Neural plasticity, which is observed in untrained individuals is a key explanatory mechanism of strength development [ 24 ], and can involve cells at the spinal and supraspinal level. Measures of neural plasticity that examine spinal and supraspinal output, such as the H-reflex and V-wave respectively, have not been measured following a period of resistance exercise in trained individuals and as such, it is not clear if trained populations have the same neural adaptation response to resistance training as untrained individuals.
The link between testosterone and changes in the corticospinal pathway has been explored in humans with artificially induced testosterone levels [ 25 ]. These increases in testosterone were concurrent with reduced threshold of the evoked potentials from transcranial magnetic stimulation TMS , indicating that testosterone can positively increase the output from a given input, within the corticospinal pathway [ 25 ].
It is plausible that artificially changing testosterone levels, via supplementation may affect strength or power, by altering the efficiency of the corticospinal pathway. The effects of DAA on neural plasticity has yet to be researched in humans. The primary objective of this study was to evaluate the effectiveness of DAA to alter basal testosterone levels over three months of resistance training.
A secondary objective was to establish potential mechanisms for changes in strength and hypertrophy. Based on our previous findings, it was hypothesised that the DAA group would experience decreased total testosterone and free testosterone. In addition, it was hypothesised that the DAA group would experience decreased strength, which would be explained by changes in the corticospinal pathway.
All relevant data are contained within the paper and supporting files. All participants gave written consent and completed a medical history check. The study was carried out by the Declaration of Helsinki. Participants were recruited from the University campus via flyers, lecture announcements and online intranet advertising. In addition, recruitment from the western Sydney area was promoted via Facebook advertising.
In response to recruitment 31 people were assessed for eligibility. Twenty-two subjects were recruited, three dropped out due to personal reasons, leaving 19 that completed the study Fig 1. A rolling recruitment strategy was conducted from 17 th of March to the 16 th of December , with participants beginning soon after they were recruited, thus participants began the study at different time periods.
Final testing was conducted at the end of the 12 week training period and the trial was ended according to a set schedule for each participant. The last day of data collection was the 10 th March The sample size for the present study was determined from the reduction in free testosterone observed in previous DAA research [ 11 ].
Free testosterone changes in the six-gram group demonstrated an effect size of 1. A Means statistical test matched pairs using G Power v 3. Power calculations were determined A Priori with an alpha level of 0.
Participant demographics are presented in Table 1. The present study was a randomised, double-blinded, and placebo-controlled research design.
Subjects attended three laboratory sessions, located at the University campus, baseline testing T1 , midpoint testing T2 and post testing T3. These testing sessions involved: fasted blood draws for serum hormonal analysis; Brightness-mode B-mode ultrasound of the quadriceps and calf muscles for hypertrophy changes; electrical stimulation of the tibial nerve to determine H-reflex and V-wave responses of the plantar flexors; and isometric maximal voluntary contraction MVC of the plantar flexor muscles.
Following T1, all participants followed a structured resistance training protocol, which was combined with their daily supplementation protocol. One participant from the placebo group did not have sufficient data for plantar flexor strength and neural measures, thus was omitted from those analyses.
All participants consumed 10 identical opaque capsules each morning with water before they had breakfast for 12 weeks. Adherence to daily supplementation was controlled for via prompts at supervised training sessions, in addition the number of pills left were compared to their set schedule each week. Participants were randomly allocated to treatment groups following a block randomisation procedure block size of four based on a computer-generated list of random numbers.
Group allocation was managed by a technical officer, while the primary investigator and participants was kept blind to group assignment throughout the experimental intervention, and data analysis. The protocol as explained in the original participant information sheet, included 1RM testing for the squat and bench press. These were omitted due to time constraints of participants on testing days, as well as the fact that isometric testing would provide a stronger match with neural testing of the plantar flexors.
As this study utilised a commercially available supplement rather than a drug, it was not expected that this study would fit the definition of a clinical trial, therefore the clinical registration of this study was performed retrospectively ANZCTR.
Participants trained four days per week, with supervised sessions conducted a minimum of once per week. The participants training was monitored using training diaries. The prescribed training involved five exercises that included 3—5 sets of various repetition maximum RM prescriptions 2RM— 10RM. These accessory exercises included: seated rows, pull-down, bent over row, biceps curl, chin-ups, bench press, overhead press, pec fly, dip and back extension.
See Table 2 for programming of measurement specific exercises. Periodisation changes were implemented at week six to improve motivation and prevent overtraining. These changes can be observed in Table 2 , with an increase in training intensity with some of the exercises, but they did not affect the overall layout of the protocol.
All participants were asked to perform 48 sessions in the gym in total average number of sessions performed During laboratory sessions, the subject was asked to lie down upon arrival. After checking for pre-testing adherence protocols fasting status participants were asked to lie down for two minutes. Blood was then extracted from the antecubital vein via venepuncture. Participants remained lying down for 20 minutes before ultrasound procedures followed.
Following ultrasound testing, the subject was seated into an isokinetic dynamometer KinCom , version 5.
After the KinCom was configured, the subject was prepared for EMG and the cathode location was determined for transcutaneous nerve stimulation. The protocol for the determination of isometric plantar flexor strength, H-wave, M max and V-waves followed. The overview of the study protocol is visually represented in Fig 2. In chronological order, the study protocol comprised of: Consent and forms; venepuncture blood draws; ultrasound testing of the quadriceps and calf muscles; EMG and stimulation preparation; isometric MVCs plantar flexors ; and determination of H-wave curve and V-waves via electrical stimulation.
Participants were instructed to fast for hours and avoid strenuous exercise and alcohol consumption the day before testing. For each participant, the initial blood draw was scheduled in the morning between —, with subsequent draws time-matched on an individual basis. Participants were asked to rest in a supine position for 20 minutes, to allow for the fluid shift in the muscles to stabilise [ 27 ]. Quality control methodology has been previously outlined [ 28 ]. A minimum of three images was obtained for each time point, with the average values from these images used for data analysis.
Images were analysed using ImageJ 1. To obtain sagittal images the probe was manipulated until the superficial, and deep aponeuroses were parallel, and the pennation fibres were straight rather than curved. Intra-experimenter reliability CV of the analysis of the sagittal images was 2. Soleus electrodes were placed at two-thirds of the distance between the medial condyle of the femur and the medial malleolus.
Two electrodes were placed on the muscle belly for the medial gastrocnemius site, and the medial malleolus landmark was used for the reference electrode. Placement of the electrodes was recorded to ensure consistency between testing sessions. Raw signals were filtered with a fourth-order Bessel filter between 20— Hz. Isometric testing was chosen over dynamic 1RM strength testing, as it was believed to be a stronger and more reliable match to the neural protocol.
The isokinetic dynamometer KinCom , version 5. The seat angle was adjusted so that there was no gap between the knee and the edge of the seat to prevent unwanted muscle activity. The participants left foot was attached to the plantar-flexion—dorsiflexion attachment with hook-and-loop straps. Two seatbelts were applied across the thighs and chest. Subjects were instructed, from complete relaxation, to contract their plantar flexors as hard and as fast as possible, holding the contraction for five seconds.
Verbal encouragement was given during MVC attempts. Visual feedback of the instantaneous torque production was displayed on a screen that participants could see. MVC was defined as the peak isometric torque N. A custom anode Aluminium foil 10x6 cm and electrode paste was applied to the anterior aspect of the thigh, proximal to the patella.
To determine nerve location a rubber-insulated probe was manipulated within the popliteal fossa until the largest evoked resting H-wave was observed from the soleus EMG trace. To map the H-M curve, H-wave threshold was approximated by increasing stimulation intensity from 10 to 30 mA 1 mA increments.
To approximate M max , the stimulus intensity was increased by 10 mA increments until a plateau was achieved over three stimulation points, with the last point defined as M max. Thirty stimulation points were created on a logarithmic scale between these two approximations. Two stimulations with 10 seconds rest between were recorded for each of the thirty points. For H-wave processing, the ascending limb was defined as data from the initial stimulation point to H max.
Data from the ascending limb was entered into a custom program coded in the statistical package R R Foundation for Statistical Computing, Vienna, Austria. These parameters are visually represented in Fig 3. V-wave data was processed by normalising the value to the maximal motor response for that time point M max.
The raw data is represented as open circles, with the sigmoid fit data represented along the solid line. The lower filled circle represents iH th , and the upper filled circle represents iH max. The Kolmogorov-Smirnov test was applied to assess normality of distribution.
In the event of a significant F ratio, post hoc comparisons were made using a Bonferroni correction. Mean differences and standard deviation were reported in results tables. Left graph depicts placebo data and right graph depicts the data from the d-aspartic group. Solid line depicts group mean. Post hoc analysis revealed that isometric plantar flexor strength increased Post hoc analysis revealed that dynamic calf strength was significantly increased by Post-hoc analysis of iH max showed a Post-hoc analysis for iH 50 also demonstrated a Post hoc analysis revealed a 1.
VM was increased 7. VI was increased 6. Percentage indicates the distance from distal to proximal with quadriceps images referenced from the centre knee joint to the ASIS and calf images referenced from lateral malleolus to the fibular head. The short-term supplementation 14 days has been shown to reduce testosterone levels in resistance-trained men [ 11 ].
Thus the primary objective of this study was to evaluate the effect of DAA supplementation on basal testosterone over a three month resistance training period. Based on our previous results, we hypothesised that DAA would reduce basal testosterone levels. The novel findings of this study were that 1 DAA did not increase or decrease testosterone levels in resistance-trained men, 2 DAA supplementation reduced levels of estradiol, 3 equivalent strength and hypertrophy gains were observed for both the placebo and DAA groups, and 4 the placebo group experienced a reduction in all gastrocnemius H-reflex parameters pertaining to current intensity.
Three months of DAA supplementation did not change basal testosterone levels in resistance-trained men. The lack of change observed in the present study suggests that the previously observed reduction in testosterone after two weeks supplementation may be transitory [ 11 ].
Aspartic acid is an amino acid found in two forms. D-aspartic acid is the form involved in testosterone production and release in the body. Because of this, it is often found in testosterone-boosting supplements. Research on the effects of D-aspartic acid on testosterone levels has yielded mixed results. Some studies have shown that D-aspartic acid can increase testosterone, while other studies have not. One study in healthy men aged 27—37 examined the effects of taking D-aspartic acid supplements for 12 days 6.
Another study in overweight and obese men taking D-aspartic acid for 28 days reported mixed results. Some men had no increase in testosterone. Another study examined the effects of taking these supplements for longer than a month. These studies did not specifically use a physically active population. However, three other studies did examine the effects of D-aspartic acid in active men.
One found no increase in testosterone in young adult men who performed weight training and took D-aspartic acid for 28 days 5. However, a three-month follow-up study using 6 grams per day showed no change in testosterone Similar research in women is not currently available, perhaps because some of the effects of D-aspartic acid are specific to the testicles 4.
D-aspartic acid may increase testosterone in inactive men or those with low testosterone. However, it has not been shown to boost testosterone in men who weight train. Several studies have examined whether D-aspartic acid improves the response to exercise, particularly weight training.
However, studies have shown that men performing weight training experienced no increases in testosterone, strength or muscle mass when they took D-aspartic acid supplements 5 , 9 , One study found that when men took D-aspartic acid and weight trained for 28 days, they experienced a 2. However, those in the placebo group experienced a similar increase of 3 pounds 1. A longer, three-month study also found that men who exercised experienced the same increase in muscle mass and strength, regardless of whether they took D-aspartic acid or a placebo Both of these studies concluded that D-aspartic acid is not effective at increasing muscle mass or strength when combined with a weight-training program.
No information is currently available about combining these supplements with other forms of exercise, such as running or high-intensity interval training HIIT. D-aspartic acid does not appear to improve muscle or strength gains when combined with a weight training.
No information is currently available regarding the effects of using D-aspartic acid with other forms of exercise. Although limited research is available, D-aspartic acid shows promise as a tool to help men who are experiencing infertility. One study in 60 men with fertility problems found that taking D-aspartic acid supplements for three months substantially increased the number of sperm they produced 8.
These improvements in sperm quantity and quality appear to have paid off. The rate of pregnancies in the partners of the men taking D-aspartic acid increased during the study. Although much of the research on D-aspartic acid has focused on men due to its supposed effects on testosterone, it may also play a role in ovulation in women Although more research is needed, D-aspartic acid may improve the quantity and quality of sperm in men with infertility.
Most studies examining the effects of D-aspartic acid on testosterone have used doses of 2. Doses of around 3 grams per day have been shown to be effective in some young and middle-aged men who were likely physically inactive 6 , 7 , 8.
However, this same dose has not been shown to be effective in active young men 5 , 9. While one short study showed a decrease in testosterone with this dose, the longer study showed no changes 9 , D-Aspartic Acid Capsules. Sanitized Product. Delivered within days. Choose an Option Qty: Qty:. Is a form of Testosterone Booster. D-Aspartic Acid Capsules Reviews:. How do you rate this product? Submit Review.
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