Not all muscle is created equal. And not all hypertrophy gets you closer to your goal. Most programs are built around chasing the pump or soreness, but that’s only one slice of the hypertrophy pie. To build a physique that performs, ages well, and adapts intelligently—you need to train across multiple cellular pathways, not just chase fatigue. This post is heavily inspired by the brilliant work of Kilo Strength Society and N1 Education, both of which are world-class resources for understanding the nuance of program design and refining your coaching skills at the cellular and biomechanical level. Let’s break it down. 1. Sarcoplasmic Hypertrophy — The Storage WarehousePathway: mTORC1 → glycolysis-driven volume → increased sarcoplasmic fluid and glycogenMechanism: Repeated submaximal effort depletes glycogen and increases cell volume. The muscle adapts by expanding the sarcoplasm (fluid + fuel space).Why this happens: Your body sees repeated energy demand and says, “I need more room to store fuel.” - Reps/Sets: 10–15 reps, 3–5 sets - Tempo: 2-0-2-0 - Rest: 30–60 sec - RIR: 0–1 - Special Methods: Myo-reps, drop sets, supersets Analogy: Think of this as upgrading the size of your warehouse—not the machinery inside. It looks big, but it doesn’t necessarily lift more. When to use it: Early hypertrophy phases, deloads, or during high-carb phases to enhance insulin sensitivity. 2. Myofibrillar Hypertrophy — The Machinery ItselfPathway: mTORC1 + satellite cell activation → increased actin/myosin densityMechanism: Heavy loads and high tension cause structural damage to contractile fibers, forcing the body to reinforce them with more protein.Why this happens: “This load is threatening structural integrity. Reinforce the scaffolding.” - Reps/Sets: 4–8 reps, 3–6 sets - Tempo: 3-1-X-1 - Rest: 2–3 min - RIR: 2–3 - Special Methods: Cluster sets, rest-pause, wave loading Analogy: This is upgrading the actual engines on your ship. It doesn’t look much bigger, but it pulls harder, faster, and longer.

Low energy is one of the most common complaints in medicine, coaching, and everyday life, yet it is one of the least precisely understood. People describe it as fatigue, burnout, brain fog, weakness, lack of motivation, or feeling “offline.” Athletes feel it when they cannot train. Patients feel it when they cannot work. High performers feel it when discipline no longer works. The problem is that “low energy” is not a diagnosis. It is a surface description of a system-level failure, and two people can experience nearly identical symptoms while the underlying biology is completely different. Treating them the same way helps one person and harms the other. To understand low energy correctly, you have to stop asking how to boost energy and start asking why energy is being limited in the first place. At the deepest level, there are two dominant failure modes. In one, the body cannot produce enough energy. In the other, the body is deliberately suppressing energy production. The first is mitochondrial damage, a capacity problem. The second is inflammatory inhibition, a regulatory decision. One is a broken engine. The other is a functioning engine with the brakes applied. Subjectively they feel similar. Biologically they are opposites. Everything that follows depends on recognizing which one you are dealing with. A simple model helps. Imagine the body as a car. The mitochondria are the engine. They take fuel and oxygen and convert them into usable energy in the form of ATP. Inflammation acts like the central control computer, deciding how much power the engine is allowed to produce. If the engine is damaged, pressing the accelerator does little. If the computer is limiting output, the engine could perform, but is being intentionally restrained. In both cases the car goes slow. Only one responds to pushing harder. Mitochondria exist inside nearly every cell and are responsible for producing ATP, the molecule that powers muscle contraction, nerve signaling, hormone synthesis, immune regulation, tissue repair, and cognition. Without adequate ATP, nothing in the body functions well. Energy production depends on intact mitochondrial membranes, functioning enzymes, proper redox balance, sufficient oxygen delivery, and a steady supply of micronutrients. When any part of this system is damaged, the maximum amount of energy the body can generate drops. This is not a motivational issue. It is a hard ceiling.

I was watching a pod cast where the podcaster was talking about mega dosing this a couple times a year to get rid of senecese cells. Does anyone have experience with this or know if it is a real functional option. I just read an old article by Anthony o er on Chris Duffins endless evolution about layering Foxo4 Dri amd other peptides. Really enjoyed the article

This Retatrutide carbs vs no-carbs discussion is a perfect example of the kind of work we’ll be doing inside the Cellular Intelligence Circle. I am attaching a video so you guys can get a sense of what to expect. Not hot takes. Not protocols copied from the internet. Not arguing teams or tribes. Instead, I’ll show you how I actually think. How I zoom out, identify what system is really being affected, and trace decisions back to first principles like cellular energetics, redox balance, signaling hierarchy, and context. You’ll see how to move beyond surface-level debates and start asking better questions. The kind of questions that cut through hype, confusion, and false certainty. The goal of the Circle isn’t to tell you what to think. It’s to teach you how to think for yourself. If you’re tired of conflicting advice, overconfident influencers, and protocols that work in theory but fall apart in real humans, this community is built for you. We’ll break down topics like peptides, metabolism, training, recovery, fat loss, and longevity in a way that connects the dots instead of fragmenting them. We kick off in February, and each month will center around a focused agenda designed to build real understanding, not just information overload. Members will get long-form breakdowns, case studies, monthly live Q&A discussions, and practical frameworks they can actually apply. If this video made you stop and rethink the question instead of picking a side, you’re exactly who this was built for. More details coming soon…. The Cellular Intelligence Circle launches February.

Over the past few years, I’ve been using GH fairly regularly. I have access to high-quality pharmaceutical-grade GH, so I didn’t overthink it. At my age (54), the difference in how I feel, recover, and sleep is definitely noticeable. That’s always been the main reason I’ve used it, and 2 - 3 IU per day was enough for me. I only increased the dose before a competition to enhance fat burning. However, after listening to and reading content from Antony and Dr. Seeds, I came to understand that constant activation of mTOR and supraphysiological levels of IGF might improve well-being and appearance as we age — but they can also accelerate aging. That said, I used GH mostly while on a ketogenic diet, where GH doesn’t significantly elevate IGF, so that likely minimized the effect. Now I’ve been off GH for two months, and I’d like to test a protocol using GHRH and GHRP, aiming for more pulsatile GH release, and therefore potentially fewer negative effects on long-term health. I have access to the following peptides: Ipamorelin Sermorelin Fragment 176–191 IGF-1 DES MK-677 PEG-MGF MOD-GRF 1-29 CJC-1295 + DAC IGF-1 LR3 What would be the best combinations for: 1. Long-term health 2. Optimal anabolism 3. Fat loss pre-competition Thanks!