Looks like you possibly omitted some things...
Despite compliance to diet and training, the Placebo group showed minor to no improvements in the 1 repetition max strength tests. Various factors affect muscle strength. One such factor to consider is limb length because individuals with longer limbs are at a biomechanical disadvantage. Another factor to keep in mind is possible overtraining/overreaching due to the intensive training program, which may result in muscle and central nervous system fatigue. The training protocol in this trial was considered high volume in nature. Interestingly, Moore & Fry (2007) have shown that high volume training can result in poor performance with significant decreases in testosterone concentrations. These results closely resemble the findings in this trial. Therefore, it is suggested that Mass FX might help in offsetting some overreaching symptoms since the Mass FX group was void of any overreaching/overtraining symptoms.
So MassFX is good for high volume training that might induce symptoms related to overreaching.
The mean percent difference increase in free testosterone from pretesting was 75.84 %. In addition, excluding the two subjects (MFX2 and MFX4), all exhibited increases in total testosterone concentrations – the subjects had minor drops (2.9 and 7.07 %, respectively).
Wow, if I read this correctly I'm suprised it made it through. This sounds like a major spin of the facts to me. Since there were only four total subjects in the MassFX grouping, the above statement removes half of the total. So, two of the four subject experienced an increase in Total Test (TT) and the other two subjects experienced a decrease in TT. Compare that to one of the four subjects in the placebo group experiencing an increase in TT. That's a huge success?
Generally, total testosterone concentrations change in relation to changes in free testosterone concentrations via SHBG concentrations (Kelly & Vankrieken, 1997; Nieschlang et al., 2004, p.643). This is due to the fact that free and protein bound testosterone in blood are in state of equilibrium (Nieschlang et al., 2004, p.643). Therefore, any changes in the concentration of free testosterone levels would result in changes in total testosterone levels. For example, increased SHBG concentrations reduce free testosterone and increases total testosterone (Anderson, 1974); therefore, it is suggested that an inverse relationship might exit between these three clinical markers. Thus, a rise in free testosterone via SHBG might result in a decrease in total testosterone and vice versa. It would have been interesting to determine whether the changes in total and free testosterone were a result of SHBG concentration differences. This could have been achieved by analyzing SHBG concentrations via a blood analysis. It is suggested that the apparent increases in free testosterone due to Mass FX (probably via SHBG inhibition) caused this decrease in total testosterone concentrations of subjects MFX2 and MFX4. These minor reductions could be attributed to a homeostatic mechanism in which the body is trying to regulate the balance of bioavailable and bound testosterone.
So MassFX is suggested to have SHGB inhibiting properties.
To determine the power of the samples used in this study, a posthoc Power Analysis (See Table 22) was performed to test an effect for Mass FX (if it existed). It was determined that the data required an 88.6% power level to detect the effect of Mass FX for the bench press outcome which was achieved. This indicates that the bench press significance was valid. There was nearly 80% power for the Free Testosterone outcome, indicating that Mass FX might have had a significant effect if the sample size was larger. The other tests had very low power to detect the effect of Mass FX, if it exists. For those variable, it is not certain if the lack of significant change was due to the small sample size or the lack of a real effect.
Again having difficulty seeing this as a "huge success."
Another recommendation for future studies would be measuring other clinical parameters such as SHBG. This would help in drawing conclusions as to whether the increases in free testosterone were a result of a decrease in SHBG production (as mentioned earlier). Measurement of other clinical markers such as testosterone metabolites, namely dihydrotestosterone (DHT) and estrogen (E), would be considered valuable. Quantifying E would help in investigating whether Mass FX modulates aromatase, an enzyme involved in the metabolism of testosterone into estrogen. In turn, this would explain if the total testosterone increases in the Mass FX group were due to feedback mechanisms via aromatase/estrogen inhibition as observed with other studies involving aromatase inhibition (Willoughby et al., 2007; Rohle et al., 2007).
Should probably also be noted, for what it's worth, that this "study" was someone's Master's thesis project needed to fulfill the requirments of a MS.
Still, pretty good numbers if you ask me! :head:
