I’m interested in hearing about everyone’s favorite cycles for both off-season and prep. Also, how do you integrate peptides, exosomes, or stem cells into your stack? My Current Stack: Off-Season: - Base Cycle: Testosterone + Primobolan + NPP - Peptide Additions: Tesamorelin + Ipamorelin + BPC-157 Prep/Cutting: - Base Cycle: Testosterone + Primobolan + Proviron - Peptide Additions: IGF-1 LR3 + MOTS-C + SS-31 Would love to hear your thoughts and any unique combinations you’ve tried!

Understanding the Muscle-Building Plateau: Insights from Santos and Haluch’s 2022 Study on Androgen Receptors and Anabolic Steroids In the pursuit of optimal muscle growth, the relationship between anabolic-androgenic steroids (AAS) and androgen receptors (AR) has been a topic of significant debate. A common theory is that long-term AAS use may downregulate androgen receptors, contributing to what many call a "muscle-building plateau." In a 2022 study by Santos and Haluch, published in Muscles, the authors critically examine this hypothesis, questioning whether AR downregulation is truly responsible for limiting muscle growth, or if this explanation oversimplifies a more complex issue. The Traditional View: AAS and Androgen Receptors Anabolic-androgenic steroids, synthetic derivatives of testosterone, are known to stimulate muscle growth by binding to androgen receptors within muscle tissue. The more AAS molecules available, the more stimulation ARs receive, leading to increased protein synthesis, hypertrophy, and muscle mass. This forms the basis of AAS efficacy in performance enhancement. However, a frequently cited concern is that prolonged AAS use may result in the body "adapting" by reducing the number of androgen receptors in muscle tissue. This downregulation, in turn, could theoretically lead to diminished gains, a point where progress stalls despite continuous steroid use—a phenomenon referred to as a muscle-building plateau. Challenging the Downregulation Hypothesis Santos and Haluch’s study revisits this widely accepted concept of AR downregulation, bringing new data and perspectives to the table. The authors argue that the idea of androgen receptor downregulation as the primary driver of muscle plateaus is not only oversimplified but may also be based on misinterpretations of how the body adapts to steroid use. One of their key critiques is the variability in how AR expression is measured in different studies. Factors such as the timing of measurements, the specific tissues analyzed, and individual differences in steroid metabolism make it difficult to draw definitive conclusions. Santos and Haluch highlight that while transient fluctuations in AR levels have been observed, these are not necessarily indicative of a permanent reduction that would halt muscle growth.

Hey everyone I'm Andrew. I used to hit the gym frequently until I had an tendon injury in my arm. After a course of a couple of years, a mixture of herbs and such helped me regain strength without surgery. However, now I'm having trouble with random muscle knots in both arms which is possibly due to overexertion when I was a truck driver. I've been to chiropractors, a massage therapist, and an acupuncturist for these knots but some are stubborn and don't want to release. They cause pain when lifting and when driving. I hope to gather some knowledge and hopefully fix my problem so I can focus on getting back to making gains.

The increase in popularity of SARMs without an understanding of the risk profile has allowed them to be coined as the ideal first exposure for the female PED user. Firstly, SARMS haven’t been approved for human use. You can’t be informed if you don’t understand the risk profile of the compound in question. In one cohort study they showed that SARMs are no more beneficial than AAS but carry a much LARGER risk profile on much smaller dosages. SARMs did provide some promise as they seem to be more tissue selective than AAS on a mg/kg comparison… but again this does not translate to the escalated dosages seen in common recreational practice and just like AAs this selectivity is lost at higher dosages. SARMs much like AAS will still cause suppression of the HPG axis. It produces a similar negative input on the feedback loop suppressing natural hormone production for a lesser return on the investment. There isn’t a single SARM to date that is approved for human use by the FDA due to risks such as acute liver damage, decreases in HDL cholesterol, increased cancer risk to name a few. From the current available evidence, the literature suggests that AAS outweigh SARMs in terms of risk profile BUT remember AAS are not without risk either. We have a much more comprehensive understanding of what those risks are in both the short and long term, meaning we can mitigate some of the potential risk by making appropriate informed decisions around protocols and deployment.

I came across an interesting article this morning and though it worth sharing. https://www.technologynetworks.com/neuroscience/news/exercise-improves-cognitive-function-but-only-when-you-move-by-choice-389835