Original Paper

HORMONE Horm Res 2008;69:343–354 Received: March 14, 2007

RESEARCH DOI: 10.1159/000117390 Accepted: August 11, 2007
Published online: March 17, 2008

Physical Effects of Short-Term Recombinant

Human Growth Hormone Administration in
Abstinent Steroid Dependency
Michael R. Graham a Julien S. Baker a Peter Evans b Andrew Kicman c
David Cowan c David Hullin d Non Thomas a Bruce Davies a
a
Health and Exercise Science Research Unit, Faculty of Health Sport and Science, University of Glamorgan,
Pontypridd; b Royal Gwent Hospital, Newport; c Drug Control Centre, Kings College London, and
d
Department of Pathology, Royal Glamorgan Hospital, Ynys Maerdy, Llantrisant, UK

Key Words creased compared to controls (p ! 0.05) and within the GH

Insulin-like growth factor-I  Physical stress  Recombinant
human growth hormone  Strength
Abstract
Background/Aims: Recombinant human growth hormone
(rhGH) as opposed to cadaver pituitary GH is misused for
physical improvement. Six days’ rhGH administration, in ab-
stinent anabolic-androgenic steroid dependents, was com-
pared with controls. Method: Male subjects (n = 48) were
randomly divided into two groups: (1): control group (C), n =
24, mean 8 SD, age 32 8 11 years, height 1.8 8 0.06 m; (2):
rhGH-using group (0.058 IU  kg–1  day–1) (GH), n = 24, mean
8 SD, age 32 8 9 years, height 1.8 8 0.07 m. Physiological
measurements included anthropometry, strength, power
and peak oxygen uptake (VO2 peak). Biochemical measure-
ments included haemoglobin, packed cell volume, glucose,
sodium, potassium, urea, creatinine, total protein, albumin,
thyroid function, testosterone, prolactin, cortisol, GH and
insulin-like growth factor-I (IGF-I). Results: Strength, peak
power output and IGF-I significantly increased and total pro-
tein, albumin and free tetra-iodothyronine significantly de-
Where applicable, the experiments described received approval for
the investigations from an institutional human research committee
here and conform with the principles of the World Medical Associa-
tion’s Declaration of Helsinki, 1975.
group (p ! 0.017). Fat-free mass index and VO2 peak signifi-
cantly increased, while body fat and thyroid-stimulating
hormone significantly decreased within the GH group (p !
0.017). Conclusions: Short-term rhGH increased strength
and power. Of therapeutic value is the possibility that mus-
cle bulk and strength could be increased in patients with
muscle-wasting conditions. Copyright © 2008 S. Karger AG, Basel
Introduction
Growth hormone (GH) exerts a stimulatory regula-
tion over insulin-like growth factor (IGF-I), a protein
produced mainly in the liver, which in conjunction with
GH has varying differential effects on body composition
[1]. Recombinant human GH (rhGH) administration has
therapeutic value as a replacement therapy for growth
hormone deficiency (GHD), increasing lean mass, reduc-
ing fat, and increasing strength [2–4]. rhGH has also been
used in research relating to certain catabolic disease
states, where administration has been shown to improve
endurance exercise [5–8].
Athletes abuse both cadaver pituitary GH and rhGH
in the belief that such effects can be extrapolated to the
healthy individual [9, 10]. The abuse of cadaver pituitary
GH has diminished in Europe, subsequent to its associa-

© 2008 S. Karger AG, Basel M.R. Graham, MBChB

0301–0163/08/0696–0343$24.50/0 Health and Exercise Science Research Unit, Faculty of Health Sport and Science
Fax +41 61 306 12 34 University of Glamorgan
E-Mail karger@karger.ch Accessible online at: Pontypridd CF37 1DL (UK)
www.karger.com www.karger.com/hre Tel. +44 144 348 2873, Fax +44 144 348 2285, E-Mail drgraham@glam.ac.uk
tion with Jacob-Creutzfeldt disease and the abundant In-
ternet availability of rhGH from China. The acclaim of
the anabolic properties of GH appeared in the under-
ground doping literature as early as 1983 [11]. Its abuse
has increased [12] despite early research demonstrating
its effect on functional abilities is no greater than exercise
alone in healthy young men [13] or elderly males [14].
Supraphysiological dosages have increased mortality
[15]. Approximately 20 IU  day–1 were given to critically
ill patients, in an intensive care unit and their catabolic
condition cannot be considered equivalent to the condi-
tion of exercising athletes or bodybuilders, who are abus-
ing rhGH.
GH and rhGH are believed to stimulate production of
class-1 isoforms of IGF-I locally in muscles and tendons.
These may have a preventative effect on rupture of mus-
cles and tendons in anabolic-androgenic steroid (AAS)-
induced hypertrophy [16]. The transmission of force from
muscle fibres to bone could be explained by the stimulat-
ing effect of GH on collagen synthesis. Such strengthened
connective tissue would provide a more strain-resistant
musculo-tendinous junction and could explain why there
is still a claimed effect of rhGH on athletic performance,
despite current scientific evidence contradicting these
postulates [17, 18].
The purpose of this study was twofold. Firstly, to ex-
amine any effects of short-term rhGH administration on
anthropometry, strength, power, endurance performance
and biochemical indices in dependent abstinent AAS-us-
ing weightlifters. Secondly, to compare such effects with
age-matched dependent abstinent AAS-using weightlift-
ing controls.
Methods
Subjects
Approval for the study was obtained from the University Eth-
ics Committee. Subjects were dependent users of AAS in previous
AAS-related studies [19]. An inclusion criterion for the study was
the abstention from any drug use for 12 weeks, confirmed by a
urinalysis drug screen performed at a World Anti-Doping Agen-
cy (WADA)-accredited laboratory. Subjects in both groups fol-
lowed synchronised training times and intensity, which were rig-
orously monitored. Subjects abstained from physical activity for
a minimum of 24 h pre-testing.
Study Design
White Caucasian male subjects (n = 48) were randomly as-
signed, using a single-blind procedure, into two groups: (1): con-
trol group (C), n = 24, mean 8 SD, age 32 8 11 years, height 1.8
8 0.06 m, and (2) rhGH-using group (GH), n = 24, mean 8 SD,
age 32 8 9 years, height 1.8 8 0.07 m.
344 Horm Res 2008;69:343–354
Physiological tests were performed in the same order for both
the experimental group and the controls. Subjects were familiar-
ised with testing procedures. Subjects were examined daily over
a period of 6 weeks between 09:00 and 11:00 h and were anony-
mous to each other. Subjects self-administered rhGH, under su-
pervision, by subcutaneous abdominal injection, in a controlled
hygienic environment.
The dosage of rhGH used was 0.019 mg  kg–1  day–1 (0.058
IU  kg–1  day–1). The rhGH certificate of analysis was provided by
GeneScience Pharmacuticals Co., Ltd. This experimental design
complied with the review of multiple studies by Hrobjartsson and
Gotzsche [20], when measuring objective outcomes in accordance
with ethical concerns and the guidelines of the Declaration of
Helsinki.
Subjects were examined prior to the commencement of rhGH
administration (day 1), 1 day after 6 days’ administration (day 7),
and 8 days after cessation (day 14). Dietary intake was strictly
monitored, using a daily dietary record assessment (Nutri-Check,
Health Options Ltd, Eastbourne, Sussex, UK).
Blood Sampling
Phlebotomy was conducted in the fasted state, following 30
min rest in the supine position [21], using the standard venepunc-
ture method (Becton Dickinson, Rutherford, N.J., USA) between
09:00 and 09:30 h accounting for diurnal biological variation of
male sex hormones [22]. Venous blood was collected into an eth-
ylenediaminetetraacetic acid (EDTA) vacutainer for assessment
of full blood count. Haemoglobin (Hb) concentration was deter-
mined immediately using the cyanmethaemoglobin method by
placing venous blood in microcuvettes (Haemocue Blood Hae-
moglobin Photometer, Haemocue Ltd, Sheffield, UK). Packed cell
volume (PCV) was measured immediately using a Hawksley mi-
crohaematocrit reader (Hawksley & Sons Ltd, Lancing, Sussex,
UK) after being centrifuged at 20,900 g for 4 min in an Analox
microhaematocrit centrifuge (Hawksley & Sons Ltd). Hb and
PCV blood samples were taken in triplicate, and the mean re-
corded. Blood was also collected into vacutainers containing se-
rum separation tubes (SST), lithium-heparin (LiH) and fluoride-
oxalate (Fx). LiH and Fx tubes were centrifuged immediately at
2,500 g for 10 min at 4 ° C, whereas the SST samples were allowed
to clot at room temperature for exactly 1 h before centrifugation.
The plasma or serum supernatant was removed and placed into
tubes (Eppendorf 쏐) and stored at –70 ° C until analysis. Serum
albumin, cortisol, prolactin (PRL), testosterone (T) and total pro-
tein were measured with chemiluminescent immunoassay on an
Advia Centaur (Bayer Diagnostics, Newbury, UK). Serum creati-
nine, free tetra-iodothyronine (fT4) glucose, potassium, sodium,
thyroid-stimulating hormone (TSH) and urea were measured by
dry-slide technology on an Ortho Vitros 950 analyzer (Ortho
Clinical Diagnostics, High Wycombe, Bucks., UK).
IGF-I was analysed using the standard Nichols Institute Diag-
nostics IGF-I immunoradiometric assay, which employs two re-
gion-restricted affinity purified polyclonal antibodies (Nichols
Institute Diagnostics, San Clemente, Calif., USA) calibrated
against the world health authority 1st IRP IGF-I 87/518. The inter-
assay coefficient of variation (CV) of IGF-I was 4.5%. The intra-
assay CV of IGF-I was 10.0, 6.3 and 5.7% at serum concentrations
of 61.5, 340.8 and 776.9 ng  ml–1 respectively.
Recombinant and pituitary GH were analysed using two im-
munofluorometric assays, one measuring 22 kDa hGH and the oth-
Graham /Baker /Evans /Kicman /Cowan /
Hullin /Thomas /Davies
er total hGH (22 and 20 kDa) 24 h after the last rhGH injection [23].
The inter-assay CVs of GH were: 10.0, 4.0, and 5.4% at 1.7, 12.1 and
22.2 ng  ml–1, respectively. The intra-assay CV of GH was !5%.
Values obtained following blood analysis for serum analytes
were adjusted to account for plasma volume changes as a conse-
quence of rhGH administration, using the equation of Dill and
Costill [24] (table 5).
Body Composition Assessment
Total body mass (TBM) was measured using a calibrated bal-
anced weighing scales (Seca, Cranlea Ltd, Birmingham, UK) and
stature was measured using a stadiometer (Seca, Cranlea Ltd).
Body mass index (BMI) was calculated by dividing the subject’s
weight in kilograms by the square of the subject’s stature in meters.
Body density was determined using hydrostatic weighing proce-
dures previously described by Goldman and Buskirk [25]. Follow-
ing a familiarisation trial, underwater weight was determined five
times. The mean of five trials was used as the criterion value. Gas-
trointestinal volume was assumed to be 0.1 l. Residual lung volume
(RLV) was estimated to be 24% of forced vital capacity and ranged
from 0.9 to 1.4 l, which was within normal limits [26]. Body fat was
estimated from body density, using the equation of Siri [27].
Fat free mass (FFM) was calculated by subtracting fat mass
from TBM. Fat free mass index (FFMI) was calculated by dividing
the subject’s FFM in kilograms by the square of the subject’s stat-
ure in meters.
Power Test (30-Second Cycle Ergometer Test)
A cycle ergometer (Monark 864, Varberg, Sweden) was cali-
brated prior to data collection [28]. Subjects were assigned to a
previously determined resistive force calculated from TBM and
multiplied by a ratio standard of 75 g  kg–1. Familiarisation with
testing protocols precluded any observable repeated bout effect
[29]. Saddle heights were adjusted to accommodate partial knee
flexion of between 170 and 175° (with 180° denoting a straight leg
position) during the down stroke. Feet were firmly supported by
toe clips and straps. Subjects were instructed to remain seated
during the test and were verbally encouraged to perform maxi-
mally. All performed a standardised 5-min warm up prior to ex-
perimental data collection [30] and were given a rolling start at 60
rpm for a 5-second period prior to resistive force application. On
the command ‘go’, the subjects began to pedal maximally, the re-
sistive force applied simultaneously, and data capture initiated.
Indices of performance were calculated from flywheel revolutions
using an inertia corrected computer programme [31]. Data trans-
fer was made possible using a mounted sensor unit and power
supply attached to the fork of the ergometer located opposite the
flywheel. The sampling frequency of the sensor was 18.2 Hz. Va-
lidity and reliability of the cycle ergometer as a test of muscle
power has been reported as r = 0.93 [32]. Throughout the study,
‘peak power output’ (PPO) refers to the highest 1-second value of
power attained during each 30-second sprint. ‘Mean power out-
put’ (MPO) refers to the average power output for the 30-second
period. ‘Fatigue index’ (FI, %) refers to drop in power from a max-
imal to a minimal value and is expressed as a percentage. Resistive
force is the mass on the cradle of the cycle ergometer.
Aerobic Testing
Functional exercise testing was performed on a motorised
treadmill (Powerjog GXC200, Birmingham, UK). Oxygen uptake
rhGH on Strength
(VO2) and respiratory exchange ratio (RER) measurements were
obtained using an online computerised gas analysis system CPX/
D (Medgraphics, Beaver Medical Ltd, UK).
Electrocardiography
A 12-lead electrocardiogram (ECG) was performed on all sub-
jects in accordance with the position statement outlined by the
American Heart Association [33]. Resting, peak and 8-min recov-
ery-exercise (-rec), heart rate (HR) and blood pressure (BP) were
recorded. Subjects underwent a functional diagnostic exercise
test, on a treadmill, using the Bruce protocol [34]. The test was
terminated at volitional exhaustion, or on achieving the predicted
peak HR, or if there were any ECG changes indicative of myocar-
dial ischaemia.
Strength Tests
Identical ‘free-weight’ equipment and strength-testing proce-
dures were utilised for the determination of one-repetition max
(1-RM) bench press and squat exercise. All testing procedures
were standardised for individual subject stature. Following stan-
dardisation, sets of 1-RM were executed with increasing resis-
tance until a subject failed on two consecutive attempts at a given
resistance. The greatest load lifted successfully was then recorded
as 1-RM. Individual trials were separated by 3-min recovery in-
tervals. The range of motion of each movement was standardised
for each subject.
The coefficients of variation of power, aerobic, anthropomet-
ric and strength testing were all !3%.
Calculations and Statistical Analyses
Data were analysed using a computerised statistical package
(SPSS 14.0 for Windows, Surrey, UK) using parametric statistics.
Significance was set at the p ! 0.05 level. Data are presented as
means 8 SD. The power of the test was calculated at 95%. Con-
firmation that all dependent variables were normally distributed
was assessed via repeated Kolmogorov-Smirnov tests. Changes in
selected dependent variables as a function of time and condition
were assessed using a two-way repeated measures analysis of vari-
ance (ANOVA). Following simple main and interaction effects,
Bonferroni-corrected paired samples t tests were applied to make
a posteriori comparison of the effect of time at each level of the
condition factor. The rate pressure product (RPP) was calculated
as HR multiplied by systolic BP (SBP).
Results
No xenobiotic AAS were detected in urine, complying
with the inclusion criterion. Demographic characteris-
tics of the subjects are presented in table 1.
BMI (kg  m–2) and FFMI (kg  m–2) significantly in-
creased within the GH group (p ! 0.017) and significant-
ly decreased on cessation of rhGH administration (p !
0.017). Percentage body fat significantly decreased within
the GH group (p ! 0.017) and remained significantly de-
creased on cessation of rhGH administration (p !
0.017).
Horm Res 2008;69:343–354 345
Table 1. Subject demographics for control group (C) vs. growth hormone (GH [administration]) group

Variable Control group Administration group

1 7 14 pre-GH, day 1 on-GH, day 7 post-GH, day 14

BM 84810.2 84810.1 83.3810.1 85.8811.6 86.4811.7a 85.2811.5a, b

BMI 26.384.4 26.384.3 26.284.3 27.583.0 27.783.1a 27.383.0a, b
Body fat 20.483.8 20.183.7 20.083.9 20.286.2 19.286.3a 19.286.0a
FFMI 20.983.3 20.983.3 20.983.3 21.981.9b 22.381.9 22.081.9b
RT 12.283.6 12.283.6 12.283.6 12.283.6 12.283.6 12.283.6
WT 4.481.1 4.381.2 4.581.1 4.781.1 4.681.3 4.581.2
TT 46812 47815 45811 4789 45813 46812
Energy intake 18,05084,100 18,10082,020 18,17583,100 17,90083,020 18,45083,900 18,10082,020
Protein intake 205860 195855 213845 207835 217865 210850

Figures are presented as means 8 SD.

BM = Body mass (kg); BMI = body mass index (kg  m–2); FFMI = fat-free mass index (kg  m–2); body fat (%); RT = resistance training
(years); WT = weight training (sessions per week); TT = training time (minutes); energy intake (kJ  day–1); protein intake (g  day–1).
a p < 0.017 = significantly different to pre-GH; b p < 0.017 = significantly different to on-GH.

Table 2. Power responses, for total body mass, strength measurements (bench press and squat) and peak oxygen uptake for control (C)
group vs. growth hormone (GH [administration]) group

Variables Control group Administration group

day 1 day 7 day 14 pre-GH, day 1 on-GH, day 7 post-GH, day 14

PPO 1,2788205 1,3038231 1,3038228 1,3458216 1,4668257a, b 1,4978253a, b

MPO 666880 688882 664890 7108105 718890 733896b
FI 20.188.8 21.988.4 21.786.5 21.787.7 19.488.7 18.488.2
RF 6.581.1 6.581.1 6.581.0 6.381.1 6.381.1 6.381.0
VO2 peak 44.887.9 45.488.3 44.688.3 41.889.8 45.489.9a 45.188.2a
RPE 19.280.7 19.080.8 19.280.7 19.280.7 18.980.6 18.880.6
RER 1.1580.09 1.1580.08 1.1680.12 1.1780.16 1.1080.09 1.1480.13
Bench press 99824 99824 100824 108818 114818a, b 114818a, b
Squat 141832 142832 142830 145827 165826a, b 164825a, b

Figures are presented as means 8 SD.

PPO = Peak power output (W); MPO = mean power output (W); FI = fatigue index (%); RF = resistive force (kg); RPE = rate of per-
ceived exertion; VO2 peak = peak oxygen uptake (ml  kg–1  min–1); RER = respiratory exchange rate; bench press (kg); squat (kg).
a p < 0.017 = significantly different to pre-GH; b p < 0.05 = significantly different to C.

Values for power outputs recorded for the cycle ergom-
eter test and values for endurance and strength are pre-
sented in table 2 and individual results for PPO are pre-
sented in figure 1. PPO significantly increased compared
with the C group and within the GH group and remained
significantly increased on cessation of rhGH administra-
tion (both p ! 0.05 and both p ! 0.017, respectively). MPO
increased significantly in the GH group compared with
the C group on cessation of rhGH administration (p !
0.05). There was no difference in FI between or within
groups.
VO2 peak increased within the GH group and re-
mained significantly increased on cessation of rhGH ad-
ministration (p ! 0.017) (table 2) and individual results
for VO2 peak are presented in figure 2.
Values for strength (bench press and squat) signifi-
cantly increased compared with the C group and within
the GH group and remained significantly increased on

346 Horm Res 2008;69:343–354 Graham /Baker /Evans /Kicman /Cowan /

Hullin /Thomas /Davies
 1,800
1,600
1,400
1,200

Power (W)
1,000
800
600
400
200
a
0
Day 1 Day 7 Day 14
Time

2,500

2,000

1,500
Power (W)

1,000

500

b
Fig. 1. Individual subject responses for 0
peak power output (W) for total body mass Day 1 Day 7 Day 14
(kg) between (a) control group (n = 24) and Time
(b) administration group (n = 24).

cessation of rhGH administration (both p ! 0.05 and
both p ! 0.017, respectively) (table 2) and individual re-
sults for bench press and squat are presented in figures 3
and 4 respectively.
Electrocardiography was unremarkable in all subjects,
demonstrating no adverse effect of rhGH on myocardial
electrical activity. Results of the effects of the drug on the
cardiovascular responses are shown in table 3. HR-rest
significantly increased compared with the C group (p !
0.05). SBP-peak significantly decreased compared with
the C group (p ! 0.05). SBP-rec significantly decreased
within the GH group on cessation of rhGH administra-
tion (p ! 0.017). RPP-rest significantly increased com-
pared with the C group (p ! 0.05). RPP-rec significantly
decreased within the GH group, 8 days following cessa-
tion of rhGH administration compared with pre-admin-
istration of rhGH (p ! 0.017).
The effects of the drug on serum analytes are present-
ed in table 4. Serum PCV, sodium, total protein, albumin,
fT4 significantly decreased and IGF-I significantly in-
creased compared to controls (all p ! 0.05) and within the
GH group (all p ! 0.017). Potassium and TSH significant-
ly decreased within the GH group (all p ! 0.017). PRL
significantly increased compared to the control group
(p ! 0.05). Comparisons between corrected and uncor-
rected metabolites are presented in table 5.
The results of hGH and rhGH analysis on day 7, 24 h
after the last rhGH injection, demonstrated that 2 of the
24 subjects were suspected as testing positive.
Discussion
Effects on Anthropometry
The findings of this study indicated that the admin-
istration of a supraphysiological dose of rhGH 0.019
mg  kg–1  day–1 for 6 days, in abstinent AAS users, signifi-
cantly decreased body fat percentage consistent with pre-

rhGH on Strength Horm Res 2008;69:343–354 347

 65
60
55
50

(ml · kg–1 · min–1)

VO2 peak
45
40
35
30
25
a
20
Day 1 Day 7 Day 14
Time points

65
60
55
(ml · kg–1 · min–1)

50
VO2 peak

45
40
35
30
25
b
20
Fig. 2. Individual subject responses for en-
Day 1 Day 7 Day 14
durance exercise (VO2 peak) between (a) Time points
control group (n = 24) and (b) administra-
tion group (n = 24).

vious research in power-lifters [9]. Circulating concentra-
tions of IGF-I and FFMI were significantly increased from
baseline, returning to baseline on cessation of rhGH.
There were no differences between protein and kilocalo-
ric dietary intakes which could have biased the treatment-
related IGF-I and body composition responses. rhGH in-
creases lipid mobilisation and oxidation, decreasing pro-
tein oxidation and increasing protein synthesis [5].
An effect of rhGH on muscle growth may be detected
by indirect measurement of lean body mass using densi-
tometry or by dual X-ray absorptiometry. As the rate of
muscle protein turnover is relatively slow, it is relatively
difficult to detect increases in muscle mass per se over
short periods using such static techniques. Measuring the
rate of protein synthesis as the rate of incorporation of
amino acids labelled with stable isotopes into muscle is a
much more sensitive method for determining the response
of muscle, but was unavailable. Consequently the indirect
method of hydrostatic underwater weighing was used.
Effects on Heart Rate and Blood Pressure
GH administration is known to increase total body
sodium and water retention, in GHD and normal sub-
jects, by activation of the renin-angiotensin system, in-
creasing aldosterone secretion, and by inhibiting atrial
natriuretic peptide secretion and by a direct action on re-
nal tubules, corroborating previous research [35, 36].
Such significant decrease in PCV and serum sodium
would corroborate this research and the expansion of
plasma volume could explain the significant elevation of
resting HR and RPP.
Previous research in athletes, administering rhGH,
has neither demonstrated effects on the HR-peak nor
SBP-peak conflicting with results in this study, where
SBP-peak was significantly decreased.
GH administration in rats for 2 weeks corroborated
the current research, impairing baroreceptor function,
via activation of the NO system, elevating HR and lower-
ing BP [37].

348 Horm Res 2008;69:343–354 Graham /Baker /Evans /Kicman /Cowan /

Hullin /Thomas /Davies
 140
130
120

Weight (kg)
110
100
90
80
70
a
60
Day 1 Day 7 Day 14
Time points

150

140

130
Weight (kg)

120

110

100

90
b
80
Fig. 3. Individual subject responses for up- Day 1 Day 7 Day 14
per body strength (bench press) between Time points
(a) control group (n = 24) and (b) admin-
istration group (n = 24).

Table 3. Heart rate (HR), systolic blood pressure (SBP) and rate pressure product (RPP) responses for control (C) group vs. growth
hormone (GH [administration]) group

Variables Control group Administration group

day 1 day 7 day 14 pre-GH, day 1 on-GH, day 7 post-GH, day 14

HR-rest 66816 67816 67814 72814 78811b 75818

HR-peak 185812 185813 183812 18587 18588 18587
HR-rec 103819 103819 104819 10088 10087 9989
SBP-rest 125812 124812 125811 126810 125812 12289
SBP-peak 199820 201818 198818 192821 190816c 188828
SBP-rec 129817 127818 126816 132810 130812 12189a, c
RPP-rest 83822 84824 85822 90818 97814b 93828
RPP-peak 367842 367840 362841 355841 351835 348852
RPP-rec 133826 131828 131827 132817 129814 119816a

Figures are presented as means 8 SD.

HR = Heart rate (bpm); SBP = systolic blood pressure (mm Hg); RPP = rate pressure product (bpm  mm Hg ! 10 –2); -rest = rest-
ing; -peak = peak; -rec = 8-min recovery.
a p < 0.017 = significantly different to pre-GH; b p < 0.017 = significantly different to on-GH; c p < 0.05 = significantly different to C.

rhGH on Strength Horm Res 2008;69:343–354 349

 220
200
180

Weight (kg)
160
140
120
100
a
80
Day 1 Day 7 Day 14
Time points

230

210

190
Weight (kg)

170

150

130

110
b
90
Day 1 Day 7 Day 14
Fig. 4. Individual subject responses for
lower body strength (squat) between (a) Time points
control group (n = 24) and (b) administra-
tion group (n = 24).

Effects on Serum Analytes penditure, by the lowering of T4 and conversion of T4 to

The significant decrease of total protein and albumin
suggested that these serum substrates may have been
used for contractile protein synthesis, which may have
been indirectly supported by the significant elevation of
urea and creatinine on cessation of rhGH. This advocated
that on rhGH cessation there may have been an element
of catabolism.
Effects on Power
The values obtained for power outputs during the
high-intensity cycle ergometry test suggest that the de-
crease in percentage body fat, increased weight and FFMI
must contribute to increased efficiency in force velocity
relationships and lead to the increased PPO observed.
The findings also indicate that the GH group were able to
produce higher PPO, maintain their performance for
longer as indicated by the MPO, without an observable
alteration in FI. An increased stimulation of energy ex-
tri-iodothyronine (T3), has been previously observed
[38], which may have contributed to the increase in PPO
and strength gains recorded.
Effects on Endurance Exercise and Strength
Previous studies in human studies have not shown an
increase in endurance exercise or strength [13, 14, 17, 18].
It has been suggested and the authors believed it to be the
case that such differences were not significant due to a
lack of power, given the relatively small sample sizes. The
significant increase in VO2 peak was supported by re-
search in conditions indicating catabolism [6–8]. Both
GH and IGF-I have a net anabolic effect, enhancing
whole-body protein synthesis over a period of days [39].
RhGH infusion over 24 h causes a net glutamine release
from skeletal muscle into the circulation and increased
glutamine synthetase mRNA levels. This can compen-
sate for reduced glutamine precursor availability, in cat-

350 Horm Res 2008;69:343–354 Graham /Baker /Evans /Kicman /Cowan /

Hullin /Thomas /Davies
Table 4. Serum analytes for control (C) group vs. growth hormone (GH [administration]) group

Variables Control group Administration group Reference

range
pre-GH on-GH post-GH
day 1 day 7 day 14 day 1 day 7 day 14

Hb 15.981.6 16.181.5 15.981.7 15.881.6 16.181.7 16.081.5 13.5–18

PCV 0.4780.04 0.4780.03 0.4780.05 0.4780.03 0.4380.01a–c 0.4780.01 0.4–0.54
Glucose 4.780.7 4.780.7 4.780.7 4.980.6 4.980.6 4.980.5 3.0–10.5
Sodium 139.688.4 141.583.1 140.585.8 140.682.7 13982.4a–c 14382.6a 136–145
K+ 4.380.4 4.380.3 4.380.3 4.580.9 4.280.3b 4.480.5 3.3–5.0
Urea 6.482.3 6.381.9 6.682.2 5.681.3b 5.781.6b 7.282.8 2.3–6.9
Creatinine 95.9817 92.3813 95.6815 103.3825 91812a, b 106824 50–100
Total protein 76.5810 78.687 76.488 75.785 71.884a–c 75.785 58–80
Albumin 44.186 45.884 4586 44.484 41.784a–c 44.185 38–50
fT4 15.681.9 15.381.8 15.981.7 15.382.0 1481.6a–c 15.181.5 9.6–26.5
TSH 1.8480.8 1.9280.7 1.8480.7 2.381.1 1.4780.8a, b 2.281.0 0.6–4.8
T 17.585.2 17.585.6 17.485.4 16.286.0 15.085.6 14.685.0 10–35
PRL 1758102 142855 1598108 2058110 196895c 1708101 120–300
Cortisol 3898162 3788125 4048146 4028133 3748135 3918150 220–720
IGF-I 179847 169850 175853 159854 317891a–c 176861 >200

Figures are presented as means 8 SD.

Hb = Haemoglobin (g  dl–1); PCV = packed cell volume (ratio); Glucose (mmol  l–1); Na+ = sodium (mmol  l–1); K+ = potassium; Urea
(mmol  l–1); Creatinine (mmol  l–1); Total protein (mmol  l–1); Albumin (mmol  l–1); fT4 = free tetra-iodothyronine (pmol  l–1); TSH =
thyroid-stimulating hormone (mU  l–1); T = testosterone (nmol  l–1); PRL = prolactin (IU  l–1); Cortisol (nmol  l–1); IGF-I = insulin-like
growth factor-1 (ng  ml–1).
a p < 0.017 = significantly different to pre-GH; b p < 0.017 = significantly different to post-GH; c p < 0.05 = significantly different

to C.

abolic states, and can account for its anticatabolic effect
[40].
Myostatin is a cytokine implicated in differentiated
skeletal muscle growth and is a member of the trans-
forming growth factor-␤ family that has gained atten-
tion due to its remarkable expression profile and dra-
matic actions. Myostatin mRNA expression is signifi-
cantly inhibited by rhGH [41]. The authors believe that
such an inhibitory effect, i.e. an anticatabolic effect is
more important in anabolism than stimulation of pro-
tein synthesis in such a cohort. This promotes a signifi-
cantly increased lean body mass which is then translated
into significantly increased aerobic performance, deter-
mined by VO2 max [41]. Myostatin is well recognised as
a negative regulator of myogenesis through control of
myoblast proliferation and inhibition of differentiation
to myotubes [42]. In humans, hypercatabolic states such
as human immunodeficiency virus associated wasting
have been categorised by marked upregulation of myo-
statin [43], but knowledge about its regulation is lim-
ited.
Myostatin inhibition has also been shown to increase
skeletal muscle mass and strength [44] and has also been
shown to preserve skeletal muscle mass in amyotrophic
lateral sclerosis in rodents [45]. More recently, mutation
of the myostatin gene has been associated with gross
muscle hypertrophy in an otherwise healthy infant [46].
There is a suggestion that the subjects in this study were
in a catabolic state, indicated by relatively low baseline
IGF-I (!200 ng  ml–1). It is possible that rhGH adminis-
tration in such potentially catabolic subjects could have
had a suppressive effect on myostatin and increased skel-
etal contractile muscle synthesis.
The effects of AAS are known to result in larger type
I, IIA, IIAB and IIC muscle fibre areas. It is possible that
previous use of AAS had increased the number of myo-
nuclei per muscle fibre to an extent that a 12-week wash-
out programme was an insufficient time interval for re-
turn of the proportion of central nuclei to baseline in
both abstinent AAS groups [47]. Therefore following ad-
ministration of rhGH, this ‘latent catabolism’ may have
been ameliorated by the combination of ‘rhGH’ and ‘AAS

rhGH on Strength Horm Res 2008;69:343–354 351

Table 5. Serum analytes for uncorrected administration group vs. corrected administration group

Variables Uncorrected administration group Corrected administration group Reference

range
pre-GH on-GH post-GH pre-GH on-GH post-GH
day 1 day 7 day 14 day 1 day 7 day 14

Hb 15.881.6 16.481.7 15.981.5 15.881.6 16.181.7 16.081.5 13.5–18

PCV 0.4780.03 0.4480.01a 0.4780.01 0.4780.03 0.4380.01a–c 0.4780.01 0.4–0.54
Glucose 4.980.6 5.080.6 4.980.5 4.980.6 4.980.6 4.980.5 3.0–10.5
Sodium 140.682.7 14282.4a 14282.4a 140.682.7 13982.4a–c 14382.6a 136–145
K+ 4.580.9 4.380.3 4.480.5 4.580.9 4.280.3b 4.480.5 3.3–5.0
Urea 5.681.3 5.881.6b 7.182.8 5.681.3b 5.781.6b 7.282.8 2.3–6.9
Creatinine 103.3825 92.7813a 105.3824 103.3825 91812a, b 106824 50–100
Total protein 75.785 73.185a 75.385 75.785 71.884a–c 75.785 58–80
Albumin 44.484 42.584a 43.985 44.484 41.784a–c 44.185 38–50
fT4 15.382.0 14.281.6a, c 15.081.5 15.382.0 1481.6a–c 15.181.5 9.6–26.5
TSH 2.381.1 1.580.8a 2.281.0 2.381.1 1.4780.8a, b 2.281.0 0.6–4.8
T 16.286.0 15.385.7 14.585.0 16.286.0 15.085.6 14.685.0 10–35
PRL 2058110 199897c 1698101 2058110 196895c 1708101 120–300
Cortisol 4028133 3818138 3898149 4028133 3748135 3918150 220–720
IGF-I 159854 323893a–c 175861 159854 317891a–c 176861 >200

Figures are presented as means 8 SD.

Values obtained following blood analysis for serum analytes were adjusted to account for plasma volume changes as a consequence
of rhGH administration, using the equation of Dill and Costill [24].
Hb = Haemoglobin (g  dl–1); PCV = packed cell volume (ratio); Glucose (mmol  l–1); Na+ = sodium (mmol  l–1); K+ = potassium; Urea
(mmol  l–1); Creatinine (mmol  l–1); Total protein (mmol  l–1); Albumin (mmol  l–1); fT4 = free tetra-iodothyronine (pmol  l–1); TSH =
thyroid-stimulating hormone (mU  l–1); T = testosterone (nmol  l–1); PRL = prolactin (IU  l–1); Cortisol (nmol  l–1); IGF-I = insulin-like
growth factor-1 (ng  l–1).
a
p < 0.017 = significantly different to pre-GH; b p < 0.017 = significantly different to post-GH; c p < 0.05 = significantly different
to control group.

pre-conditioning’ and account for the significant increase
in strength. This latent catabolic condition would be dis-
similar to GHD and may explain why drug-free athletes
cannot achieve the same strength increases.
Effect on the Central Nervous System
PRL was significantly elevated compared with the con-
trol group, but did not adversely affect the PPO. We sug-
gest this was in part a consequence of the peripheral con-
version of T4 to T3, counteracting any diminished central
fatigue affected by the lowered serotonergic activity [48].
Conclusion
In previous studies, supraphysiological doses of rhGH
increased muscle protein synthesis, but did not increase
strength, either in fit young men or in highly trained
athletes. In the present study, rhGH administration in-
creased lean body mass, strength and power. In contrast,
in this unique study, these subjects were experienced for-
mer AAS users, in a latent catabolic phase, which may
have been ameliorated by the anabolic effect of rhGH
administration. This would suggest that the time period
of a 2-year ban, following a doping offence, is too short.
Our findings are of relevance because they reflect the
situation where athletes may switch from using AAS to
the use of rhGH to circumvent such a dope test (table 5).
Research is being conducted in an attempt to detect
rhGH use in sport [49] based on the ratio of its isoforms,
and to formulaic interpretation of IGF-I and N-terminal
extension peptide of procollagen type III (P III P) [50].
WADA needs to subject the tests to the rigour of an evi-
dential challenge. The WADA procedure requires two
sets of recombinant and two sets of pituitary assays to be
conducted before a sample is considered positive for
rhGH administration. The threshold values are not yet
in the public domain, the method of detection still being
refined and research is still being conducted. Any ben-
efit on athletic performance is yet to be elucidated.

352 Horm Res 2008;69:343–354 Graham /Baker /Evans /Kicman /Cowan /

Hullin /Thomas /Davies
 Of therapeutic value, these results suggest the possi-
bility that muscle bulk and strength could be increased
by the inhibition of myostatin in patients with muscle-
wasting conditions, catabolic respiratory conditions, or
rehabilitation post-trauma, using a dosage of 0.04–0.05
mg  kg–1  day–1 for up to 12 months [51–53]. However,
doses as high as 0.1 mg  kg–1  day–1 have been used for 2
weeks, without adverse effects [54].
Acknowledgements
The design, execution, data handling, interpretation, and
manuscript preparation were entirely the responsibility of the au-
thors. We would like to acknowledge the contribution of Chris-
tiaan Bartlett for his assistance in the analysis of IGF-I and urine
steroid screen and the contribution of Prof. Martin Bidlingmaier
for the two immunofluorometric assays for analysis of the GH
isoforms.

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