 kg, 95% CI: –0.61; 0.41, p = 0.70). One trial
[29] showed that muscle strength (isometric back
strength) and maximal explosive strength (jump
height) did not increase in the group treated with GH
(2.00 kg, 95% CI: –1.29; 5.29, p = 0.23 and –1.30 cm,
95% CI: –2.19; 0.41, p < 0.01, respectively). Summary
data on GH treatment showed that GH lacked effect
on the relative change in muscle strength (–0.02, 95%
ДИ: –0.05; 0.02, р = 0.36) (Fig. 3).
The general estimates obtained for the effects were
tested for stability by excluding each trial from the
analysis and recalculating the results with subsequent
evaluation of their heterogeneity by the χ2 test. The
effects did not change in magnitude for all outcomes
under study, indicating that the conclusions of the pri-
mary meta-analysis were sufficiently grounded.
Visual examinations of the funnel plots did not
reveal signs of publication bias.
DISCUSSION
Our meta-analysis of the data from RCTs showed
that GH treatment does not increase the muscle
strength in recreational athletes and athletes engaged
in strength sports, although significantly increasing
the lean body mass and nearly significantly tending to
decrease the fat mass [23, 29, 32]. A reasonable ques-
tion arises in this respect as to why an increase in lean
body mass does not lead to an increase in strength.
The problem is that the methods used to quantitatively
assess the lean body mass (dual-energy X-ray absorp-
tiometry) are unreliable in differentiating the solid and
liquid components of the lean body mass [33]. It is
noteworthy in this context that GH significantly
increases the extracellular water volume [30, 34] by
increasing sodium retention and activating the renin–
angiotensin system and thus increases water absorp-
tion in the renal tubular system and intestine [35, 36].
Water retention is likely to make a major contribution
to the increase in lean body mass.
Measuring the fractional rate of muscle protein
synthesis is a far more sensitive method to estimate the
muscle response as compared with evaluating the
change in muscle mass for a period between two time
points. The method measures the protein synthesis
rate as the rate at which amino acids labeled with sta-
ble isotopes are incorporated in muscle tissue. Studies
with the method have shown that GH does not affect
muscle protein synthesis in healthy young adults. The
finding is supported by the results obtained for well-
trained weight-lifters in a nonrandomized trial, where
the fractional rate of muscle protein synthesis and the
protein degradation rate measured for the total body
did not differ from the respective baseline values after
2-week GH treatment [37]. In addition, it has been
well documented that GH and insulin-like growth fac-
tor 1 (IGF-1) stimulate collagen synthesis in tendons
and skeletal muscles, suggesting a stimulatory role in
muscle and tendon connective tissues for the hor-
mones [24, 38, 39]. Boesen et al. [40] have observed
no difference in between a group receiving GH and a
group receiving placebo in a study where muscle
strength recovery was assessed in healthy young
adults after 2-week limb immobilization and subse-
quent 6-week rehabilitation via GH/placebo treat-
ment combined with exercise. GH used at 33–
50 μg/kg/day increased the tendon transversal cross-
sectional area and tendon modulus without changing
the myofibril morphology. The combination of GH
treatment and exercise was not observed to exert a
favorable effect on the skeletal muscle growth during
rehabilitation. Assuming that GH potentiates collagen
synthesis, GH doping may help an athlete to train
more often and with a higher intensity and may reduce
risk of muscle and tendon injuries, thus indirectly
improving the sports results.
In total, our results make it possible to think that
GH does not affect the morphology of the myofibril
system in skeletal muscles. An increase observed in
lean body mass is explained by an increase in extracel-
lular water, indicating that supraphysiological doses of
GH exert only a limited anabolic effect. The erroneous
feeling of higher performance may be explained by
subjective changes in kinesthesia that arise from mus-
cle swelling and higher rigidity due to an increase in
tissue collagen because the GH/IGF-1 axis plays a
central role in regulating collagen metabolism in mus-
cle, tendon, and bone tissues [41].
Our analysis has certain limitations. First, publica-
tion bias cannot be fully excluded. Although we per-
formed statistical testing for publication bias, it is
important to understand that such tests have a low
power in meta-analyses of few trials. In addition, the
sample sizes were too low, rendering it impossible to
analyze the effects in particular subgroups after strati-
fication by sex, treatment duration, and treatment
type.
Second, the trials included were few, although not
heterogeneous, and the statistical conclusions con-
cerning the heterogeneity determinants might there-
fore be incorrect.
HUMAN PHYSIOLOGY Vol. 45 No. 4 2019
 EFFECT OF GROWTH HORMONE ADMINISTRATION ON THE MASS AND STRENGTH 457

(a)
GH treatment Placebo Std. Mean difference Std. Mean Difference
Study or subgroup Mean SD Total Mean SD Total Weight IV, Random, 95% CI IV, Random, 95% CI
Deyssig 1993 –0.8 5.0001 8 –0.9 6.0001 10 8.3% 0.02 [–0.91, 0.95]
Ehmborg 2005 –1 1.6772 20 –0.4 3.1752 10 12.4% –0.26 [–1.02, 0.51]
Graham 2007 –1 1.9039 24 –0.2 0.3808 24 21.6% –0.57 [–1.15, 0.01]
Hansen 2005 –0.6 0.9723 8 0.6 1.6928 8 6.8% –0.82 [–1.86, 0.21]
Meinhardt 2010 –2 1.1095 32 –0.6 1.3868 32 25.8% –1.10 [–1.63, –0.57]
Wolthers 1999 –0.7 1.6279 8 0.8 1.2806 8 6.5% –0.97 [–2.02, 0.09]
Yarasheski 1992 –1.4 1.3001 7 –0.2 1.5 9 6.7% –0.80 [–1.84, 0.24]
Healy 2003 0.2 2.2023 6 0.3 2.7586 5 5.1% –0.04 [–1.22, 1.15]
Crist 1988 –1.5 1.794 8 –0.4 0.478 8 6.8% –0.79 [–1.82, 0.24]

Total (95% CI) 121 114 100.0% –0.67 [–0.93, –0.40]

Heterogeneity: Таu2 = 0.00; Chi2 = 7.49, df = 8 (P = 0.48); I2 = 0%
Test for overall effect: Z = 4.86 (P < 0.00001) –4 –2 0 2 4
(b)
GH treatment Placebo Mean difference Mean Difference
Study or subgroup Mean SD Total Mean SD Total Weiqht IV, Random, 95% CI IV, Random, 95% CI
Deyssig 1993 4.6 5.2999 8 1.1 2.2 10 2.8% 3.50 [–0.42, 7.42]
Ehmborg 2005 2.9 3.8792 20 0.4 6.0823 10 2.5% 2.50 [–1.64, 6.64]
Hansen 2005 1.9 3.4655 8 –0.5 2.9069 8 4.3% 2.40 [–0.73, 5.53]
Meinhardt 2010 3.3 1.9415 32 0.6 1.1095 32 70.6% 2.70 [1.93, 3.47]
Wolthers 1999 1.3 5.0596 8 -0.7 5.0596 8 1.7% 2.00 [–2.96, 6.96]
Yarasheski 1992 4.5 1.5875 7 1.6 2.1 9 13.0% 2.90 [1.09, 4.71]
Healy 2003 3.4 1.6279 6 0.2 3.4655 5 3.9% 3.20 [–0.11, 6.51]
Crist 1988 2.7 5.58 8 1 6.02 8 1.3% 1.70 [–3.99, 7.39]

Total (95% CI) 97 90 100.0% 2.72 [2.07, 3.38]

Heterogeneity: Таu2 = 0.00; Chi2 = 0.53, df = 7 (P = 1.00); I2 = 0%
Test for overall effect: Z = 8.20 (P < 0.00001) –4 –2 0 2 4
(c)
GH treatment Placebo Mean difference Mean Difference
Study or subgroup Mean SD Total Mean SD Total Weiqht IV, Random, 95% CI IV, Random, 95% CI
Ehmborg 2005 2.5 2.879 20 0.2 0.1323 10 49.1% 0.94 [0.14, 1.74]
Moller 1995 5.74 6.8659 8 1 1.1961 8 28.8% 0.91 [–0.14, 1.95]
Yarasheski 1992 4.1 1.852 7 1.4 1.2 9 22.1% 1.69 [0.49, 2.88]

Total (95% CI) 35 27 100.0% 1.10 [0.54, 1.66]

Heterogeneity: Таu2 = 0.00; Chi2 = 1.20, df = 2 (P = 0.55); I2 = 0%
Test for overall effect: Z = 3.83 (P = 0.00001)
–4 –2 0 2 4
(d)
GH treatment Placebo Mean difference Mean Difference
Study or subgroup Mean SD Total Mean SD Total Weiqht IV, Random, 95% CI IV, Random, 95% CI
Ehmborg 2005 1.8 1.4431 20 0.3 1.9251 10 31.1% 1.50 [0.15, 2.85]
Meinhardt 2010 1.7 1.6642 32 –0.2 1.9415 32 69.9% 1.90 [1.01, 2.79]

Total (95% CI) 52 42 100.0% 1.78 [1.04, 2.52]

Heterogeneity: Таu2 = 0.00; Chi2 = 0.24, df = 1 (P = 0.63); I2 = 0%
Test for overall effect: Z = 4.71 (P < 0.00001) –4 –2 0 2 4
(e)
GH treatment Placebo Mean difference Mean Difference
Study or subgroup Mean SD Total Mean SD Total Weiqht IV, Random, 95% CI IV, Random, 95% CI
Doessing 2010 0.049 0.028 10 0.047 0.028 10 42.2% 0.00 [–0.02, 0.03]
Yarasheski 1992 0.022 0.01 7 0.018 0.03 9 57.8% 0.00 [0.02, 0.02]

Total (95% CI) 17 19 100.0% 0.00 [–0.01, 0.02]

Heterogeneity: Таu2 = 0.00; Chi2 = 0.01, df = 1 (P = 0.90); I2 = 0%
Test for overall effect: Z = 0.39 (P = 0.70) –0.10 –0.05 0 0.05 0.10

Fig. 2. Effects of GH on the body composition, including (a) fat mass (SD), (b) lean body mass (kg), (c) total water (SD),
(d) extracellular water (kg), and (e) fractional rate of muscle protein synthesis (% per hour).

Third, the GH dosing regimens used in clinical tri- i.e., the doses might be higher than in the majority of
als may differ from the doping regimens used in sports. the trials included in our analysis. However, it is still
Athletes presumably receive GH at 15–180 μg/kg unclear whether the effect of GH administration is
three or four times a week in 4- to 6-week cycles [1]; dose dependent.

HUMAN PHYSIOLOGY Vol. 45 No. 4 2019

458 SERGEEVA et al.

(a)
GH treatment Placebo Std. Mean difference Std. Mean Difference
Study or subgroup Mean SD Total Mean SD Total Weight IV, Random, 95% CI IV, Random, 95% CI
Deyssig 1993 5.4 4.3001 8 6.1 5.8999 10 7.2% –0.70 [–5.42, 4.02]
Yarasheski 1992 4.2 1.5875 7 4.4 0.9 9 92.8% –0.20 [–1.51, 1.11]

Total (95% CI) 15 19 100.0% –0.24 [–1.50, 1.03]

Heterogeneity: Таu2 = 0.00; Chi2 = 0.04, df = 1 (P = 0.84); I2 = 0%
Test for overall effect: Z = 0.37 (P = 0.71) –4 –2 0 2 4
(b)
GH treatment Placebo Std. Mean difference Std. Mean Difference
Study or subgroup Mean SD Total Mean SD Total Weight IV, Random, 95% CI IV, Random, 95% CI
Deyssig 1993 3.7 4.3999 8 5.3 7.4 10 22.2% –1.60 [–7.11, 3.91]
Yarasheski 1992 8.8 3.1749 7 9.7 2.7 9 77.8% –0.90 [–3.84, 2.04]

15 19 100.0% –1.06 [–3.65, 1.54]

Total (95% CI)
Heterogeneity: Таu = 0.00; Chi = 0.05, df = 1 (P = 0.83); I2 = 0%
2 2

Test for overall effect: Z = 0.80 (P = 0.43) –4 –2 0 2 4

(c)
GH treatment Placebo Std. Mean difference Std. Mean Difference
Study or subgroup Mean SD Total Mean SD Total Weight IV, Random, 95% CI IV, Random, 95% CI
Deyssig 1993 0.0388 0.0346 8 0.0438 0.0842 10 41.0% –0.00 [–0.06, 0.05]
Deyssig 1993 0.0504 0.0622 8 0.104 0.1175 9 17.4% –0.05 [–0.14, 0.03]
Meinhardt 2010 0.0387 0.1301 32 0.0596 0.1242 32 34.8% –0.02 [–0.08, 0.04]
Yarasheski 1992 0.54 0.141 7 0.5 0.144 9 6.8% –0.04 [–0.10, 0.18]

Total (95% CI) 55 60 100.0% –0.02 [–0.05, 0.02]

Heterogeneity: Таu2 = 0.00; Chi2 = 1.47, df = 3 (P = 0.69); I2 = 0%
Test for overall effect: Z = 0.85 (P = 0.40) –0.2 –0.1 0 0.1 0.2

Fig. 3. Effects of GH on muscle strength: (a) the biceps brachii muscle (1RM, kg), (b) the quadriceps femoris muscle (1RM, kg),
and (c) relative change in muscle srength.

Fourth, quality of a meta-analysis depends on CONFLICT OF INTEREST

quality of the trials included. Only some of the trials
included in our analysis are possible to consider as
methodologically high quality. Potential limitations
include an unclear or inadequate allocation blinding,
lack of blinding, and small sample size-related limita-
tions.
CONCLUSIONS
It should be noted that there is still no reliable trial
that has clearly characterized the effects on myofibril
protein synthesis and strength parameters for mid-
term or long-term GH administration used alone or in
combination with various training protocols. Athletes
and training specialists should comprehensively
understand not only the mechanisms whereby exercise
affects the body, but also the mechanisms whereby
drugs exert their effects on physiological systems. In
view of this, it is desirable to perform quality trials with
validated outcomes to evaluate the pharmacological
effects of GH.
ACKNOWLEDGMENTS
We are grateful to R.V. Tambovtseva, doctor of science
(biol.)., professor, head of the Volkov Chair of Biochemis-
try and Bioenergetics of Sports, for help in writing the arti-
cle and working with literature sources.
The authors declare that they have no real or potential
conflict of interest with respect to publication of this article.
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Translated by T. Tkacheva
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