I’ve seen it, and so have you. We coach the same workout all day. Some athletes thrive on the challenge, and others don’t look as good. We second-guess ourselves: “Did I scale them right?” “Was that the right workout today?” But sometimes the answer is simpler. It’s not the workout that needs a closer look, it’s the athlete who is struggling. This is where mitochondria enter the conversation.
MetFix is the only commercial entity concerned with the care and feeding of the mitochondria.
I’ll admit that line didn’t land at first. Mito-what? It sounded like textbook science, not a coach’s job. But experience has taught me that when Coach Glassman makes a claim that doesn’t make sense right away, it’s worth listening to. If I don’t understand it yet, it usually means there’s something big I’m missing. That’s why, when I heard Pete Shaw’s lecture at the first Foundations Course, the line finally clicked: capacity lives or dies inside the mitochondria. What we call fitness is really mitochondrial function expressed on the gym floor.
If we’re going to talk about fitness and health, we have to care about mitochondria, because talking about performance without them is like talking about a drag race without talking about the engines.
So let’s look under the hood. Nearly every cell in your body is built around these engines. Mature red blood cells and lens cells of the eye are the exception. Red blood cells carry oxygen, but they do not have mitochondria. Most tissues do. The mitochondria you “see” in performance live mainly in skeletal muscle, the heart, and the nervous system. Those are the engines that move the load and keep output steady. But mitochondria in organs like the liver, pancreas, and gut set the fuel mix and metabolic signals that determine whether those performance engines run clean or overheat. At the cellular level, each mitochondrion fires like a cylinder, turning the fuel you eat into ATP, the cell’s universal energy currency. Mitochondria turn fuel into ATP. That’s where we get the horsepower. Nutrition sets the fuel mix, and training controls how hard the engine has to work. This tiny engine explains what coaches see every day: elbows drop, midlines soften, footwork gets sloppy, while someone right beside them stays crisp and in control. Mitochondria determine who has the power to do the work, who adapts, who fades, and who can show up again tomorrow. Performance and health share the same mechanism: when these engines adapt, athletes get fitter; when they run on the wrong fuel for too long, dysfunction isn’t far behind.
The mitochondria don’t care about food brands or nutrition fads; they care about substrates. Everything—fat, carbohydrate, and protein—gets broken down into acetyl-CoA, the molecule they burn to produce ATP. Fat enters through beta-oxidation. Carbohydrate runs through glycolysis and pyruvate oxidation, and amino acids contribute during fasting or excess intake. In metabolic terms, fat is the long, clean burn; carbohydrate is the fast, hot flame. With oxygen, a molecule of fat yields roughly three times more ATP than a molecule of glucose. That difference shows up on the gym floor, where fat supports steady output and repeat efforts, while glucose is powerful but limited—one feels sustainable, the other urgent.
Metabolic flexibility is the capacity to burn the right fuel at the right time. When mitochondria are efficient and abundant, fat supports the easy gears and glucose is reserved for speed. When they’re limited, so too is the capacity to burn fat. The engine runs too hot, too soon. More glucose is burned without oxygen through glycolysis. Coaches see the result: athletes who look in distress instead of control, faces flushed, breathing panicked, pace collapsing long before the clock demands it, recovery slowing to a crawl. Without metabolic flexibility, training becomes futile suffering instead of driving adaptation.
What we see as poor performance is often early metabolic disease. The same engines that decide who holds form in a workout also decide who drifts toward chronic disease. When mitochondrial oxidative capacity is limited, athletes rely more heavily on glucose and fatigue sooner. Chronic overexposure to refined carbohydrate and industrial seed oils drives the overload, increasing oxidative stress and eroding the ability to adapt. First, performance breaks. Then health breaks. Diabetes, fatty liver, cardiovascular disease, and cancer—many of them begin with the same failing engine. Research in cancer metabolism, insulin resistance, and cardiometabolic disease increasingly identifies mitochondrial dysfunction as an upstream driver of metabolic disease. Workout performance is the first test of metabolic health, and coaches administer it every day. Doctors use a similar principle with exercise stress tests, unmasking cardiovascular problems that are silent at rest. Long before fasting insulin climbs above 5 µIU/mL or the triglyceride-to-HDL ratio rises past 2.0, coaches can see the engine struggling on the gym floor.
Back to what we see all the time—one athlete keeps mechanics sharp and breathing steady, while the other fades early: red face, slumped posture, confusion in the eyes. What you’re noticing is the engine beginning to fail. One engine is responsive; the other is overheating and struggling to convert fuel into power. Scaling won’t fix a failing engine; you have to change what goes into the tank.
When adaptation stalls, it’s usually a fuel problem, not a programming problem. Fasting can help restore insulin sensitivity and reset energy signaling. If you want mitochondria that make power and recover fast, you need adequate protein, sufficient total energy, and food that supports stable blood sugar so training can stay consistent. The principle is the same moving from sick to well as it is from well to fit, but the dose changes: total intake, macros, training load, and recovery have to be fitted for the athlete in front of you.
This is the care and feeding of mitochondria. In MetFix terms, mitochondria are the biological engine behind work capacity across broad time and modal domains. Mitochondria drive metabolism and control capacity—and they’re trainable. Give them a consistent signal and they expand, giving you more capacity to make energy, hold output longer, and recover faster between bouts. Remove the signal and they diminish. The same workout feels harder, breathing spikes sooner, and recovery slows. Coaches measure it with a stopwatch and record it with a whiteboard.
Coach the mitochondria, and you coach both performance and health.
Hollis Molloy is a career coach and Certified CrossFit Level 4 Trainer who served on the CrossFit HQ Seminar Staff from 2007 to 2025 and has owned CrossFit Santa Cruz since 2008. He continues his work as CrossFit Santa Cruz while expanding into MetFix Santa Cruz and serves as a member of the MetFix Academy Staff, teaching and developing education for coaches on metabolic health and performance.
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Great work Hollis! Loved this article!
Perfect. We’ll use this with the students.
Hi Hollis. Your argument that mitochondrial efficiency and fat oxidation are foundational for long‑term health is compelling. The nuance I’d add is that fat oxidation is not a universal starting point. It is a capacity that depends on a network of hormonal, autonomic, mucosal, and neuroimmune systems that vary dramatically between individuals. These differences create distinct physiological phenotypes, and those phenotypes determine whether fat is the preferred fuel under specific training conditions.
Fat oxidation is capacity‑dependent, not choice‑dependent! Even before discussing phenotyping, mainstream physiology shows that fat metabolism is shaped by:
* insulin sensitivity (insulin suppresses lipolysis)
* cortisol and HPA axis tone (stress shifts metabolism toward glycolysis)
* thyroid hormones (T3/T4 regulate mitochondrial throughput)
* catecholamines (mobilize fat but increase sympathetic drive)
* leptin and adiponectin (govern fat‑mass signaling and oxidation efficiency)
* FGF21 (regulates fasting metabolism and mitochondrial switching)
* mTOR/AMPK balance (anabolic vs. catabolic signaling)
* incretin hormones like GLP‑1 (control nutrient sensing and metabolic switching)
* gut integrity and fermentation (SCFA drive endogenous GLP‑1 and fat oxidation)
* neuroimmune activation (inflammation shifts mitochondria toward glycolysis)
NOTE: The above pathways differ widely between individuals. That variability alone makes a universal fat‑dominant model physiologically unrealistic.
Phenotypes determine whether fat is the preferred fuel. Some practitioners use the term Metabolic Type to describe predictable constellations of autonomic tone, oxidation rate, nutrient sensing, and gut‑brain signaling. Whether we call them “Metabolic Types” or simply “physiological phenotypes,” the underlying variability is measurable:
* HRV and cortisol curves reflect autonomic dominance
* SCFA levels and mucosal markers reflect nutrient sensing
* fasting insulin and post‑meal behavior reflect metabolic switching
* thyroid patterns reflect mitochondrial throughput
* leptin and adiponectin reflect fat‑mass signaling
* motility and fermentation patterns reflect gut‑brain communication
These phenotypes explain why some individuals can access fat easily while others physiologically cannot—yet. So fat is not the preferred fuel under all training conditions. Even in metabolically healthy individuals, fat is not the dominant fuel during:
* high‑intensity intervals
* threshold work
* sprinting
* power training
* heavy strength training
* any effort above ~65–75% VO₂max
Fat oxidation cannot meet ATP demand at these intensities. Carbohydrate becomes the preferred fuel by necessity, not by choice. This is a fundamental principle of exercise physiology that seems to be overlooked in most cases. Some phenotypes do not prefer fat even at lower intensities!
There are well‑documented phenotypes where fat is not the efficient or preferred fuel:
* sympathetic‑dominant phenotypes (high cortisol, high catecholamines → glycolytic bias)
* slow‑oxidizer phenotypes (low thyroid, low adiponectin, low SCFA → sluggish fat oxidation)
* high‑insulin phenotypes (insulin blocks lipolysis → carbohydrate reliance)
* neuroimmune phenotypes (inflammation shifts mitochondria toward glycolysis)
* low‑GLP‑1 phenotypes (poor nutrient sensing → impaired metabolic switching)
These individuals do not begin in a fat‑dominant state, and training them as if they do often produces poor outcomes.
The type of exercise that optimizes health therefore varies by phenotype, and a lot of trainers emphasize steady‑state, fat‑dominant, zone‑2‑centric training for all of their clients. This is highly effective for some phenotypes—but not all. There are phenotypes for whom other modalities are more beneficial:
* strength training improves insulin sensitivity, adiponectin, thyroid conversion, and mitochondrial density
* glycolytic intervals improve metabolic flexibility in high‑insulin or low‑thyroid phenotypes
* autonomic repair (breathwork, low‑intensity movement) is essential for sympathetic‑dominant phenotypes
* mixed‑fuel training is necessary for individuals with rigid metabolic switching
* higher‑intensity work is required for those with low mitochondrial throughput
So a one‑size‑fits‑all fat‑dominant approach does not match the physiological diversity seen in real clients. Fat‑dominant metabolism is the destination—not the universal starting point!
Your model describes the ideal end‑state:
* fat for steady output, carbohydrate for intensity, flexible switching.
The question is not whether fat oxidation is desirable—it is. The question is whether a given client is ready for fat‑dominant metabolism today. Some are. Many are not—until autonomic, mucosal, incretin, thyroid, or neuroimmune bottlenecks are resolved.
A readiness‑based model doesn’t contradict your framework; it completes it. It explains the real‑world variability that trainers and clinicians see every day and provides a physiological basis for why two people doing the same workout can look metabolically worlds apart.