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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. 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(-1) plain flour (D0); 3 g.d(-1) of d-aspartic acid (D3); and 6 g.d(-1) 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. 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). 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.
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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
Abstract
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 yearsexperience 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
1
plain flour (D0); 3 g.d
1
of d-aspartic acid (D3); and 6 g.d
1
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
Background
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 [5]. 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: g.melville@uws.edu.au
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
DOI 10.1186/s12970-015-0078-7
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
in humans.
Aspartic acid (C
4
H
7
NO
4
)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 [6]. 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 [9]. StAR is a key regulator for the transport of
cholesterol from outside the mitochondrial membrane
to the inner membrane [7]. 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 [7]. In vitro
rats studies demonstrated that DAA increased levels of
testosterone, luteinizing hormone, progesterone [6] and
growth hormone [10]. This is believed to occur due to
the accumulation of DAA in the anterior pituitary and
testes [10]. Additional in vitro studies on isolated rat
testes [6] and Leydig cells [11] 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
1
[6].
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. [12] demonstrated
that after 12 days of supplementation (3.12 g.d
1
), levels
of testosterone were significantly increased by 42% (4.5
6.4 ng.ml
1
). They recruited a cohort of healthy sedentary
male IVF patients (2737 years), with low initial testoster-
one levels (~4.55 ng.ml
1
). Contrastingly Willoughby and
Leutholtz, reported that after 29 days of supplementation
(3 g.d
1
) 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
1
)
[13]. 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 5.88.6 ng.ml
1
(2030 nmol.l
1
), [4,14] and untrained men range from
about 4.96.6 ng.ml
1
(1723 nmol.l
1
) [15-17]. Further-
more current research has only explored one dose response
of DAA, 3 g.d
1
[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
1
). 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
DAA.
Methods
Subjects
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 1836;
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
1
(n= 8) 6 g.d
1
(n=8)
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).
Experimental procedures
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
(Figure1).Thesupplementalperiodoftwoweekswas
chosen as this has been previously shown to be a suffi-
cient time period to see a change in total testosterone
levels [12].
1-RM testing
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
12 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 participants 1-RM was achieved within five
attempts and adequate rest between attempts was adhered
to (35 mins) [18].
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
(7:0010:00 am) for each particular participant, to prevent
any effect of diurnal variation. Whole blood was collected
using serum separator tubes (SSTII 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
and albumin.
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
Training standardisation
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 810. If the repetition range wasnt 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).
Dietary intake
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.
Statistical analysis
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
2
), sex-hormone-
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
T1þT2
2

was conducted, with the
baseline scores: PRE ¼T1þT2
2

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).
Results
Analysis of the POST values revealed no main effect for
group with E
2
(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
5.1 ng.ml
1
). FT in group D6 was significantly decreased
(429.1 to 363.4 pmol.l
1
) as compared to D0 (439.6 to
480.9 pmol.l
1
) (P = 0.005) but not D3 (534.9 to 524.3
pmol.l
1
) (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).
Discussion
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. [12], 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. [12] (6.3 and 4.5 ng.ml
1
respectively),
presumably because the cohort in the Topo et al. study
were sedentary [12]. In resistance training literature, total
testosterone levels range from 5.88.6 ng.ml
1
[4,14] for
trained individuals and 4.96.6 ng.ml
1
for untrained
[15-17]. The increase in testosterone observed in Topo
et al. [12] 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 [13], 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%,
withaparalleldecreaseinfreetestosterone~15.3%
(see Table 2). Previous research has demonstrated that in
resistance trained men, free testosterone can increase due
to training [19]. 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-
tosteroneamaximumeffectivedosage(MED)isobserved
in rat studies [6]. At the higher dosages there were signifi-
cantly increased accumulation of d-aspartic acid observed
in the pituitary and testes [6]. A dose response increase
in total testosterone was observed until 1 μmol.g
1
.Each
increase in dose past 1 μmol.g
1
theriseintestosterone
was reduced [6]. It could be theorised that 6 g.d
1
may be
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 [7], 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
[1]. 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
(4.9-8.6 ng.ml
1
) 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
or negatively.
Conclusion
Many testosterone boosting supplements are commer-
cially available without sufficient research to support
their efficacy. The present study has demonstrated that
3 g.d
1
of d-aspartic acid was inadequate to affect any
hormonal markers and that 6 g.d
1
significantly reduced
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
1
)
Time Placebo 3 g.d
1
6 g g.d
1
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
1
)
Placebo 3 g.d
1
6 g g.d
1
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*
Estradiol (pmol.l
1
)
Placebo 3 g.d
1
6 g g.d
1
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
1
)
Placebo 3 g.d
1
6 g g.d
1
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
Δ4.19 ± 5.90 0.31 ± 4.29 0.19 ± 1.46
Albumin (g.l
1
)
Placebo 3 g.d
1
6 g g.d
1
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
Δ1.63 ± 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
1
over
a longer period and observe any correlations between
basal testosterone levels and changes in hypertrophy and
strength.
Competing interests
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.
Authorscontributions
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.
Acknowledgments
The authors thank the volunteers who participated in the study.
Received: 19 November 2014 Accepted: 5 March 2015
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Melville et al. Journal of the International Society of Sports Nutrition (2015) 12:15 Page 6 of 6
... Observationally, soy proteins, rich in glutamate and aspartate, are reported to lower the androgen levels but no large RCTs have been conducted to test their health effects; in addition, animal experiment results suggest that glutamate and aspartate can decrease the testosterone levels [10,11], and diverse epidemiological studies suggest that consumption of soy, fruits, and vegetables are linked with reduced risk of recurrence and increased survival rate of prostate cancer and breast cancer [12][13][14][15]. In a RCT of men, D -aspartate can reduce testosterone [16]. Despite these studies, however, up to now a causal relationship between serum levels of amino acids, such as glutamate and aspartate, and prostate and breast cancers remains elusive. ...
... For example, aspartate can improve liver metabolism [55], and glutamate can modulate the body weight [56], regulate the release of hormones [57] and lipid metabolism [58], probably owing to its impact upon the TCA cycle and ATP production [59]. Aspartate might also operate by lowering androgens [10], and high level of circulating androgens is a risk factor for prostate cancer, a notion for which there is, however limited, evidence in human studies [16]. ...
Article
Full-text available
Background Respectively, prostate cancer (PCa) and breast cancer (BC) are the second most and most commonly diagnosed cancer in men and women, and they account for a majority of cancer-related deaths world-wide. Cancer cells typically exhibit much-facilitated growth that necessitates upregulated glycolysis and augmented amino acid metabolism, that of glutamine and aspartate in particular, which is tightly coupled with an increased flux of the tricarboxylic acid (TCA) cycle. Epidemiological studies have exploited metabolomics to explore the etiology and found potentially effective biomarkers for early detection or progression of prostate and breast cancers. However, large randomized controlled trials (RCTs) to establish causal associations between amino acid metabolism and prostate and breast cancers have not been reported. Objective Utilizing two-sample Mendelian randomization (MR), we aimed to estimate how genetically predicted glutamate and aspartate levels could impact upon prostate and breast cancers development. Methods Single nucleotide polymorphisms (SNPs) as instrumental variables (IVs), associated with the serum levels of glutamate and aspartate were extracted from the publicly available genome-wide association studies (GWASs), which were conducted to associate genetic variations with blood metabolite levels using comprehensive metabolite profiling in 1,960 adults; and the glutamate and aspartate we have chosen were two of 644 metabolites. The summary statistics for the largest and latest GWAS datasets for prostate cancer (61,106 controls and 79,148 cases) were from the Prostate Cancer Association Group to Investigate Cancer Associated Alterations in the Genome (PRACTICAL) consortium, and datasets for breast cancer (113,789 controls and 133,384 cases) were from Breast Cancer Association Consortium (BCAC). The study was performed through two-sample MR method. Results Causal estimates were expressed as odds ratios (OR) and 95% confidence interval (CI) per standard deviation increment in serum level of aspartate or glutamate. Aspartate was positively associated with prostate cancer (Effect = 1.043; 95% confidence interval, 1.003 to 1.084; P = 0.034) and breast cancer (Effect = 1.033; 95% confidence interval, 1.004 to 1.063; P = 0.028); however, glutamate was neither associated with prostate cancer nor with breast cancer. The potential causal associations were robust to the sensitivity analysis. Conclusions Our study found that the level of serum aspartate could serve as a risk factor that contributed to the development of prostate and breast cancers. Efforts on a detailed description of the underlying biochemical mechanisms would be extremely valuable in early assessment and/or diagnosis, and strategizing clinical intervention, of both cancers.
... On the other side, one study reveal that there is no increase in testosterone level of young adult men who took D aspartic acid for 28 days with performed weight training [23]. One study found that two week of taking high-dose D aspartic acid supplements of 6 grams per day decrease the testosterone level in young men who weight trained [24]. The analysis of above research is that there is no effect of D aspartic acid on muscles and testosterone level combined with weight training. ...
Article
Full-text available
D-Aspartic acid is a non-essential amino acid which is present in vertebrates and invertebrates for stimulating the different hormones in endocrine system. Its nature to rotate the plane polarized light in right direction deter it to act as building block of proteins. This review is focuses on the contribution of D-Aspartic acid in Hypothalamus, Pituitary and Leydig cell of vertebrate’s testis for the production of GnRH, LH and Testosterone respectively. In hypothalamus gland, it is elucidated that D-Aspartic acid is transform into NMDA (n-methyl D-aspartate) by reacting with SAM-CH_3 molecule. Furthermore, the NMDA will activate the KISS-1 neuron to stimulate the gonadotropin releasing hormone (GnRH). The D-Aspartic acid action activate the NMDA-R along with glycine to facilitate the calcium ion movement after depolarization to form gonadotropin (luteinizing hormone LH and follicle-stimulating hormone FSH) in pituitary gland. In vitro, the direct action of D-Aspartic acid in Leydig cell initiate intracellular signalling through second messenger cAMP and MAPK by binding with NMDA-R to stimulate pregnenolone. There is an limited research available about the direct action of D-aspartic acid in Leydig cell to finish the dependence of testosterone production on neuronal activity of brain (mental causation). The male infertility will eradicate by the chemical treatment of D-aspartic acid instead of surgery.
... In the study of Melville et al. in 2015, two weeks of DAA consumption (three grams daily) had no effects on testosterone levels. In addition, six grams of DAA daily decreased the testosterone level (41). In addition, no effects on testosterone were seen in a long-term period (12 weeks) consumption of DAA (18). ...
Article
Full-text available
Context: D-Aspartic acid (DAA) is an amino acid found in the brain and reproductive system. Some investigations have reported beneficial effects of DAA on brain function and reproductive system health by increasing testosterone through the hypothalamic-pituitary-gonadal axis. However, its effect on body composition is unknown. Given testosterone's role in muscle growth, this study aimed to evaluate the effect of DAA supplementation on the body composition of trained males. Evidence Acquisition: PubMed, Scopus, Embase, and Web of Science (until 1 August 2021) were searched for this systematic review. Inclusion criteria assumed as clinical trials assessed the effect of DAA on body composition in trained males. After including articles by keywords, the articles were reviewed for meeting the eligibility criteria. Three independent researchers conducted the search and full-text review. Results: Among 134 articles located during the primary search, five articles (47 interventions and 43 controls) were included in the study based on eligibility criteria. All included clinical trials had a low risk of bias. A review of the relevant literature concludes that different doses of DAA (three grams, six grams, 7.12, and 12 grams) in different intervention periods (two weeks, four weeks, and 12 weeks) have no effects on body composition in trained males. Conclusions: DAA supplementation is a low-level booster of testosterone and has no significant effect on the testosterone level in professional male athletes, and cannot alter the body composition.
... In addition, it plays the role of a neurotransmitter in the central nervous system. The acid itself and its salts are used as components of drugs, activating immunity, and due to a decrease in pH -increases the eff ectiveness of antibacterial agents [15,16]. ...
Article
Full-text available
Postpartum endometritis is one of the most widespread pathologies in animal husbandry. They often occur on the background of exposure on animals stress factors, microclimate disorders, complete feeding, which is accompanied by decrease of the resistance, leads to increasing morbidity, etc. The aim of the research is to develop a method of prevention of postpartum endometritis in cows using cell-free probiotics "Bacinil" and "Lactimet" with 4 % suspension of aspartic acid. Complex use of integrated cell-free probiotics "Bacinyl" and "Lactimet" with 4% suspension of asparagic acid for the prevention of postpartum endometritis in doses of 7.5 and 10 ml each at 3-fold use once a day for 3 days in a row allowed to obtain 100% preventive efficacy. The mechanism of action of probiotic "Bacinil" is based on the high activity of components of its composition - immunostimulants (lipopolysaccharides), bacteriocins and enzymes, probiotic "Lactimet" due to biosynthetic lactic acid and a complex of fermentation products. Complex application of probiotics and aspartic acid increases their bacteriostatic activity, which allows more actively suppress the proliferation of pathogenic and opportunistic microflora, complicating the flowing of postpartum endometritis; promotes liquefaction of exudate accumulated in the uterine cavity due to enzymes included in probiotic "Bacinil"; leads to activation of local immunity of endometrial tissues due to immunostimulating activity of components of "Bacinil" and "Lactimet" probiotics; creation of low pH level in the uterine cavity due to aspartic acid and biosynthetic lactic acid. Key words: cows, postpartum endometritis, prophylaxis, acellular probiotics, aspartic acid.
... Specifically, basal testosterone levels in resistance-trained men ranged from around 5.8 to 8.6 ng/mL and in untrained men from around 4.9 to 6.6 ng/mL. In addition, Melville and coworkers [145] evaluated the effects of two doses of D-Asp (3 g and 6 g) administered for 2 weeks on basal testosterone levels. In line with Willoughby and Leutholtz [144], they confirmed that 3 g/day of D-Asp did not affect testosterone levels and that 6 g/day significantly reduced testosterone levels, without any concomitant change in estradiol. ...
Article
Full-text available
The endogenous amino acids serine and aspartate occur at high concentrations in free D-form in mammalian organs, including the central nervous system and endocrine glands. D-serine (D-Ser) is largely localized in the forebrain structures throughout pre and postnatal life. Pharmacologically, D-Ser plays a functional role by acting as an endogenous coagonist at N-methyl-D-aspartate receptors (NMDARs). Less is known about the role of free D-aspartate (D-Asp) in mammals. Notably, D-Asp has a specific temporal pattern of occurrence. In fact, free D-Asp is abundant during prenatal life and decreases greatly after birth in concomitance with the postnatal onset of D-Asp oxidase expression, which is the only enzyme known to control endogenous levels of this molecule. Conversely, in the endocrine system, D-Asp concentrations enhance after birth during its functional development, thereby suggesting an involvement of the amino acid in the regulation of hormone biosynthesis. The substantial binding affinity for the NMDAR glutamate site has led us to investigate the in vivo implications of D-Asp on NMDAR-mediated responses. Herein we review the physiological function of free D-Asp and of its metabolizing enzyme in regulating the functions of the brain and of the neuroendocrine system based on recent genetic and pharmacological human and animal studies.
... Bibliografía: [184][185][186][187][188][189][190][191] ...
Book
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This book is intended for anyone passionate about nutrition and sports supplementation. It aims to introduce readers to what regards the subject, combining areas such as nutrition, biological chemistry, the physiology of the exercise, food science and pharmacology. It is by no means intended to replace a good book on each of these areas, just try to give a general snapshot of each of the substances that are currently being used in the world of supplementation sports, its functions, applications, benefits and doses that are usually used. Heber E. Andrada October 5, 2020
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Schizophrenia has been conceptualized as a neurodevelopmental disorder with synaptic alterations and aberrant cortical–subcortical connections. Antipsychotics are the mainstay of schizophrenia treatment and nearly all share the common feature of dopamine D2 receptor occupancy, whereas glutamatergic abnormalities are not targeted by the presently available therapies. D-amino acids, acting as N-methyl-D-aspartate receptor (NMDAR) modulators, have emerged in the last few years as a potential augmentation strategy in those cases of schizophrenia that do not respond well to antipsychotics, a condition defined as treatment-resistant schizophrenia (TRS), affecting almost 30–40% of patients, and characterized by serious cognitive deficits and functional impairment. In the present systematic review, we address with a direct and reverse translational perspective the efficacy of D-amino acids, including D-serine, D-aspartate, and D-alanine, in poor responders. The impact of these molecules on the synaptic architecture is also considered in the light of dendritic spine changes reported in schizophrenia and antipsychotics’ effect on postsynaptic density proteins. Moreover, we describe compounds targeting D-amino acid oxidase and D-aspartate oxidase enzymes. Finally, other drugs acting at NMDAR and proxy of D-amino acids function, such as D-cycloserine, sarcosine, and glycine, are considered in the light of the clinical burden of TRS, together with other emerging molecules.
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Testosterone deficiency, defined as low total testosterone combined with physical, cognitive, and sexual signs and/or symptoms, is a common finding in adult men. Functional hypogonadism (FH) is defined as borderline low testosterone (T) secondary to aging and/or comorbid conditions such as diabetes, obesity, and/or metabolic syndrome. The relationship between FH and metabolic disorders is multifactorial and bidirectional, and associated with a disruption of the hypothalamic–pituitary–gonadal axis. Resolution of FH requires the correct diagnosis and treatment of the underlying condition(s) with lifestyle modifications considered first-line therapy. Normalization of T levels through dietary modifications such as caloric restriction and restructuring of macronutrients have recently been explored. Exercise and sleep quality have been associated with T levels, and patients should be encouraged to practice resistance training and sleep seven to nine hours per night. Supplementation with vitamin D and Trigonella foenum-graecum may also be considered when optimizing T levels. Ultimately, treatment of FH requires a multidisciplinary approach and personalized patient care.
Preprint
Full-text available
Background: Respectively, prostate cancer and breast cancer are the second most and most commonly diagnosed cancer in men and woman, and they account for major cancer-related deaths world-wide. Special attention aiming to find potentially effective early detection of, and intervention strategies against, prostate cancer (PCa) and breast cancer need to be paid. Objective: Utilizing Mendelian randomization (MR), we aimed to estimate how genetically predicted glutamate and aspartate levels affected prostate and breast cancers development. Methods: Single nucleotide polymorphisms (SNPs) were selected as instrumental variables (IVs) to predict the serum levels of glutamate and aspartate from the publicly available genome-wide association studies (GWASs), which were conducted to associate genetic variations with blood metabolite levels using comprehensive metabolite profiling in 1,960 adults and the glutamate and aspartate we chosen were two of 644 metabolites. The summary statistics for the largest and latest GWAS datasets for prostate cancer (61,106 controls and 79,148 cases) were from the Prostate Cancer Association Group to Investigate Cancer Associated Alterations in the Genome (PRACTICAL) consortium and datasets for breast cancer (113,789 controls and 133,384 cases) were from Breast Cancer Association Consortium (BCAC). The analyses were performed through two-sample MR method. Results: Serum level of aspartate was positively associated with prostate cancer (Effect = 1.043; 95% confidence interval, 1.003 to 1.084; P = 0.034) and breast cancer (Effect = 1.033; 95% confidence interval, 1.004 to 1.063; P = 0.028); however, glutamate was neither associated with prostate cancer and breast cancer. The potential causal associations were robust to the sensitivity analysis. Conclusions: Our study found that the level of serum aspartate could serve as a risk factor that contributed to the development of prostate and breast cancers. Efforts detailing the underlying mechanism(s) would be extremely valuable in early assessment/diagnosis and strategizing clinical intervention of both cancers.
Article
Free d-aspartate is abundant in the mammalian embryonic brain. However, following the postnatal onset of the catabolic d-aspartate oxidase (DDO) activity, cerebral d-aspartate levels drastically decrease, remaining constantly low throughout life. d-Aspartate stimulates both glutamatergic NMDA receptors (NMDARs) and metabotropic Glu5 receptors. In rodents, short-term d-aspartate exposure increases spine density and synaptic plasticity, and improves cognition. Conversely, persistently high d-Asp levels produce NMDAR-dependent neurotoxic effects, leading to precocious neuroinflammation and cell death. These pieces of evidence highlight the dichotomous impact of d-aspartate signaling on NMDAR-dependent processes and, in turn, unveil a neuroprotective role for DDO in preventing the detrimental effects of excessive d-aspartate stimulation during aging. Here, we will focus on the in vivo influence of altered d-aspartate metabolism on the modulation of glutamatergic functions and its involvement in translational studies. Finally, preliminary data on the role of embryonic d-aspartate in the mouse brain will also be reviewed.
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Testosterone is one of the most potent naturally secreted androgenic-anabolic hormones, and its biological effects include promotion of muscle growth. In muscle, testosterone stimulates protein synthesis (anabolic effect) and inhibits protein degradation (anti-catabolic effect); combined, these effects account for the promotion of muscle hypertrophy by testosterone. These physiological signals from testosterone are modulated through the interaction of testosterone with the intracellular androgen receptor (AR). Testosterone is important for the desired adaptations to resistance exercise and training; in fact, testosterone is considered the major promoter of muscle growth and subsequent increase in muscle strength in response to resistance training in men. The acute endocrine response to a bout of heavy resistance exercise generally includes increased secretion of various catabolic (breakdown-related) and anabolic (growth-related) hormones including testosterone. The response of testosterone and AR to resistance exercise is largely determined by upper regulatory elements including the acute exercise programme variable domains, sex and age. In general, testosterone concentration is elevated directly following heavy resistance exercise in men. Findings on the testosterone response in women are equivocal with both increases and no changes observed in response to a bout of heavy resistance exercise. Age also significantly affects circulating testosterone concentrations. Until puberty, children do not experience an acute increase in testosterone from a bout of resistance exercise; after puberty some acute increases in testosterone from resistance exercise can be found in boys but not in girls. Aging beyond 35-40 years is associated with a 1-3% decline per year in circulating testosterone concentration in men; this decline eventually results in the condition known as andropause. Similarly, aging results in a reduced acute testosterone response to resistance exercise in men. In women, circulating testosterone concentration also gradually declines until menopause, after which a drastic reduction is found. In summary, testosterone is an important modulator of muscle mass in both men and women and acute increases in testosterone can be induced by resistance exercise. In general, the variables within the acute programme variable domains must be selected such that the resistance exercise session contains high volume and metabolic demand in order to induce an acute testosterone response.
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Full-text available
D-aspartic acid is an amino acid present in neuroendocrine tissues of invertebrates and vertebrates, including rats and humans. Here we investigated the effect of this amino acid on the release of LH and testosterone in the serum of humans and rats. Furthermore, we investigated the role of D-aspartate in the synthesis of LH and testosterone in the pituitary and testes of rats, and the molecular mechanisms by which this amino acid triggers its action. For humans: A group of 23 men were given a daily dose of D-aspartate (DADAVIT) for 12 days, whereas another group of 20 men were given a placebo. For rats: A group of 10 rats drank a solution of either 20 mM D-aspartate or a placebo for 12 days. Then LH and testosterone accumulation was determined in the serum and D-aspartate accumulation in tissues. The effects of D-aspartate on the synthesis of LH and testosterone were gauged on isolated rat pituitary and Leydig cells. Tissues were incubated with D-aspartate, and then the concentration (synthesis) of LH and cGMP in the pituitary and of testosterone and cAMP in the Leydig cells was determined. In humans and rats, sodium D-aspartate induces an enhancement of LH and testosterone release. In the rat pituitary, sodium D-aspartate increases the release and synthesis of LH through the involvement of cGMP as a second messenger, whereas in rat testis Leydig cells, it increases the synthesis and release of testosterone and cAMP is implicated as second messenger. In the pituitary and in testes D-Asp is synthesized by a D-aspartate racemase which convert L-Asp into D-Asp. The pituitary and testes possesses a high capacity to trapping circulating D-Asp from hexogen or endogen sources. D-aspartic acid is a physiological amino acid occurring principally in the pituitary gland and testes and has a role in the regulation of the release and synthesis of LH and testosterone in humans and rats.
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Recent advances in molecular biology have elucidated some of the mechanisms that regulate skeletal muscle growth. Logically, muscle physiologists have applied these innovations to the study of resistance exercise (RE), as RE represents the most potent natural stimulus for growth in adult skeletal muscle. However, as this molecular-based line of research progresses to investigations in humans, scientists must appreciate the fundamental principles of RE to effectively design such experiments. Therefore, we present herein an updated paradigm of RE biology that integrates fundamental RE principles with the current knowledge of muscle cellular and molecular signalling. RE invokes a sequential cascade consisting of: (i) muscle activation; (ii) signalling events arising from mechanical deformation of muscle fibres, hormones, and immune/inflammatory responses; (iii) protein synthesis due to increased transcription and translation; and (iv) muscle fibre hypertrophy. In this paradigm, RE is considered an ‘upstream’ signal that determines specific downstream events. Therefore, manipulation of the acute RE programme variables (i.e. exercise choice, load, volume, rest period lengths, and exercise order) alters the unique ‘fingerprint’ of the RE stimulus and subsequently modifies the downstream cellular and molecular responses.
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It was hypothesized that d-aspartic acid (D-ASP) supplementation would not increase endogenous testosterone levels or improve muscular performance associated with resistance training. Therefore, body composition, muscle strength, and serum hormone levels associated with the hypothalamo-pituitary-gonadal axis were studied after 28 days of resistance training and D-ASP supplementation. Resistance-trained men resistance trained 4 times/wk for 28 days while orally ingesting either 3 g of placebo or 3 g of D-ASP. Data were analyzed with 2 × 2 analysis of variance (P < .05). Before and after resistance training and supplementation, body composition and muscle strength, serum gonadal hormones, and serum D-ASP and d-aspartate oxidase (DDO) were determined. Body composition and muscle strength were significantly increased in both groups in response to resistance training (P < .05) but not different from one another (P > .05). Total and free testosterone, luteinizing hormone, gonadotropin-releasing hormone, and estradiol were unchanged with resistance training and D-ASP supplementation (P > .05). For serum D-ASP and DDO, D-ASP resulted in a slight increase compared with baseline levels (P > .05). For the D-ASP group, the levels of serum DDO were significantly increased compared with placebo (P < .05). The gonadal hormones were unaffected by 28 days of D-ASP supplementation and not associated with the observed increases in muscle strength and mass. Therefore, at the dose provided, D-ASP supplementation is ineffective in up-regulating the activity of the hypothalamo-pituitary-gonadal axis and has no anabolic or ergogenic effects in skeletal muscle.
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The purpose of this study was to examine the influence of an 8-wk high-intensity resistance training program on muscular strength and basal serum testosterone in male veteran sprint runners. Twelve healthy veteran sprint runners, ages 45-79, were recruited as subjects and randomly assigned to an experimental (n = 8) or control (n = 4) group. Measured in both groups before and after the resistance training period were body mass, total skinfolds, isoinertial strength (bench press, leg press), peak torque (knee extensors, knee flexors), and basal testosterone levels. ANOVA revealed significant increases (p < 0.05) in both the isoinertial and isokinetic strength of the experimental group following resistance training. However, no significant increase in basal testosterone level was observed in that group after 8 weeks of resistance training. The results suggest significant improvements in muscular strength in veteran male sprint runners following 8 weeks of high-intensity resistance training. Furthermore, the strength gains are not explained by changes in basal serum testosterone and may be due to neurological, physiological, and morphological factors.
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Hypogonadism is a common condition which occurs more frequently in older men. It is characterized by low testosterone (T) and is associated with symptoms which are often nonspecific. A key symptom is low libido, but it can also be associated with erectile dysfunction, reduced muscle mass and strength, increased body fat, reduced bone mineral density and osteoporosis, reduced vitality, and depressed mood. Hypogonadism is linked with a variety of comorbid conditions including erectile dysfunction, metabolic syndrome, diabetes, obesity, and osteoporosis. However, the condition is often underdiagnosed. T supplementation in hypogonadism is associated with a range of benefits including improved sexual function, increased lean body mass and/or reduced fat mass, and improved bone mineral density. A variety of T supplementation formulations are available. Although there is no evidence of increased risk of initiating prostate cancer with T supplementation, it is contraindicated in men with prostate cancer. It is important that primary care physicians are aware of both the signs and symptoms of hypogonadism, the monitoring and testing that is required and the merits and advantages of the various T preparations to ensure optimal management of the condition with a treatment approach that best suits patients' needs.
The effects of a 24-weeks' progressive training of neuromuscular performance capacity on maximal strength and on hormone balance were investigated periodically in 21 male subjects during the course of the training and during a subsequent detraining period of 12 weeks. Great increases in maximal strength were noted during the first 20 weeks, followed by a plateau phase during the last 4 weeks of training. Testosterone/cortisol ratio increased during training. During the last 4 weeks of training changes in maximal strength correlated with the changes in testosterone/cortisol (P<0.01) and testosterone/SHBG (P<0.05) ratios. During detraining, correlative decreases were found between maximal strength and testosterone/cortisol ratio (P<0.05) as well as between the maximal strength and testosterone/SHBG ratio (P<0.05). No statistically significant changes were observed in the levels of serum estradiol, lutropin (LH), follitropin (FSH), prolactin, and somatotropin. The results suggest the importance of the balance between androgenic-anabolic activity and catabolizing effects of glucocorticoids during the course of vigorous strength training.
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D-Aspartic acid (D-Asp) is an endogenous amino acid which occurs in many marine and terrestrial animals. In fetal and young rats, this amino acid occurs prevalently in nervous tissue, whereas at sexual maturity it occurs in endocrine glands and above all in pituitary and testes. Here, we have studied if a relationship exists between the presence of D-Asp and the hormonal activity.The following results were obtained: 1) Both D-Asp and testosterone are synthesized in rat testes in two periods of the animal's life: before birth, about the 17th day after fertilization and, after birth, at sexual maturity. 2) Immunocytochemical studies have demonstrated that this enantiomer is localized in Leydig and Sertoli cells. 3) In vivo experiments, consisting of i.p. injection of D-Asp to adult male rats, demonstrated that this amino acid accumulates in pituitary and testis (after 5 h, the accumulation was of 12 and 4-fold over basal values, respectively); simultaneously, luteinizing hormone, testosterone and progesterone significantly increased in the blood (1.6-fold, p < 0.05; 3.0-fold, p < 0.01 and 2.9-fold, p < 0.01, respectively). 4) Finally, in vitro experiments, consisting of the incubation of D-Asp with isolated testes also demonstrated that this amino acid induces the synthesis of testosterone. These results suggest that free D-Asp is involved in the steroidogenesis.
Article
The optimal volume of resistance exercise to prescribe for trained individuals is unclear. The purpose of this study was to randomly assign resistance trained individuals to 6-weeks of squat exercise, prescribed at 80% of a 1 repetition-maximum (1-RM), using either one, four, or eight sets of repetitions to failure performed twice per week. Participants then performed the same peaking program for 4-weeks. Squat 1-RM, quadriceps muscle activation, and contractile rate of force development (RFD) were measured before, during, and after the training program. 32 resistance-trained male participants completed the 10-week program. Squat 1-RM was significantly increased for all groups after 6 and 10-weeks of training (P < 0.05). The 8-set group was significantly stronger than the 1-set group after 3-weeks of training (7.9% difference, P < 0.05), and remained stronger after 6 and 10-weeks of training (P < 0.05). Peak muscle activation did not change during the study. Early (30, 50 ms) and peak RFD was significantly decreased for all groups after 6 and 10-weeks of training (P < 0.05). Peak isometric force output did not change for any group. The results of this study support resistance exercise prescription in excess of 4-sets (i.e. 8-sets) for faster and greater strength gains as compared to 1-set training. Common neuromuscular changes are attributed to high intensity squats (80% 1-RM) combined with a repetition to failure prescription. This prescription may not be useful for sports application owing to decreased early and peak RFD. Individual responsiveness to 1-set of training should be evaluated in the first 3-weeks of training.
Article
Neuromuscular and hormonal adaptations to prolonged strength training were investigated in nine elite weight lifters. The average increases occurred over the 2-yr follow-up period in the maximal neural activation (integrated electromyogram, IEMG; 4.2%, P = NS), maximal isometric leg-extension force (4.9%, P = NS), averaged concentric power index (4.1%, P = NS), total weight-lifting result (2.8%, P less than 0.05), and total mean fiber area (5.9%, P = NS) of the vastus lateralis muscle, respectively. The training period resulted in increases in the concentrations of serum testosterone from 19.8 +/- 5.3 to 25.1 +/- 5.2 nmol/l (P less than 0.05), luteinizing hormone (LH) from 8.6 +/- 0.8 to 9.1 +/- 0.8 U/l (P less than 0.05), follicle-stimulating hormone (FSH) from 4.2 +/- 2.0 to 5.3 +/- 2.3 U/l (P less than 0.01), and testosterone-to-serum sex hormone-binding globulin (SHBG) ratio (P less than 0.05). The annual mean value of the second follow-up year for the serum testosterone-to-SHBG ratio correlated significantly (r = 0.84, P less than 0.01) with the individual changes during the 2nd yr in the averaged concentric power. The present results suggest that prolonged intensive strength training in elite athletes may influence the pituitary and possibly hypothalamic levels, leading to increased serum levels of testosterone. This may create more optimal conditions to utilize more intensive training leading to increased strength development.