R E S E A R C H A R T I C L E Open Access
Three and six grams supplementation of d-aspartic
acid in resistance trained men
Geoffrey W Melville
, Jason C Siegler and Paul WM Marshall
Background: Although abundant research has investigated the hormonal effects of d-aspartic acid in rat models,
to date there is limited research on humans. Previous research has demonstrated increased total testosterone levels
in sedentary men and no significant changes in hormonal levels in resistance trained men. It was hypothesised that
a higher dosage may be required for experienced lifters, thus this study investigated the effects of two different
dosages of d-aspartic acid on basal hormonal levels in resistance trained men and explored responsiveness to
d-aspartic acid based on initial testosterone levels.
Methods: Twenty-four males, with a minimum of two years’experience in resistance training, (age, 24.5 ± 3.2 y;
training experience, 3.4 ± 1.4 y; height, 178.5 ± 6.5 cm; weight, 84.7 ± 7.2 kg; bench press 1-RM, 105.3 ± 15.2 kg)
were randomised into one of three groups: 6 g.d
plain flour (D0); 3 g.d
of d-aspartic acid (D3); and 6 g.d
of d-aspartic acid (D6). Participants performed a two-week washout period, training four days per week. This continued
through the experimental period (14 days), with participants consuming the supplement in the morning. Serum was
analysed for levels of testosterone, estradiol, sex hormone binding globulin, albumin and free testosterone was
determined by calculation.
Results: D-aspartic acid supplementation revealed no main effect for group in: estradiol; sex-hormone-binding-globulin;
and albumin. Total testosterone was significantly reduced in D6 (P = 0.03). Analysis of free testosterone showed that
D6 was significantly reduced as compared to D0 (P = 0.005), but not significantly different to D3. Analysis did not
reveal any significant differences between D3 and D0. No significant correlation between initial total testosterone
levels and responsiveness to d-aspartic acid was observed (r = 0.10, P = 0.70).
Conclusions: The present study demonstrated that a daily dose of six grams of d-aspartic acid decreased levels of
total testosterone and free testosterone (D6), without any concurrent change in other hormones measured. Three
grams of d-aspartic acid had no significant effect on either testosterone markers. It is currently unknown what effect
this reduction in testosterone will have on strength and hypertrophy gains.
Keywords: D-aspartic acid, Resistance training, Testosterone, Estradiol, SHBG
The anabolic hormone testosterone is considered to be
a key determinant of training induced improvements
in hypertrophy and strength. Circulating testosterone
increases other anabolic hormones and directly interacts
with androgen receptors and satellite cells, causing a
cascade of events leading to protein synthesis and muscle
growth [1,2]. Research has previously demonstrated corre-
lations between testosterone levels and training related
strength gains [3,4]. Furthermore exogenous elevation of
testosterone to supraphysiological levels, via administra-
tion of anabolic steroids has been shown to drastically
improve strength and hypertrophy . Currently it is
unknown whether boosting testosterone levels within
normal physiological levels (mid-range to upper-range)
will have a significant effect on strength and hypertrophy.
Nonetheless, the supplement industry is endorsing tes-
tosterone boosters to improve training related gains.
D-aspartic acid is currently recommended as a viable
product to significantly raise testosterone, however re-
search in humans only supports this recommendation
* Correspondence: firstname.lastname@example.org
School of Science & Health, University of Western Sydney, Campbelltown
Campus, Locked Bag 1797, Penrith, NSW 2751, Australia
© 2015 Melville et al.; licensee BioMed Central. This is an Open Access article distributed under the terms of the Creative
Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and
reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain
Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article,
unless otherwise stated.
Melville et al. Journal of the International Society of Sports Nutrition (2015) 12:15
in untrained men with below average testosterone levels.
Moreover there is no information about the effect of
different doses of d-aspartic acid on testosterone levels
Aspartic acid (C
)isanα-amino acid which
is known to exist in two isoforms, l-aspartic acid and
d-aspartic acid. (2R)-2-aminobutanedioic acid or d-aspartic
acid (DAA), previously believed to be exclusive to brain
tissue in octopus, squid and cuttlefish, has more recently
been shown to exist in mammals . Free DAA is found
in tissues and cells related to the central nervous and
endocrine systems [7,8]. DAA is believed to stimulate the
production and release of testosterone through multiple
pathways of the hypothalamic-pituitary-gonadal (HPG)
axis. It has been shown to increase steroidogenic acute
regulatory protein (StAR) gene expression in rat Leydig
cells . StAR is a key regulator for the transport of
cholesterol from outside the mitochondrial membrane
to the inner membrane . By increasing levels of StAR
DAA may indirectly increase testosterone, as the trans-
portation of cholesterol is believed to be the rate limit-
ing step in the production of testosterone . In vitro
rats studies demonstrated that DAA increased levels of
testosterone, luteinizing hormone, progesterone  and
growth hormone . This is believed to occur due to
the accumulation of DAA in the anterior pituitary and
testes . Additional in vitro studies on isolated rat
testes  and Leydig cells  indicate that DAA increased
the rate of testosterone synthesis in a dose dependent
manner. In these animals the maximal effective dose of
DAA, which elicited the greatest hormonal response
(LH, testosterone and progesterone), was 1 μmol.g
In humans the effects of different dosages of DAA on
basal testosterone is unclear.
To date only two studies on DAA supplementation have
been conducted on humans. Topo et al.  demonstrated
that after 12 days of supplementation (3.12 g.d
of testosterone were significantly increased by 42% (4.5–
). They recruited a cohort of healthy sedentary
male IVF patients (27–37 years), with low initial testoster-
one levels (~4.55 ng.ml
). Contrastingly Willoughby and
Leutholtz, reported that after 29 days of supplementation
) and resistance training, levels of total testoster-
one and free testosterone were not significantly altered. In
this study resistance trained men (age: 22.8 ± 4.67 years
old; training age: > 1 year) were recruited and this cohort
exhibited higher initial testosterone levels (~7.96 ng.ml
. The difference in outcome between these two studies
may in part be explained by training status and accom-
panying basal testosterone levels. Basal testosterone levels
of RT men range from approximately 5.8–8.6 ng.ml
), [4,14] and untrained men range from
about 4.9–6.6 ng.ml
) [15-17]. Further-
more current research has only explored one dose response
of DAA, 3 g.d
[12,13], hence the maximum effective dose
for humans is yet to be determined.
Supplement companies are currently recommending
three grams of DAA once to twice a day, and these rec-
ommendations have been drawn from the only dosage
studied in humans (3 g.d
). It is reasonable to believe
that in RT males, a higher dose may be required to fur-
ther increase testosterone levels. As such the primary
aim of this study was to evaluate the effects of two doses
of d-aspartic acid (3 g and 6 g) on basal testosterone
levels in resistance trained men. A secondary aim was to
establish if a relationship exists between initial testoster-
one levels and responsiveness to DAA. It was hypothe-
sised that; (a) testosterone levels would be unchanged in
the 3 g group; (b) testosterone levels would be increased
in the 6 g group; and (c) lower initial testosterone levels
would correspond with an increased responsiveness to
The institutional review board approved the study and
participants provided written informed consent prior to
testing and participation. A total of twenty-four partici-
pants from the local area completed this study (Table 1).
To be eligible participants had to be: male; aged 18–36;
have no acute or chronic medical conditions; have the
ability to bench press 100% bodyweight; and had been per-
forming regular resistance training exercise for at least
three days per week for the previous two years. None of
the participants were supplementing their diet with any
ergogenic or testosterone booting supplements prior to
testing. All participants provided written consent and
completed a medical history check. The study was ap-
proved by the University of Western Sydney human re-
search ethics committee, and carried out in accordance
with the declaration of Helsinki.
Experimental approach to the problem
This was a randomised, double-blinded, and placebo-
controlled design to examine the effects of d-aspartic acid
supplementation on basal testosterone levels following
a two week supplementation protocol. Participants were
assigned to one of three experimental groups: placebo
Table 1 Participant demographics
Placebo (n= 8) 3 g.d
(n= 8) 6 g.d
Age (years) 24.24 ± 2.26 23.16 ± 2.16 26.06 ± 4.26
Training age, (years) 2.94 ± 0.78 3.25 ± 1.04 4.00 ± 1.91
Height (m) 1.84 ± 0.03 1.74 ± 0.07 1.78 ± 0.06
Body Mass (kg) 89.41 ± 3.59 79.50 ± 6.07 85.12 ± 7.95
1 RM Bench (kg) 111.56 ± 15.17 97.50 ± 12.82 106.86 ± 15.74
Data are mean ± SD.
Melville et al. Journal of the International Society of Sports Nutrition (2015) 12:15 Page 2 of 6
(D0), three grams of DAA (D3) and six grams of DAA
(D6). All participants consumed 10 opaque capsules each
morning with breakfast for two weeks. They contained
either: six grams of flour (D0, n = 8); a mixture of three
grams each of flour and DAA (D3, n = 8); or six grams
of DAA (D6, n = 8). Participants were randomly allo-
cated to treatment groups following a block randomisa-
tion procedure based on a computer-generated list of
random numbers. Placebo, mixed and supplement were
provided in identical opaque capsules to improve blinding.
Group allocation was managed by a technical officer,
whilst investigators were kept blind to group assign-
ment throughout the intervention. All participants followed
an upper/lower body split resistance training program for a
full month, with the initial two weeks of training (washout
period) performed without supplementation (Figure 1).
Three timepoints were used to obtain testing data: T1, T2
and T3 (Figure 1).
Testing sessions consisted of a fasted blood draw, then
1-RM bench press evaluation. Initial baseline blood mea-
sures were taken at two timepoints (T1 & T2) and aver-
aged to ensure accuracy in baseline assessment of these
markers (Figure 1). After T1 prescribed training com-
menced for four weeks. After testing session T2 daily sup-
plementation begun with training continuing as before.
Post-measures were taken after these last two weeks of
training and supplementation, at the end of week 4
chosen as this has been previously shown to be a suffi-
cient time period to see a change in total testosterone
Bench press dynamic strength one repetition max (1-RM)
was measured before the standardisation period (T1), be-
ginning of experimental period (T2) and post experiment
period (T3) (Figure 1), as part of eligibility testing. Correct
form included depth to the level of the chest, with feet not
leaving the floor, and the backside not leaving the bench
at any point during the repetition. The protocol for 1-RM
testing involved one warm up set of 10 reps at approxi-
mately 50% of their estimated 1-RM, followed by two
more warm ups at approximately 70% and 80% with only
1–2 reps. After the warm ups participants attempted
1-RMs with incrementally increasing weight. The weight
achieved prior to the failed attempt was recorded as
the 1-RM. A participant’s 1-RM was achieved within five
attempts and adequate rest between attempts was adhered
to (3–5 mins) .
Fasted blood draws
All blood draws were obtained via venepuncture of the
antecubital vein after a 12 hour fast. Participants were
also instructed to avoid strenuous exercise and alcohol
consumption the day before the draw. Blood draws were
conducted by a trained phlebotomist and subsequent
draws were planned for the same time of morning
(7:00–10:00 am) for each particular participant, to prevent
any effect of diurnal variation. Whole blood was collected
using serum separator tubes (SST™II Advance, BD Vacutai-
ner®). They were then allowed to clot for 45 minutes and
centrifuged using a fixed angle rotor centrifuge: ADAMS®
Compact II Centrifuge, V:227 (Becton Dickinson & Co)
(828 × g, at 2700 rpm) for 15 minutes in an air condi-
tioned room (19°C). Serum was aliquoted and stored
at −80°C until analysis (Douglas Hanly Moir Path-
ology, Macquarie Park, NSW, Australia). Single analysis
of serum was conducted for total testosterone, estradiol,
sex-hormone-binding-globulin (SHBG) and albumin. Tes-
tosterone and SHBG was measured via electrochemilumi-
nescent (ECL) immunoassay, on a Roche E170 system
(Roche Diagnostics). Albumin was measured via bromo-
cresol green (BCG) succinate buffer method, on an Abbott
16000. Estradiol was measured via chemiluminescent mi-
croparticle immunoassay on an Abbott i2000. Free testos-
terone was calculated from total testosterone, SHBG
Figure 1 Timeline of the study. After completion of T1, subjects began training four days per week. Daily supplementation commenced after
T2 ( ). T1-3 included fasted blood draws ( ).
Melville et al. Journal of the International Society of Sports Nutrition (2015) 12:15 Page 3 of 6
Participants trained for four days per week over a one
month period. The prescribed training for each exercise
consisted of four sets of a repetition maximum range
of 8–10. If the repetition range wasn’t met, participants
were asked to lower or raise the weight in the next ses-
sion. Exercises during the upper body session were: bar-
bell bench press; overhand pulldown; barbell overhead
press and underhand pulldown. The lower body session
consisted of: back squat; good morning; leg extensions;
and straight leg calf raises. Adherence was monitored
via training diaries and supervised sessions (minimum
1 × per week).
Participants were asked to control their diet, by avoiding
any major changes throughout the study duration. To
monitor their diet they were asked to weigh and re-
corded their food intake for three days each of the first
and last week; two training days and one non-training
day. These three days were averaged to get a daily mean
for week one and four. The food diaries were entered
into CalorieKing (Australian Edition 4.0), then analysed
for caloric and macronutrient daily intakes (protein, car-
bohydrates and fats) and normalised to bodyweight.
Analyses were conducted using IBM SPSS Statistics for
Windows version 21.0 (Armonk, NY: IBM Corp), and
the level of significance was set at P < 0.05. Data are
shown as mean ± S.D. The distribution was tested for
normality using the Kolmogorov-Smirnov test. Paired
sample statistics were run on total testosterone (TT),
free testosterone (FT), estradiol (E
binding-globulin (SHBG), and albumin (ALB) to deter-
mine the stability of these blood measures over the
standardisation period. As these measures were found to
be unchanged they were each computed (averaged) into
one baseline measure. Univariate analysis of the absolute
change scores: Δ¼T3−
was conducted, with the
baseline scores: PRE ¼T1þT2
as covariates (Figure 1).
Pairwise comparisons with Bonferroni correction were
performed if a group effect was observed. To explore the
responsiveness of the supplement, linear regression ana-
lysis was conducted on the baseline and change scores
of TT and FT, of the experimental groups (n= 16).
Analysis of the POST values revealed no main effect for
group with E
(P = 0.47), SHBG (P = 0.07) and ALB (P =
0.32). Post values of D6 TT were significantly reduced
(~12.5%) as compared to the pre values (P = 0.03; 5.9 to
). FT in group D6 was significantly decreased
(429.1 to 363.4 pmol.l
) as compared to D0 (439.6 to
) (P = 0.005) but not D3 (534.9 to 524.3
) (P = 0.06) (Figure 2). Diet analysis revealed no
significant changes in macronutrient (CHO: P = 0.74;
PRO: P = 0.99; FAT: P = 0.54) and caloric intakes (P = 0.64)
during the study. Regression analysis revealed no signifi-
cant correlation between baseline total testosterone levels
and total testosterone change (r = 0.10, P = 0.70), and no
significant correlation between baseline free testosterone
and free testosterone change (r = 0.32, P = 0.23).
The primary findings of the current study were, 1) resist-
ance trained men consuming six grams of d-aspartic
acid daily demonstrated significant reductions in total
and free testosterone after 14 days of d-aspartic acid
supplementation, and 2) the responsiveness to d-aspartic
acid supplementation was unaffected by initial testoster-
one levels (total or free) in resistance trained men.
Our results demonstrate that in resistance trained men
three grams daily of d-aspartic acid had no significant
effect on total testosterone, estradiol, sex-hormone-
binding-globulin, and albumin. This is contrary to the evi-
dence provided by Topo et al. , where the cohort con-
sumed the same dose over 12 days and reported elevated
total testosterone levels (~42%). Baseline testosterone
levels of the current study were higher than values
found in Topo et al.  (6.3 and 4.5 ng.ml
presumably because the cohort in the Topo et al. study
were sedentary . In resistance training literature, total
testosterone levels range from 5.8–8.6 ng.ml
trained individuals and 4.9–6.6 ng.ml
[15-17]. The increase in testosterone observed in Topo
et al.  was likely due to the fact that testosterone levels
were low enough for d-aspartic acid to have an effect. In
comparison our results in the D3 group mirror the results
seen in the study by Willoughby & Leutholtz , where
Figure 2 The absolute change of free testosterone. *statistically
significant (P < 0.05).
Melville et al. Journal of the International Society of Sports Nutrition (2015) 12:15 Page 4 of 6
the total testosterone levels fall within levels observed in
resistance trained males [4,14].
It was observed in the six gram group that total testos-
terone was significantly reduced from baseline by ~12.5%,
(see Table 2). Previous research has demonstrated that in
resistance trained men, free testosterone can increase due
to training . A reduction in calculated free testosterone
in this study is due to a reduction in total testosterone, an
increase in the binding proteins or a combination of the
two occurring. Within the context of increasing total tes-
in rat studies . At the higher dosages there were signifi-
cantly increased accumulation of d-aspartic acid observed
in the pituitary and testes . A dose response increase
in total testosterone was observed until 1 μmol.g
increase in dose past 1 μmol.g
was reduced . It could be theorised that 6 g.d
affecting negative feedback mechanisms of the HPG axis,
thus reducing pituitary initiated production of luteinizing
hormone and in turn testosterone levels. Furthermore
d-aspartic acid could also be over-accumulating within
the testes. This may be creating a disruptive effect on
the mobilisation of cholesterol from the outer membrane
to the inner , which would attenuate testosterone pro-
duction. As this was the first study to administer a six
gram dosage of d-aspartic acid, these mechanisms can
only be speculated due to the lack of data available on the
utilisation of d-aspartic acid in humans.
The reductions in testosterone observed in this study
are important to consider, owing to the negative impact
it could have on training gains within this population.
Resistance trained men have higher levels of strength
and hypertrophy compared to novice trainers and also
exhibit higher basal testosterone levels [4,13-17], which
suggest a link between basal total testosterone levels and
training related gains. A decrease in total testosterone
with a concurrent decrease in free testosterone could re-
duce the likelihood of interaction with androgen recep-
tors in muscles and nerves, which would reduce the
speed of testosterone initiated muscle protein synthesis
. Over time this could translate into reduced training
gains. Conversely, alterations of testosterone within nor-
mal physiological ranges may not be clinically signifi-
cant. Research indicates that when total testosterone
levels are observed outside of normal healthy ranges
) it affects strength and hypertrophy. In
the case of hypogonadism where testosterone levels are
low this negatively affects strength and hypertrophy, and
with the use of steroids a positive affect is seen [5,20].
The changes observed in the current study reflect minor
alterations with respect to normal physiological ranges.
It is currently unknown if these fluctuations are detri-
mental to training gains.
A potential limitation of this research may be the study
length. The short term nature of a two week supplementa-
tion period will answer only acute hypotheses. The ob-
served reduction in testosterone may rebound, or even
decrease further and a longer term training study would
be able to better explain the effects of this supplement.
Moreover it would be able to delineate changes in
strength and or hypertrophy, and observe whether
d-aspartic acid affects training related gains positively
Many testosterone boosting supplements are commer-
cially available without sufficient research to support
their efficacy. The present study has demonstrated that
of d-aspartic acid was inadequate to affect any
hormonal markers and that 6 g.d
total testosterone and free testosterone levels, with
no concurrent change in other hormones tested. It is
Table 2 PRE (Baseline), POST (T3), and Change Scores (Δ)
of hormonal markers
Total Testosterone (ng.ml
Time Placebo 3 g.d
6 g g.d
PRE 6.03 ± 1.48 6.95 ± 1.44 5.85 ± 1.10
POST 6.07 ± 1.35 6.91 ± 1.71 5.12 ± 1.16
Δ0.05 ± 0.80 −0.03 ± 0.68 −0.74 ± 0.95*
Free Testosterone (pmol.l
Placebo 3 g.d
6 g g.d
PRE 439.62 ± 132.64 534.88 ± 127.65 429.13 ± 93.98
POST 480.87 ± 133.48 524.25 ± 101.67 363.38 ± 78.09
Δ41.25 ± 52.48 −10.63 ± 66.31 −65.75 ± 79.25*
Placebo 3 g.d
6 g g.d
PRE 118.50 ± 20.91 117.56 ± 30.58 107.50 ± 24.22
POST 125.12 ± 23.88 112.5± 34.51 104.75 ± 34.03
Δ6.63 ± 14.94 −5.06 ± 19.52 −2.75 ± 23.46
SHBG Pre (nmol.l
Placebo 3 g.d
6 g g.d
PRE 34.56 ± 16.55 32.56 ± 10.72 33.56 ± 11.82
POST 30.38 ± 12.39 32.88 ± 12.53 33.75 ± 10.98
Δ−4.19 ± 5.90 0.31 ± 4.29 0.19 ± 1.46
Placebo 3 g.d
6 g g.d
PRE 46.38 ± 2.08 45.06 ± 2.60 45.50 ± 1.49
POST 44.75 ± 1.67 45.00 ± 2.33 45.50 ± 2.56
Δ−1.63 ± 1.33 −0.06 ± 1.82 0.00 ± 2.35
Data is presented as: mean ± standard devia tion.
*statistically significant (P < 0.05).
PRE values are an average of T1 and T2.
Melville et al. Journal of the International Society of Sports Nutrition (2015) 12:15 Page 5 of 6
currently unknown if any negative consequences of this
reduction, with respect to strength and hypertrophy will
occur over time. The need for longer-duration research
utilising six grams of d-aspartic acid is clear. Future
research should explore supplementation of 6 g.d
a longer period and observe any correlations between
basal testosterone levels and changes in hypertrophy and
The d-aspartic acid supplement used in this study was commercially sourced.
The authors have no undisclosed professional relationships with companies
or manufacturers that would benefit from the results of the present study.
The authors declare that they have no competing interests.
GM, PM and JS contributed to the study conception and design, GM
acquired the data, performed data analysis and interpreted the data; all
authors were involved in drafting the manuscript and have given final
approval of the published version.
The author’s thank the volunteers who participated in the study.
Received: 19 November 2014 Accepted: 5 March 2015
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