Most people think muscle growth and mitochondria live in separate worlds. Muscle growth is about lifting heavy weights, eating protein, and activating anabolic pathways. Mitochondria are about endurance, cardio, and oxygen. One is for strength athletes and bodybuilders, the other is for runners and cyclists. That way of thinking is incomplete and it creates many of the problems people run into with stalled progress, chronic fatigue, poor recovery, and overcomplicated protocols that look impressive but quietly undermine long term adaptation. Muscle is not just a contractile tissue designed to move joints. It is a highly metabolically active organ system. Inside every muscle fiber are thousands of mitochondria producing energy, lipid membranes that organize signaling, redox systems that determine whether stress becomes adaptation or damage, and genetic machinery that decides what gets built next. A helpful way to think about muscle is as a city. The contractile proteins are the machinery, the mitochondria are the power plants, the membranes are the wiring and roads, and the nucleus is city hall making decisions. If the city builds bigger machines faster than it upgrades power plants and infrastructure, the system becomes fragile. That is exactly what happens when muscle growth outpaces mitochondrial adaptation. Mitochondria are often described as the powerhouse of the cell, but that description leaves out most of what makes them important. Mitochondria do not just make energy. They produce signaling molecules that tell the cell how to adapt. They help determine whether fuel comes from fat, carbohydrate, or amino acids. They influence inflammation, repair, and cell survival. They even provide structural support for signaling proteins through their membranes. Mitochondria are not passive batteries. They are decision making centers. A confusing paradox in training is that heavy resistance training improves mitochondrial function but often reduces mitochondrial density relative to muscle size. This does not mean resistance training is bad for mitochondria. It means muscle fibers can grow faster than mitochondria are built unless the right signals are included. An easy way to visualize this is to imagine drawing dots on a balloon. As the balloon inflates, the dots move farther apart. The dots did not disappear, but their density decreased. This is what happens when hypertrophy outpaces mitochondrial biogenesis.

Most conversations about mitochondria start in the wrong place. They start with energy production, ATP output, or how to “boost” mitochondria. That framing misses the real problem. Mitochondria don’t usually fail because they can’t make energy. They fail because the physical structure that allows energy to be made cleanly and efficiently becomes unstable. Once structure is compromised, every attempt to push energy production creates more noise, more oxidative stress, and more dysfunction. This is why people can have “normal” labs yet feel exhausted, wired, inflamed, or unable to recover. The issue isn’t fuel. It’s architecture. To understand this, we need to zoom in to the level of mitochondrial structure. Inside every mitochondrion is an inner membrane that folds inward into structures called cristae. These folds are not random. They are precisely shaped, tightly regulated, and essential for efficient energy production. Cristae dramatically increase surface area, but more importantly, they organize the electron transport chain into coherent, functional units. The electron transport chain is not just a series of enzymes floating in space. It is a spatially organized system embedded in the inner membrane. Distance between complexes, membrane curvature, lipid composition, and membrane tension all matter. A helpful analogy is an accordion. When the folds are evenly spaced, elastic, and well aligned, air flows smoothly and predictably. When the folds become stiff, warped, or collapsed, airflow becomes turbulent and inefficient. The same thing happens with electrons inside mitochondria. Electrons enter the electron transport chain and move through complexes I, II, III, and IV. As they move, they pump protons across the inner membrane, creating a proton gradient called membrane potential. ATP synthase then uses that gradient to produce ATP. When cristae structure is intact, electrons flow smoothly, protons are distributed evenly, ATP is produced efficiently, and reactive oxygen species remain low. When cristae structure is compromised, electrons leak, protons accumulate unevenly, membrane potential becomes excessive or unstable, and reactive oxygen species rise.

@Anthony Castore Can you provide your feedback on the below... it is Dr. Seeds feedback on using methylene blue as an indicator for function status of Mitochondria. @Anthony Castore *** Dr. Seeds Feedback - Short answer: No. Methylene blue is not a safe or reliable non-medical way to check liver or kidney function. Here’s a clear explanation without getting technical or giving instructions. Why methylene blue does not work as a liver/kidney test 1. It’s not a diagnostic marker Methylene blue is a dye and redox-active compound. Changes in urine color after exposure do not reflect how well your liver or kidneys are working. - Blue or green urine ≠ good or bad kidney function - Faster or slower color change ≠ liver performance Those changes mainly reflect: - How the dye is processed chemically - Hydration status - Gut absorption - Individual metabolism Not organ health. 2. The body handles it in multiple ways Methylene blue: - Is partially metabolized in the liver - Is partially excreted by the kidneys - Is chemically reduced to leucomethylene blue (colorless) Because of this, you cannot isolate liver vs kidney function based on what you see. Too many variables = no meaningful conclusion. 3. Color changes are misleading Urine color after exposure can change due to: - Dose size - Timing - Gut absorption - Gut bacteria - Hydration - Other foods, dyes, or supplements This makes it uninterpretable outside a controlled medical setting. Historical / medical context (important distinction) In the past, methylene blue was used by doctors for very specific purposes, such as: - Certain lab-based kidney flow studies (obsolete now) - Specialized surgical or imaging contexts ⚠️ These were: - Controlled - Measured - Clinically supervisedNot self-tests. Modern medicine does not use methylene blue to assess routine liver or kidney function. Safety note (important)

This article is about one simple but deeply misunderstood idea: before you try to make mitochondria faster, stronger, or more powerful, you have to make them stable. And mitochondrial stability is not primarily about enzymes, supplements, peptides, or signaling molecules. It is about structure. Specifically, it is about membranes, and at the center of those membranes sits a phospholipid called cardiolipin. Most people think of mitochondria as engines. Engines burn fuel and make energy. When energy feels low, the instinct is to add more fuel or push the engine harder. But mitochondria are not engines in the mechanical sense. They are closer to power plants built out of flexible walls, electrical gradients, and flowing electrons. If the walls of the power plant are damaged, leaky, or poorly organized, no amount of fuel will restore output. In fact, pushing fuel through a damaged system often makes things worse. To understand why, we need to go down to the molecular level and build back up. Mitochondria are double-membrane organelles. The outer membrane is relatively smooth and permissive. The inner membrane is where the magic happens. It folds inward into structures called cristae. These folds massively increase surface area, and that surface area is packed with the electron transport chain. The electron transport chain is not a single thing; it is a series of protein complexes embedded in the inner membrane that pass electrons from one to the next, ultimately creating a proton gradient that drives ATP synthesis. This system is not rigid. It is dynamic, fluid, and responsive to stress, fuel availability, redox state, and training load. The inner membrane has to be both strong and flexible at the same time. That balance is determined by its lipid composition. This is where cardiolipin enters the picture. Cardiolipin is a unique phospholipid found almost exclusively in the inner mitochondrial membrane. Unlike most phospholipids, which have two fatty acid tails, cardiolipin has four. This gives it a distinctive shape that allows it to curve membranes, stabilize protein complexes, and act like molecular glue holding the respiratory chain together.

I am a 51 year old man. I work in the Operating room scrubbing in on nasty sugeries for sick people. Got into peptides after I had my G6 Prostate removed in June. My goal is cognitive and longevity. My father has late stage Parkinsons disease. I currently take Semax. Selank and Ta1 with low dose Reta Gym rat my whole life. I was wanting to stack Epitalon, NAD+, MotsC, SS31 and Slu. I work overnights so nights I work in gonto bed about 6am. Up by 1230. My off days I go to bed around 230 and will sleep till about 1030 or 11. I train 4 to 5 days a week. My diet isnt terrible but could always be better. I see all kinds of protocols. Ive seen run Epitalon to start. 10 days. 10mg before bed. Then start NAD for 3 weeks. Add in 4 weeks of daily SS31, then follow with Mots at 5mg 3 days a week. Add Slu anytime. I see variations of this all over but I just want to do it right. Ive seen you can do 2.5mg of SS31 daily with 1 mg morning fasted and night of Mots. Seems to be a lot of ways. Really like this page. Appreciate all your information.